Uncommon Descent Serving The Intelligent Design Community

Homologies, differences and information jumps

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

shark-553666_1280In recent posts, I have been discussing some important points about the reasonable meaning of homologies and differences in the proteome in the course of natural history. For the following discussion, just to be clear, I will accept a scenario of Common Descent (as explained in many recent posts) in the context of an ID approach. I will also accept the very reasonable concept that neutral or quasi-neutral random variation happens in time, and that negative (purifying) selection is the main principle which limits random variation in functional sequences.

My main points are the following:

  1. Given those premises, homologies through natural history are certainly an indicator of functional constraints, because they mean that some sequence cannot be significantly transformed by random variation. Another way to express this concept is that variation in a functional sequence with strong functional constraints is not neutral, but negative, and therefore negative selection will in mot cases suppress variation and conserve the functional sequence through time. This is a very important point, because it means that strong homologies through time point to high functional complexity, and therefore to design. I have used this kind of argument, for example, for proteins like the beta chain of ATP synthase (highly conserved from LUCA to humans) and Histone H3 (highly conserved in all eukaryotes).
  2. Differences between homologues, instead, can have two completely different meanings:
  •  2a) They can be the result of accumulating neutral variation in parts of the molecule which are not functionally constrained
  • 2b) They can be the expression of differences in function in different species and contexts

I do believe that both 2a and 2b happen and have an important role in shaping the proteome. 2b, in particular, is often underestimated. It is also, in many cases, a very good argument for ID.

 

Now, I will try to apply this reasoning to one example. I have chosen a regulatory protein, one which is not really well understood, but which has certainly an important role in epigenetic regulation. The protein is called “Prickle”, and we will consider in particular the one known as “Prickle 1”. It has come to my attention trough an interesting paper linked by Dionisio (to whom go my sincere thanks and appreciation):

Planar polarization of Vangl2 in the vertebrate neural plate is controlled by Wnt and Myosin II signaling

In brief, Prickle is a molecule implied, among other things, in planar polarization events and in the regulation of neural system in vertebrates.

Let’s have a look at the protein. From Wikipedia:

Prickle is part of the non-canonical Wnt signaling pathway that establishes planar cell polarity.[2] A gain or loss of function of Prickle1 causes defects in the convergent extension movements of gastrulation.[3] In epithelial cells, Prickle2 establishes and maintains cell apical/basal polarity.[4] Prickle1 plays an important role in the development of the nervous system by regulating the movement of nerve cells.[5

And:

Mutations in Prickle genes can cause epilepsy in humans by perturbing Prickle function.[12] One mutation in Prickle1 gene can result in Prickle1-Related Progressive Myoclonus Epilepsy-Ataxia Syndrome.[2] This mutation disrupts the interaction between prickle-like 1 and REST, which results in the inability to suppress REST.[2] Gene knockdown of Prickle1 by shRNA or dominant-negative constructs results in decreased axonal and dendritic extension in neurons in the hippocampus.[5] Prickle1 gene knockdown in neonatal retina causes defects in axon terminals of photoreceptors and in inner and outer segments.[5]

The human protein is 831 AAs long.

Its structure is interesting: according to Uniprot, in the first part of the molecule we can recognize 4 domains:

1 PET domain:  AAs 14 – 122

3 LIM zinc-binding doamins:  AAs 124 – 313

In the rest of the sequence (AAs 314 – 831) no known domain is recognized.

Here is the FASTA sequence of the human protein, divided in the two parts (red: 4 domain part; blue: no domain part):

 

>sp|Q96MT3|PRIC1_HUMAN Prickle-like protein 1 OS=Homo sapiens GN=PRICKLE1 PE=1 SV=2
MPLEMEPKMSKLAFGCQRSSTSDDDSGCALEEYAWVPPGLRPEQIQLYFACLPEEKVPYV
NSPGEKHRIKQLLYQLPPHDNEVRYCQSLSEEEKKELQVFSAQRKKEALGRGTIKLLSRA
VMHAVCEQCGLKINGGEVAVFASRAGPGVCWHPSCFVCFTCNELLVDLIYFYQDGKIHCG
RHHAELLKPRCSACDEIIFADECTEAEGRHWHMKHFCCLECETVLGGQRYIMKDGRPFCC
GCFESLYAEYCETCGEHIGVDHAQMTYDGQHWHATEACFSCAQCKASLLGCPFLPKQGQI
YCSKTCSLGEDVHASDSSDSAFQSARSRDSRRSVRMGKSSRSADQCRQSLLLSPALNYKF
PGLSGNADDTLSRKLDDLSLSRQGTSFASEEFWKGRVEQETPEDPEEWADHEDYMTQLLL
KFGDKSLFQPQPNEMDIRASEHWISDNMVKSKTELKQNNQSLASKKYQSDMYWAQSQDGL
GDSAYGSHPGPASSRRLQELELDHGASGYNHDETQWYEDSLECLSDLKPEQSVRDSMDSL
ALSNITGASVDGENKPRPSLYSLQNFEEMETEDCEKMSNMGTLNSSMLHRSAESLKSLSS
ELCPEKILPEEKPVHLPVLRRSKSQSRPQQVKFSDDVIDNGNYDIEIRQPPMSERTRRRV
YNFEERGSRSHHHRRRRSRKSRSDNALNLVTERKYSPKDRLRLYTPDNYEKFIQNKSARE
IQAYIQNADLYGQYAHATSDYGLQNPGMNRFLGLYGEDDDSWCSSSSSSSDSEEEGYFLG
QPIPQPRPQRFAYYTDDLSSPPSALPTPQFGQRTTKSKKKKGHKGKNCIIS

So, this is a very interesting situation, which is not so rare. We have the first part of the sequence (313 AAs) which configures well known and conserved domains, while “the rest”(517 AAs)  is apparently not understood in terms of structure and function.

So, to better understand what all this could mean, I have blasted those two parts of the human molecule separately.

(Those who are not interested in the technical details, can choose here to go on to the conclusions  🙂 )

The first part of the sequence (AAs 1 – 313) shows no homologies in prokaryotes. So, we are apparently in the presence of domains which appear in eukaryotes.

In fungi, we find some significant, but weak, homologues. The best hit is an expect of 2e-21, with 56 identities and 93 positives (99.4 bits).

Multicellular organisms have definitely stronger homologies:

C. elegans:  144 identities, 186 positives, expect 2e-90 (282 bits)

Drosophila melanogaster:  202 identities, 244 positives, expect 5e-152 (447 bits)

Let’s go to non vertebrate chordates:

Cephalochordata (Branchiostoma floridae):  222 identities, 256 positives, expect 6e-165 (484 bits)

Tunicata (Ciona intestinalis): 196 identities, 241 positives, expect 2e-149 (442 bits)

Now, vertebrates:

Cartilaginous fishes (Callorhincus milii): 266 identities, 290 positives, expect 0.0 (588 bits)

Bony fishes (Lepisosteus oculatus): 274 identities, 292 positives, expect 0.0 (598 bits)

Mammals (Mouse): 309 identities, 312 positives, expect 0.0 (664 bits)

IOWs, what we see here is that the 4 domain part of the molecule, absent in prokaryotes, is already partially observable in single celled eukaryotes, and is strongly recognizable in all multicellular beings. It is interesting that homology with the human form is not very different between drosophila and non vertebrate chordates, while there is a significant increase in vertebrates, and practical identity already in mouse. That is a very common pattern, and IMO it can be explained as a mixed result of different functional constraints and neutral evolution in different time splits.

Now, let’s go to “the rest” of the molecule: AAs 314 – 831 (518 AAs). No recognizable domains here.

What is the behaviour of this sequence in natural history?

Again, let’s start again from the human sequence and blast it.

With Prokaryotes: no homologies

With Fungi: no homologies

C. elegans: no homologies

Drosophila melanogaster: no homologies

Let’s go to non vertebrate chordates:

Cephalochordata (Branchiostoma floridae):  no significant homologies

Tunicata (Ciona intestinalis): no significant homologies

So, there is no significant homology in the whole range of eukaryotes, excluding vertebrates and including chordates which are not vertebrates.

Now, what happens with vertebrates?

Here are the numbers:

Cartilaginous fishes (Callorhincus milii): 350 identities, 429 positives, expect 0.0 (597 bits)

Bony fishes (Lepisosteus oculatus): 396 identities, 446 positives, expect 0.0 (662 bits)

Mammals (Mouse): 466 identities, 491 positives, expect 0.0 (832 bits)

IOWs, what we see here is that the no domain part of the molecule is practically non existent in prokaryotes, in single celled eukaryotes and in all multicellular beings which are not vertebrates. In vertebrates, the sequence is not only present in practically all vertebrates, but it is also extremely conserved, from sharks to humans. So, we have a steep informational jump from non chordates and non vertebrate chordates, where the sequence is practically absent, to the very first vertebrates, where the sequence is already highly specific.

What does that mean from an ID point of view? It’s simple:

a) The sequence of 517 AAs which represents the major part of the human protein must be reasonably considered highly functional, because it is strongly conserved throughout vertebrate evolution. As we have said in the beginning, the only reasonable explanation for high conservation throughout a span of time which must be more than 400 million years long is the presence of strong functional constraints in the sequence.

b) The sequence and its function, whatever it may be (but it is probably an important regulatory function) is highly specific of vertebrates.

We have here a very good example of a part of a protein which practically appears in vertebrates while it is absent before, and which is reasonably highly functional in vertebrates.

So, to sum up:

  1. Prickle 1 is a functional protein which is found in all eukaryotes.
  2. The human sequence can be divided in two parts, with different properties.
  3. The first part, while undergoing evolutionary changes, is rather well conserved in all eukaryotes. Its function can be better understood, because it is made of known domains with known structure.
  4. The second part does not include any known domain or structure, and is practically absent in all eukaryotes except vertebrates.
  5. In vertebrates, it is highly conserved and almost certainly highly functional. Probably as a regulatory epigenetic sequence.
  6. For its properties, this second part, and its functional sequence, are a very reasonable object for a strong design inference.

 

I have added a graph to show better what is described in the conclusions, in particular the information jump in vertebrates for the second part of the sequence:

Graph3

Note: Thanks to the careful checking of Alicia Cartelli, I have corrected a couple of minor imprecisions in the data and the graph (see posts #83 and #136). Thank you, Alicia, for your commitment. The sense of the post, however, does not change.

Those who are interested in the evolutionary behaviour of protein Prickle 2 could give a look at my posts #127 and #137.

Comments
@975: the genetic pathways active along the proximodistal, anteroposterior, and dorsoventral axes of cephalopod limbs are homologous (specifically, orthologous) to the networks that regulate limb development in arthropods and vertebrates. Hh signaling could regulate the number of sucker rows along the anteroposterior axis of cephalopod limbs, similar to the manner in which Hh specifies digit number along the anteroposterior axis of vertebrate limbs our discovery that cephalopod arms and tentacles evolved by parallel recruitment of the same genetic program that orchestrates appendage formation in arthropods and vertebrates suggests that this program was present in the bilaterian common ancestor. the ancestral appendage developmental program was not a latent developmental feature that was redeployed each time that limbs evolved, but rather it might have been a continuously activated network that controlled formation of outgrowths in general. This raises the question of whether other foot-derived outgrowths/appendages (e.g., in sea slugs) evolved by co-option of the same developmental program that cephalopods, arthropods, and vertebrates use to build appendages. Although the results presented here suggest that an ancient and conserved developmental genetic program facilitated the origin of cephalopod limbs, they also indicate that fine-scale regulatory changes may have played a role in the diversification of cephalopod limb morphologies. Finally, we note that while the data presented here point to the existence of a deeply conserved genetic program for appendage development across Bilateria, this does not imply that the limbs of cephalopods, arthropods, and vertebrates are homologous structures, or that limbs were present in the common ancestor. Rather, these results show that homologous developmental mechanisms underlie the multiple parallel origins of limbs in bilaterians. Evolution of limb development in cephalopod mollusks Oscar A Tarazona,1,2 Davys H Lopez,1 Leslie A Slota,2 and Martin J Cohn1,2 eLife. 2019; 8: e43828. doi: 10.7554/eLife.43828 OLV
20 years later? Field Homology: Still a Meaningless Concept Briscoe S.D. Brain Behav Evol 2019;93:1–3 DOI:10.1159/000500770 https://www.karger.com/Article/FullText/500770 Field homology: a meaningless concept. Northcutt RG Eur J Morphol. 1999 Apr;37(2-3):95-9. OLV
It would be very interesting to see if any protein information jumps were required in these cases: Evolution of limb development in cephalopod mollusks Oscar A Tarazona,1,2 Davys H Lopez,1 Leslie A Slota,2 and Martin J Cohn1,2 eLife. 2019; 8: e43828. doi: 10.7554/eLife.43828 OLV
Homology in Development and the Development of the Homology Concept Manfred D. Laubichler Integrative and Comparative Biology, Volume 40, Issue 5, October 2000, Pages 777–788, DOI: 10.1093/icb/40.5.777 Homology: A Concept in Crisis (?) http://www.arn.org/docs/odesign/od182/hobi182.htm OLV
Homology, neocortex, and the evolution of developmental mechanisms Steven D. Briscoe, Clifton W. Ragsdale Science 12 Oct 2018: Vol. 362, Issue 6411, pp. 190-193 DOI: 10.1126/science.aau3711 The six-layered neocortex of the mammalian pallium has no clear homolog in birds or non-avian reptiles. Recent research indicates that although these extant amniotes possess a variety of divergent and nonhomologous pallial structures, they share a conserved set of neuronal cell types and circuitries. These findings suggest a principle of brain evolution: that natural selection preferentially preserves the integrity of information-processing pathways, whereas other levels of biological organization, such as the three-dimensional architectures of neuronal assemblies, are less constrained. We review the similarities of pallial neuronal cell types in amniotes, delineate candidate gene regulatory networks for their cellular identities, and propose a model of developmental evolution for the divergence of amniote pallial structures. OLV
You said, Origenes: The microRNA genetic sequences do not fall into the expected common descent pattern. We noted that the differences are explained by loss of miRNA over evolutionary history. You then responded @963 to Thomson et al. by waving your hands. Are you trying to say that miRNA can't be lost? Zachriel
Zachriel, when I wrote:
Origenes: Invoking selective and total extinction of all the intermediate forms of a sequence in natural history, without offering any specifics, is not handwaving but constitutes valid criticism of Gpuccio’s argument?
I was obviously talking about your "valid criticism" of Gpuccio's argument — not about Thomson et al, which is unrelated to Gpuccio's argument. So, your reply:
Zachriel: They did offer specifics. Did you read the paper?
doesn't make any sense. Origenes
Origenes: Invoking selective and total extinction of all the intermediate forms of a sequence in natural history, without offering any specifics, is not handwaving They did offer specifics. Did you read the paper? They statistically analyzed RNA datasets showing that RNA losses constitute between about a third of the implied evolutionary changes. While the study isn't conclusive, caution in interpreting the data is certainly warranted. You latch onto anything that supports your claim, while disregarding anything that undermines it. Eugene: What is this hierarchy but a mental concept? So is "round". Eugene: I can informally say that seeing that the sun is “round” is indeed an observation. So? It means that recognizing a pattern is a type of observation. If you look at a wolf and a mouse, do you observe they both have hair? It's clear that all observations are theory-laden. The question seems to be whether the nested hierarchy is something "real" or whether it is an artifact of classification. Zachriel
Zachriel, The sun is not a circle. Nor is it like a circle because it is 3D. With these corrections, I can informally say that seeing that the sun is "round" is indeed an observation. So? Are you saying that it is the same as biological taxonomy? A hierarchy assumes not only an observation of a single event or object (as in the example of observing that the sun is round), it also represents relations between multiple objects, which is not the same as observing that the sun is "round". This is because in contrast to the direct observation of the sun, in the case of taxonomy, you are using theoretical abstractions. So a hierarchy in biology is a mathematical concept. One can easily do an isomorphic transform of the hierarchy without changing the actual objects or relations this hierarchy represents. What is this hierarchy but a mental concept? Can you see, hear, touch, taste or smell it? Can you measure it? When you see a beetle, you do not directly observe its place in the hierarchy, do you? What you observe is only its own properties (body plan, colour, size, etc.). You placing it in a hierarchy is a mental exercise. In a word, a hierarchy is not a (direct) observation but depends upon a theory. EugeneS
Zachriel: Still not a valid criticism of Thomson et al.
Invoking selective and total extinction of all the intermediate forms of a sequence in natural history, without offering any specifics, is not handwaving but constitutes valid criticism of Gpuccio's argument? You are a joke. ---- BTW I did not criticize Thomson et al. Origenes
EugeneS: This does not change the mathematical truth that a sphere is an ellipsoid We used scare-quotes @960, and it's clear you are avoiding an answer. We're talking about someone looking up in the sky and seeing the sun. Do they see that it is round? Is recognizing a pattern an observation? round, shaped like or approximately like a circle All observations are theory-laden, even something as simple as noting the existence of an object. However, most uses of the word observation include recognizing objects and patterns. Origenes, Still not a valid criticism of Thomson et al. Zachriel
Zachriel: Handwaving. If you have an objection, you have to grapple with the specifics.
Wow it's a bit rich coming from you don't you think? Origenes
Zachriel, "The sun's diameter only varies about ten parts per million." This does not change the mathematical truth that a sphere is an ellipsoid: x^2/a^2 + y^2/b^2 + z^2/c^2 = 1 with a = b = c. "You did not answer the question". I have stated what I think quite clearly. I showed you that you haven't got an understanding of the scientific method because you cannot distinguish an observation/data from a scientific model. You can try and answer yourself your silly question about roundness. First though define 'roundness' empirically without invoking mathematical models. Because this discussion is digressing more and more from the OP, I'd rather stop here. I can see no benefit in continuing it, Zachriel. EugeneS
Origenes: Translation: The data used so far doesn’t fit. Handwaving. If you have an objection, you have to grapple with the specifics. Origenes: Translation: Nope! MicroRNA also doesn’t fit. So, don’t use microRNA genetic sequences when you seek support for the tree of life. Handwaving. If you have an objection, you have to grapple with the specifics. Zachriel
Zachriel,
“Recent progress in resolving the tree of life continues to expose relationships that resist resolution, which drives the search for novel sources of information (...).” [Thomson et al.]
Translation: The data used so far doesn't fit. We need to try something else. >> Hey guys, how about microRNA?
“Our results indicate that miRNA data have far less phylogenetic utility in resolving the tree of life than is currently recognized and we urge ample caution in their interpretation.” [Thomson et al.]
Translation: Nope! MicroRNA also doesn't fit. So, don't use microRNA genetic sequences when you seek support for the tree of life. >> Ok, got it. Origenes
EugeneS: I would say that the geometric form of the sun can be approximated by an ellipsoid (not a circle, btw). The sun's diameter only varies about ten parts per million. You didn't answer the question. Is seeing the roundness of the sun an observation? Scientist writing in notebook: • Monday, Sun is round. • Tuesday, Sun is round. • Wednesday, Sun is round. -- Edited for clarity. Zachriel
I would say that the geometric form of the sun can be approximated by an ellipsoid (not a circle, btw). When you characterize something using abstractions you are not observing already, you are reasoning. Characterization is classification. When the hand of a meter is showing voltage, you are observing. Observation finishes as soon as you are making statements about the observation (voltage high or low), in particular making specific predictions (high voltage will lead to a fuse burning out). EugeneS
Origenes: The microRNA genetic sequences do not fall into the expected common descent pattern. MicroRNAs form a nested hierarchy. The nested hierarchy of microRNAs is not completely different from traditional hierarchies (e.g. mammals are still nested within vertebrates), but does differ in many places. Many of these differences are due to incomplete lineage sorting and microRNAs dropping out of genomes. See Thomson et al., Estimating Phylogeny from microRNA Data: A Critical Appraisal, PNAS 2014: "Our results indicate that miRNA data have far less phylogenetic utility in resolving the tree of life than is currently recognized and we urge ample caution in their interpretation." EugeneS: The sun is a thing. If you want to be pedantic, the observation is sensation and memory. An object is a conjecture of the mind based on the persistence of the sensation. In any case, would you say the sun is "round"? That is, it forms a "circle"? Or do you think it is not an observation? And the sun's movement across the sky? Is this not an "arc"? Or is this not an observation too? Zachriel
Zachriel, "So is an ellipse. Are you saying that when we see the sun move across the sky that this is not an observation? More facepalm. The sun is a thing. An ellipse is a mental (mathematical) generalization, i.e. a concept. A primary school student could tell you what is wrong in what you post here. A thing objectively exists and does not care what we call it, an ellipsoid or a cube nor how we relate it to other things. Classification is a mental activity. Read a book. This time a relevant one though ;) EugeneS
Zachriel: What you mean is that the nested hierarchy is not observed in every instance. However, the overall pattern remains.
No, that's not what I mean.
The microRNA genetic sequences do not fall into the expected common descent pattern. That is, when compared across different species, microRNAs do not align with the evolutionary tree. As one scientist explained, “I've looked at thousands of microRNA genes and I can't find a single example that would support the traditional [evolutionary] tree.” (Dolgin) While there remain questions about these new phylogenetic data, “What we know at this stage,” explained another evolutionist, “is that we do have a very serious incongruence.” In other words, different types of data report very different evolutionary trees. The conflict is much greater than normal statistical variations. “There have to be,” added another evolutionist, “other explanations.” One explanation is that microRNAs evolve in some unexpected way. Another is that the traditional evolutionary tree is all wrong. Or evolutionists may consider other explanations. But in any case, microRNAs are yet another example of evidence that does not fit evolutionary expectations. Once again, the theory will need to be modified in complex ways to fit the new findings. more ...
Origenes
bill cole: Based on observation it is a way to organize the observations contingent on a mechanism that would validate the hypothesis? The nested hierarchy exists regardless of any explanatory framework. There are specific correlations. For instance, having hair and mammary glands correlates with bellows lungs. EugeneS: A hierarchy is a mental concept So is an ellipse. Are you saying that when we see the sun move across the sky that this is not an observation? Origenes: The nested hierarchy is an observation [hypothesis] that leads to specific and verifiable empirical predictions. What you mean is that the nested hierarchy is not observed in every instance. However, the overall pattern remains. Zachriel
Zachriel: The nested hierarchy is an observation [hypothesis] that leads to specific and verifiable empirical predictions.
Indeed, here are those predictions — each of them has failed: Genomic features are not sporadically distributed. Gene and host phylogenies are congruent. Gene phylogenies are congruent. The species should form an evolutionary tree. Origenes
Zachriel, Facepalm. Your indoctrination stops you from distinguishing clearly between what is given in observation, what is assumed, and what is deduced. A hierarchy is a mental concept, Zachriel. Natural phenomena don't care if they fit into a hierarchy or not. We cannot observe a hierarchy. Again you confuse the map with the territory. Typical of evolutionists' wishful thinking ;) You conflate artificial selection with natural selection. In situ evolution can only cause oscillations around already existing functional attractors. Complex functional novelty (attractors) can only be achieved by design. It is so in practice and it is so in theory (never mind the scientifically sterile ToE). Your examples with Galileo only obfuscate the truth. If you demonstrated (not hypothesised or posited) an evolutionary path to at least a single novel protein, that would have been a different matter. As of today, you have no case. The key point in getting a functional system of any sort is intelligent design. Simply because inanimate nature does not care about function. Function is already a pointer to design because the key thing in being functional is "in order to" i.e. teleology, foresight, which is non-existent in inanimate nature. Function's subsequent evolvability is irrelevant. EugeneS
Z
No. The nested hierarchy is an observation. Common descent is the hypothesis. While the latter may or may not be true, the former is an observation of the distribution of traits.
Would you say it is an observation? Based on observation it is a way to organize the observations contingent on a mechanism that would validate the hypothesis? bill cole
EugeneS: They artificially steer events in the test tube towards a goal and then declare it a result of natural events. And Galileo artificially dropped stones from the Tower of Pisa. Some experiments are in nature, some in the lab. Each experiment reveals some aspect or other of evolution. In particular, some lab experiments select for function, but don't design the particular structures. The pathways have to be selectable. Some lab experiments simply allow organisms to evolve on their own, though the environment is obviously artificial. That's what we mean by "in the lab". Still other experiments simply observe nature. EugeneS: A hierarchy is not an observation, it is a result of human classification (i.e., fundamentally, a theory). No more than observing a planet trace an elliptical orbit is a result of human classification. Rather, the nested hierarchy refers to specific and predictable correlations between traits. EugeneS: we then formulate a theory to propose an interpretation of scientific observations (an example of such an interpretation is a nested hierarchy) No. The nested hierarchy is an observation. Common descent is the hypothesis. While the latter may or may not be true, the former is an observation of the distribution of traits. EugeneS: The theory of evolution as it stands completely fails to account for huge sudden increases of complex functional information in living systems. Sudden, as in millions of years; spans of time so vast that they defy simple human comprehension. EugeneS: Are you saying ToE is not falsifiable because a direct observation would take millions of years? No. Simply that your proposed observation is precluded by the Theory of Evolution. In other words, a strawman. There are many other observations that would falsify evolution that doesn't require millions of years of observations. Zachriel
Wait a minute, Zachriel. "The Theory of Evolution posits that complex macroevolution takes place over millions of years, so a direct observation would be a falsification of the Theory of Evolution." Did you read what you had typed? Are you saying ToE is not falsifiable because a direct observation would take millions of years? EugeneS
"That’s not what evolution experiments do." It is exactly what some of them do, Zachriel. They artificially steer events in the test tube towards a goal and then declare it a result of natural events. That is complete fraud. Fortunately, not every researcher is like that. "The nested hierarchy is an observation." No, completely wrong. A hierarchy is not an observation, it is a result of human classification (i.e., fundamentally, a theory). What you observe is natural phenomena. Given specific useful metrics, we can reason about natural phenomena by formulating theories. E.g. we can observe protein molecules in different organisms, measure and compare them. Consider protein structure homology. Based on observations and on assumptions (such as common descent), we then formulate a theory to propose an interpretation of scientific observations (an example of such an interpretation is a nested hierarchy) and predict future observations (such as future discovered species will be within an existing hierarchy). "We were referring to human design." The theory of evolution as it stands completely fails to account for huge sudden increases of complex functional information in living systems. The only reliably empirically known source of complex functional information is design, as I am sure you know. Why only human? What about animals who surely can design nests, develop hunting or escape tactics, can communicate with one another and consequently use code, train their young, etc.?! EugeneS
EugeneS: Phylogeny is not evidence, it is an interpretation. The nested hierarchy is an observation that leads to specific and verifiable empirical predictions. EugeneS: There are no direct observations of macroevolution. The Theory of Evolution posits that complex macroevolution takes place over millions of years, so a direct observation would be a falsification of the Theory of Evolution. On the other hand, we have ample evidence of intermediates for many complex structures, supporting the Theory of Evolution. EugeneS: If you allude to co-optation, it is irrelevant. No. We were referring to human design. "Hold this here until I can nail it together." Zachriel
"In design, we often hold pieces into place where they have no function, until we can affix all the necessary parts. That’s not what evolution experiments do." If you allude to co-optation, it is irrelevant. The switching between functions is a function in itself, which must be assumed for co-optation to be feasible. Intelligence must already be present in the system for co-optation to occur. That kills the argument completely. I never liked Ken Miller's argumentation. EugeneS
Zachriel: I like you when you are explicitly repetitive! :) Alicia: As Mung says: Good to have you back. gpuccio
Zachriel You have no evidence. Phylogeny is not evidence, it is an interpretation. There are no direct observations of macroevolution. What can be observed is nowhere near Darwinian grand claims. EugeneS
EugeneS: You must be joking. No. Zachriel
"direct observations of evolution" You must be joking. EugeneS
Alicia Cartelli: I’m impressed at your stupidity. And we're impressed by your being impressed at our stupidity! And we've missed your brilliant mind. Good to have you back. Mung
EugeneS: What I am saying is simply that {evolution} cannot do much in the wild. Yes, that's your claim. EugeneS: In most cases of studies in the lab they are trying to sell artificial selection (guided search and active control) for natural selection (unguided search and passive control by elimination). In design, we often hold pieces into place where they have no function, until we can affix all the necessary parts. That's not what evolution experiments do. EugeneS: In order to produce statistically significant information gains in reality intelligence is absolutely needed. It does not happen otherwise. Yes, that's your claim. However, the evidence from phylogeny, and direct observations of evolution, both natural and artificial, contradict your claim. Zachriel
Zachriel, You are ramming through an open door (or preaching to the choir, whichever you like more). I do not deny the phenomenon of evolution. What I am saying is simply that it cannot do much in the wild. In most cases of studies in the lab they are trying to sell artificial selection (guided search and active control) for natural selection (unguided search and passive control by elimination). In order to produce statistically significant information gains in reality intelligence is absolutely needed. It does not happen otherwise. EugeneS
EugeneS: Under this OR there is ample room for philosophical maneuvering. Someone does a clever experiment involving active search and control of a system to steer it towards a goal state and then conveniently labels it ‘evolution demonstrated in action’. The definition concerned selection. Evolution is a process involving variation and selection. Biological evolution is an instance of this process. Origenes: where did these well-wrought fitness landscapes come from From symmetry. gpuccio: 1) You seem to agree that Szostak’s results do not apply to the “larger non experimental world”. The experiment shows that proteins are rare in sequence space but not exceedingly so, and that there are selectable pathways to improved function. The actual biological process probably didn't start from random sequences, but from already structured peptides. gpuccio: 2) Hayashi’s results apply to the “larger non experimental world” for what they are. They show that RV and NS can partially retrieve a function which has been artificially compromised, but not completely, but that they cannot retrieve the highly functional wildtype sequence. The experiment shows that proteins are rare in sequence space but not exceedingly so, and that there are selectable pathways to improved function. The actual biological process probably didn't start from random sequences, but from already structured peptides. gpuccio: 3) Stop equivocationg on the word “function”. ID is not about any impossibility of “novel function” to evolve, as you seem to imply. ID is, and always has been, about the impossibility of “new original complex function” A protein is complex, though certainly not a complex as a protein complex. gpuccio: It started as an ATP-binding protein, and ended as a strongly ATP-binding protein. That's right. The experiment shows that proteins are rare in sequence space but not exceedingly so, and that there are selectable pathways to improved function. The actual biological process probably didn't start from random sequences, but from already structured peptides. Zachriel
Wow you guys have dragged things on for this long? I'm impressed at your stupidity. To add to the stupidity: “simple ATP binding does not provide any advantage” “Simple ATP binding is completely useless, and it subtracts ATP to the environment.” “They don’t, and you seem to agree that a weak ATP binding is no advantage to a living cell.” {“(it binds ATP, whcih can be defined as a function), but in no way is biologically functional, least of all naturally selectable (even in its “evolved” form, it does not confer any reproductive advantage).” “The final protein was still biologically useless, and not naturally selectable.” I’ll argue against any one of these statements. Alicia Cartelli
Zachriel: "It *started* as an ATP-binding protein, the experiment shows there is a selectable pathway to improved function." It started as an ATP-binding protein, and ended as a strongly ATP-binding protein. The only function which was improved was ATP binding. The final protein was still biologically useless, and not naturally selectable. gpuccio
Zachriel: So, let me understand: 1) You seem to agree that Szostak's results do not apply to the “larger non experimental world”. Then why do you and others continuously quote them in defense of your theory? Those results are not pertinent. If you were defending the esistence and validity of protein engineering, you would be welcome to quote that paper. As you are defending neo darwinism, which requires naturally selectable functions, you are not. 2) Hayashi's results apply to the “larger non experimental world” for what they are. They show that RV and NS can partially retrieve a function which has been artificially compromised, but not completely, but that they cannot retrieve the highly functional wildtype sequence. 3) Stop equivocationg on the word "function". ID is not about any impossibility of "novel function" to evolve, as you seem to imply. ID is, and always has been, about the impossibility of "new original complex function" to evolve in the absence of conscious intelligent intervention. Please, try to criticize our theory for what it is, not for what is convenient for you. gpuccio
Zachriel: (...) the effectiveness of evolution depends on the shape of the fitness landscape.
If mutation, recombination, and selection only work well on certain kinds of fitness landscapes, yet most organisms are sexual, and hence use recombination, and all organisms use mutation as a search mechanism, where did these well-wrought fitness landscapes come from, such that evolution manages to produce the fancy stuff around us? (...) No one knows. ['Investigations', Kauffman]
Origenes
Zachriel, "a natural or artificial process" A big OR indeed. Under this OR there is ample room for philosophical maneuvering. Someone does a clever experiment involving active search and control of a system to steer it towards a goal state and then conveniently labels it 'evolution demonstrated in action'. If one decides though to make a clear distinction between the two kinds of selection, there is a lot less left for evolution. Mung, Yes, an oxymoron it is indeed. Another popular evolutionary oxymoron is the phrase "natural process" ;) EugeneS
What happens in Zachriel's program is directed evolution, which is itself an oxymoron. Mung
EugeneS: Will you say there is a selectable path from wheat flour to the pie? Selection, meaning "a natural or artificial process that results or tends to result in the survival and propagation of some individuals or organisms but not of others with the result that the inherited traits of the survivors are perpetuated", doesn't apply to your example. The closest would be someone saying there's no way that flour (or, for comparison, feces) can make a pie, and someone providing a recipe (or not). Zachriel
Zachriel, "There is a selectable path". Selectable by whom? You are playing word games again. Again you conflate natural with artificial selection. E.g. 1. Take 1 glassful of wheat flour. 2. Take 1 egg. 3. Add a pinch of salt. 4. Add a bit of sugar. 5. Mix together. 6. Put in the oven. 7. Bake for 5 minutes at 150 degrees. 8. Take the baked pie out of the oven and serve. Will you say there is a selectable path from wheat flour to the pie? EugeneS
gpuccio: The “larger non experimental world” is not endowed with columns selecting ATP binding molecules. It can select ATP binding molecules only if they confer a reproductive advantage. No ones says that the artificial ATP-binding molecule would provide a reproductive advantage in an organism. Why would you think that? Certainly Szostak never made that claim. gpuccio: Must I remind you that Hayashi’s main result is that he could not find the wildtype functional form in his experimental context? But it provides a reproductive advantage, which you just said was definitive. gpuccio: Szostak found a pathway from some rare random sequences, appropriately selected artificially (see previous post) to an ATP binding protein It *started* as an ATP-binding protein, the experiment shows there is a selectable pathway to improved function. gpuccio: Nylonase “evolved” from penicillinases. And so? It shows that novel functions can evolve. Zachriel
Zachriel: "There are selectable pathways from random sequences to functional proteins. Novel functions can evolve from existing proteins, such as nylonase. Proteins form into families, indicating that they share common ancestors." Which pathways? Szostak found a pathway from some rare random sequences, appropriately selected artificially (see previous post) to an ATP binding protein which may be functional in a large sense (it binds ATP, whcih can be defined as a function), but in no way is biologically functional, least of all naturally selectable (even in its "evolved" form, it does not confer any reproductive advantage). Nylonase "evolved" from penicillinases. And so? We have a few examples of molecular microevolution such as that. Lenski's Cit+ is another example. Must I remind you that the problem is complex functionality, and that a pathway should be something which generates complexity through stepwise simple variation? Isolated examples of simple variation, which is no way build new complex functions, are no example of "pathways". Finally, while it is certainly possible that some protein families share a common ancestor, there is no evidence of that for the 2000 superfamilies which constitute the observable proteome. gpuccio
Zachriel: "You don’t apply your own instruction, but merely wave your hands. You have to show why the results, or the results of Hayashi et al., do not apply in the larger non-experimental world." I have done that repeatedly. Just because you don't agree, it does not mean that I have not done it. For the Szostak case, it's very simple. The "larger non experimental world" is not endowed with columns selecting ATP binding molecules. It can select ATP binding molecules only if they confer a reproductive advantage. They don't, and you seem to agree that a weak ATP binding is no advantage to a living cell. Therefore, Szostak's results do not apply to the "larger non experimental world". Hayashi is a competely different context, and has completely different meanings. Again, we have discussed it in detail. Must I remind you that Hayashi's main result is that he could not find the wildtype functional form in his experimental context? gpuccio
EugeneS: all you have to do is demonstrate that selectable paths exist between different proteins. There are selectable pathways from random sequences to functional proteins. Novel functions can evolve from existing proteins, such as nylonase. Proteins form into families, indicating that they share common ancestors. Zachriel
Now, Zachriel, all you have to do is demonstrate that selectable paths exist between different proteins. Good luck! EugeneS
EugeneS: Function must exist before it is naturally selected. That is correct. EugeneS: Complex functions cannot be created by random modification from existing ones. That is incorrect. Evolution doesn't search the entire landscape, but only those regions that are connected. Consequently, the effectiveness of evolution depends on the shape of the fitness landscape. Zachriel
Zachriel has no argument, only say-so and hand waving. Function must exist before it is naturally selected. Natural selection is an informationfilter so cannot create new information. Consequently it isonly chance thatthey have at their disposalto create information with. Cmplex functions cannot be created by random modification from existing ones. Therefore probabilistic barriers do exist. In the real world the only source of statistically significant amounts of novelty is intelligence. That is supported by observation. EugeneS
EugeneS: Perhaps, a most striking illustration of such conflation was in an interview by Robert Pennock (Michigan State Uni) who was quoted as saying that the famous computer project Avida was not a simulation but an example of evolution. It is an example of evolution, but not a simulation of biological evolution. Zachriel
"That’s something very easy to demonstrate in silico." All evolutionists conflate intelligent artificial selection with natural selection. Perhaps, a most striking illustration of such conflation was in an interview by Robert Pennock (Michigan State Uni) who was quoted as saying that the famous computer project Avida was not a simulation but an example of evolution. Whereas, in fact, even a simulation would be a huge exaggeration. EugeneS
EugeneS: Says who? That's something very easy to demonstrate in silico. gpuccio: I am strongly reminding you that, when we derive conclusions from experiments, we have to be fully aware of the meaning of those restrictions, and of how they influence the results. Sure. Let's see how you apply that instruction. gpuccio: “On the other hand, you should be honest enough to admit that there is no evidence that proteins with a naturally selectable function exist in random libraries, at least at reasonable library sizes. Papers like Szostak’s do not support such a conclusion in any way.” You don't apply your own instruction, but merely wave your hands. You have to show why the results, or the results of Hayashi et al., do not apply in the larger non-experimental world. Querius: what are the chances that you’ll ever get a straight answer from Zachriel regarding the selective advantage of ATP? ATP-binding, which is probably what you meant, is a common cellular mechanism, so obviously provides an advantage to the cell. If you mean does the artificial protein provide an advantage within the context of a cell, the answer is no. It's not integrated with the rest of the cell's mechanisms, so would be detrimental. However, the experiment only attempts to show that sequences of amino acids that fold into functional proteins are rare, but not exceedingly so, within random sequence space. Are you claiming this is the only possible protein that might be found in random sequence space, that they happened to pick the only one that might exist? Zachriel
gpuccio, Looking over the last ~600 postings, what are the chances that you'll ever get a straight answer from Zachriel regarding the selective advantage of ATP? Instead, you will continue to receive a stream of unsupported assertions from someone who exists in the plural. ;-) -Q Querius
Zachriel: "You continue to ignore our argument. Experiments always artificially restrict variables in order to test other variables." I am ignoring nothing. I am strongly reminding you that, when we derive conclusions from experiments, we have to be fully aware of the meaning of those restrictions, and of how they influence the results. What is not clear in my simple statement? "On the other hand, you should be honest enough to admit that there is no evidence that proteins with a naturally selectable function exist in random libraries, at least at reasonable library sizes. Papers like Szostak’s do not support such a conclusion in any way." Do you agree, or not? gpuccio
Zachriel, "Selection is very adept at balancing countervailing considerations." Says who? NS is not considering anything. It is not balancing anything. It is mere culling of complete no-hopers. It is only intelligence that can choose between alternatives for a pragmatic/quality of service goal. NS can't because it is neither intelligent not teleological. Nature (and consequently natural selection) cannot choose. Saying otherwise is like saying MS Windows is achievable exclusively by sorting. NS is incapable of producing novel functions. Like I say, all evolutionists conflate artificial selection with natural selection. EugeneS
gpuccio: On the other hand, you should be honest enough to admit that there is no evidence that proteins with a naturally selectable function exist in random libraries, at least at reasonable library sizes. Papers like Szostak’s do not support such a conclusion in any way. You continue to ignore our argument. Experiments always artificially restrict variables in order to test other variables. gpuccio: Hayashi is a completely different context: it is about partial retrieval of an existing, and partially surviving function. We have already discussed the differences. Hayashi et al. is artificial selection, but the criterion is reproductive. And yes, it starts with a random sequence, a few of which increase the reproductive capability of the phage. Zachriel
Zachriel: We agree on some important points. I absolutely agree that proteins with a definable function exist in random libraries, and that there is an artificially selectable pathway to improved function for them. Otherwise, how could bottom up protein engineering work? On the other hand, you should be honest enough to admit that there is no evidence that proteins with a naturally selectable function exist in random libraries, at least at reasonable library sizes. Papers like Szostak's do not support such a conclusion in any way. Hayashi is a completely different context: it is about partial retrieval of an existing, and partially surviving function. We have already discussed the differences. gpuccio
gpuccio: As I have explained before. simple ATP binding does not provide any advantage, indeed it is a potential problem. If you mean in isolation ATP-binding is not beneficial, that is certainly correct. As already pointed out, this is an experiment to determine whether proteins exist in random sequences, and whether there is a selectable pathway to improved function. The answer to both of these questions is yes. gpuccio: The essential nature of natural selection (selecting only for properties and levels which give reproductive advantage) is certainly not a detail! Yes, and Galileo dropping stones from the Leaning Tower of Pisa is not the same as a landslide. It's a simplification that helps understand the underlying process. Zachriel
Zachriel: A breeder or nature selects from a population. A breeder selects from a population for some purpose or goal. This is selection for some future state envisioned by the breeder. Natural selection has no purpose or goal and has no orientation towards some desirable future. It doesn't care. In nature some members of a population produce more offspring than other members. That's not selection for anything. Mung
Zachriel: "ATP-binding is a common cellular activity, so, of course ATP-binding provides a selective advantage. ATP-binding was chosen for just this reason." That is completely false. As I have explained before. simple ATP binding does not provide any advantage, indeed it is a potential problem. Molecules bind ATP to use its chemical energy to accomplish specific tasks. Simple ATP binding is completely useless, and it subtracts ATP to the environment. "Sure, but that doesn’t mean we can’t tease apart the details of how the process works." The essential nature of natural selection (selecting only for properties and levels which give reproductive advantage) is certainly not a detail! gpuccio
gpuccio: Have you any evidence that a weak binding to ATP can give even a small selective advantage in a natural population, and that therefore it can be fixed? ATP-binding is a common cellular activity, so, of course ATP-binding provides a selective advantage. ATP-binding was chosen for just this reason. gpuccio: Natural selection selects only for properties and levels which give reproductive advantage. Other experiments have shown similar results, such as Hayashi et al. and phages. Keep in mind that the scientific method usually entails eliminating most of the complexity of nature in order to study a single attribute. That's why Galileo dropped stones from the Leaning Tower of Pisa, and why Aristotle was confused about gravity and inertia. gpuccio: Natural selection selects only for properties and levels which give reproductive advantage. Sure, but that doesn't mean we can't tease apart the details of how the process works. Zachriel
Zachriel: The difference is not simply semantic. Artificial selection selects for any pre-defined property, at any pre-defined level. Natural selection selects only for properties and levels which give reproductive advantage. Can you agree on that? gpuccio
Zachriel: Let's not play games. Have you any evidence that a weak binding to ATP can give even a small selective advantage in a natural population, and that therefore it can be fixed? Yes or no, please. gpuccio
Mung: Natural selection doesn’t know anything about traits or reproduction. It doesn’t know advantage from disadvantage. It is blind and unintelligent. We said "select" not "know". Not sure why you want to quibble over semantics, though. What we can show is that environmental constraints will *cause* heritable changes *due* to differences in phenotype. Mung: From, not for. You're still arguing semantics — poorly. A breeder or nature selects from a population. A breeder or nature selects for bigger teeth. Zachriel
Zachriel: Natural selection selects for traits which provide a reproductive advantage. Natural selection doesn't know anything about traits or reproduction. It doesn't know advantage from disadvantage. It is blind and unintelligent.
“The stronger progeny must be already there; it is not produced by natural selection…selection is made from already existing entities.” - Colin Patterson
From, not for. For is teleological. For is purposeful. Do you believe natural selection is teleological and purposeful Zachriel? Mung
Mung: Artificial selection selects for. Natural selection selects from. Keefe & Szostak select from random sequences. Natural selection selects for traits which provide a reproductive advantage. Zachriel
Artificial selection selects for. Natural selection selects from. Huge difference. HT: David Abel Mung
gpuccio: It is not a magnifying glass. It’s a completely different process. If the original random sequences didn't bind to ATP, then they couldn't be amplified. Even a small selective advantage can be fixed in a natural population. gpuccio: It doesn’t. It's an experiment. It's like you saying that Galileo dropping stones from the Leaning Tower of Pisa doesn't tell us anything about stones falling in nature. It's artificial dropping! What the experiment shows is that ATP-binding was present in the original randomized population, and that there are selectable pathways to increased function. Zachriel
Zachriel: "Think of artificial selection as a magnifying glass." It is not a magnifying glass. It's a completely different process. "The original proteins bound to the substrate. If this provides even a small advantage to an organism..." It doesn't. That's why artificial selection can select those proteins, and natural selection can't. We have already discussed Hayashi many times, I don't think that here it's the time to do it again. gpuccio
EugeneS: One of them is statistically significant functional information gains over the natural history. There are both theoretical and empirical reasons to believe that natural selection and natural sources of variation can explain increases in complexity over biological history. EugeneS: In the lab, yes. Almost never in the wild. Natural selection has been observed in the wild, and observed rates of evolution by natural selection are much faster than required to explain the historical record. EugeneS: When a system’s behaviour is a function of more than one parameter, it is up to a decision maker to make compromises between two non-dominating optimal solutions (Pareto front). Selection is very adept at balancing countervailing considerations. Zachriel
"If this provides even a small advantage to an organism," In the lab, yes. Almost never in the wild. Natural selection is too coarse-grained control for it. Apart from that, in a multi-criteria optimization setting such as: Sensitivity vs. robustness. Chemical activity vs. chemical stability. ... The control by NS is too rudimentary for this. When a system's behaviour is a function of more than one parameter, it is up to a decision maker to make compromises between two non-dominating optimal solutions (Pareto front). For example, I have 10 dollars to spend in a shop. I want to minimize expense and maximize the amount of shopping I do. Two things at the same time. Many solutions are possible. I have to intelligently choose which one I want. The situation is even more interesting when my criteria are conflicting. E.g. I may want my system to be chemically active but only as and when needed. The point is, to create such systems takes intelligent purposive choice making. This kind of systems are practically impossible to achieve without intelligence. This hardly leaves anything from your overly optimistic evolutionistic picture of ToE being an overarching theory for biology. RV+NS is critically insufficient to explain decision making systems such as living organisms. The code base of all known life is not amenable to naturalistic explanations at all. EugeneS
Zachriel, "Sure, and there are many unanswered questions in biology, as well." Sure. One of them is statistically significant functional information gains over the natural history. What can be observed is noise or information losses. The only credibly experimentally established source of statistically significant functional information is intelligence. EugeneS
"So now we both agree that the biological Theory of Evolution doesn’t explain everything about biology." Of course, it does not. Nor does it explain statistically significant information gains as shown in the OP. EugeneS
EugeneS: There are profound things there that complicate the picture. Sure, and there are many unanswered questions in biology, as well. That doesn't mean there isn't two broad unifying theories in physics, and recent developments have brought scientists closer to a single theory; the discovery of the Higgs boson, and the possible detection of gravitational waves. Zachriel
EugeneS: There is a threshold of sensitivity below which “stuff does not happen” in situ. The original proteins bound to the substrate. If this provides even a small advantage to an organism, then fixation may occur according to population genetics. For instance, the enzyme might bind to a toxin, or an invader. Or it may assist some other enzyme by making the substrate more easily available. Zachriel
"However, it shows that there is a great deal of unification within physics. " That is an oversimplification. There are profound things there that complicate the picture. So the answer is, no. Some researchers believe it will always be a no. EugeneS
"Think of artificial selection as a magnifying glass." That is the whole point. There is a threshold of sensitivity below which "stuff does not happen" in situ. In the lab, in an intelligently guided experiment, yes, sure. In reality though, it becomes noise. EugeneS
EugeneS: Physics: 2 > 1, isn’t it? However, it shows that there is a great deal of unification within physics. Meanwhile scientists are attempting to unify both theories into a single edifice. EugeneS: I agree that the origin of life cannot be explained by the theory of evolution. That is a remarkable coincidence of our views. So now we both agree that the biological Theory of Evolution doesn't explain everything about biology. Zachriel
Zachriel, Physics: 2 > 1, isn't it? Do I take your phrase as an agreement with mine? Biology (largely explanative): The phrase "stuff happens" explains everything even better because it is absolutely correct in all cases. Do you think it is any worth? I agree that the origin of life cannot be explained by the theory of evolution. That is a remarkable coincidence of our views. But I suspect this is for entirely different reasons. I think that biology is a lot more than chemistry. You apparently don't. EugeneS
gpuccio: Simply binding ATP is of no use, indeed it can only deplete ATP, making it nor available for useful processes. The experiment shows that functional proteins are rare in random sequences, but not exceedingly so. gpuccio: b) In your statements, you aptly avoid to make any distinction between artificial selection and natural selection. That's immaterial to the point that weakly functioning proteins exist among random sequences, and that there is a selectable pathway to improved function. Think of artificial selection as a magnifying glass. Another example is where a gene for infectivity was replaced in a phage with a random sequence. See Hayashi et al., Can an Arbitrary Sequence Evolve Towards Acquiring a Biological Function?, Journal of Molecular Biology 2003. Eugenes: Now, stick to biology and tell us what in biology the theory of evolution does not explain. The biological Theory of Evolution is largely explanative of biological phenomena. However, it does not explain the origin of life. Eugenes: In physics, there is no overarching theory. In physics there are just two, albeit inconsistent, overarching theories, quantum theory and general relativity. Zachriel
Zachriel, In physics, there is no overarching theory. In mathematics, there is none either. Don't you think it is a bit suspicious that in biology, which is way more complex than our contemporary understanding of physics or mathematics, allegedly, there is one grand theory that purports to explain every biological phenomenon. EugeneS
Zachriel, "The word “evolution” has many uses" I am glad you admit it. Now, stick to biology and tell us what in biology the theory of evolution does not explain. EugeneS
Me_Think: The only thing which seems to be extinct here is common sense. gpuccio
Zachriel: Just as an aside, I would like to remind you that in the Szostak paper there is another basic bias, less important than those I have already highlighted, but which deserves to be mentioned. As the random library was built from random DNA sequences selected to be ORFs (avoiding stop codons, and requiring a start codon for translation), we should consider an additional factor of 3 orders of magnitude in the results, because the probability for a random sequence of nucleotides to be an ORF coding for 80 AAs is about 1:1000. So, the final figure, if related to random nucleotide sequences rather than to random AA sequences, should be 1:10^14. gpuccio
Me @ 645
I will try 3d model search. If that too doesn’t bring up anything useful, it means there is no reason for intermediary protein sequence to be preserved or-as zac says- the intermediaries are extinct.
Well, 3d model search too didn't bring up anything useful, so the conclusion is: the intermediaries are extinct. (atleast IMO) Me_Think
Zachriel: I will not insist on your rather ambiguous use of the concept of chemical specificity. It's not really important. I want to remind you, however, that: a) ATP binding is a common cellular function because ATP is a common source of stored energy for chemical reactions. So, a lot of systems bind ATP to couple that energy to some other biochemical reaction. Simply binding ATP is of no use, indeed it can only deplete ATP, making it nor available for useful processes. b) In your statements, you aptly avoid to make any distinction between artificial selection and natural selection. As you know, I have dedicated a whole thread to that problem (https://uncommondesc.wpengine.com/intelligent-design/natural-selection-vs-artificial-selection/). That's why I used the world "engineered". Simply backpedaling to the generic word "selection" does not solve the problem. c) Again, you should say: "Biologists already know that if there is a naturally selectable function, then natural evolution can usually optimize the structure." On the other end, if there is an artificially selectable function, then only artificial evolution can optimize the structure. gpuccio
gpuccio: Weak binding to ATP is a function, but it is not a naturally selectable function ATP binding is a common cellular function. gpuccio: The original protein has low specificity. Engineered evolution increases the specificity. It shows that simple selection for function can increase the binding capability of the protein, that there is a selectable pathway. gpuccio: In no way we can assume that those sequences presented any folding comparable to that of known functional proteins, while the engineered protein derived from them certainly presented some definite ordered folding. Of course. That's the whole point. Biologists already know that if there is a selectable function, then evolution can usually optimize the structure. The question was where the initial function came from in primordial life. While modern cells don't start with random sequences — junk DNA is naturally enriched — , primordial cells may not have had the same resources. Using random sequences provides a floor to the frequency of proteins with selectable function. gpuccio: The binding of Hydrogen to Oxygen to make water is specific and strong. Oxygen-binding is generally indiscriminate. Hemoglobin has a special affinity for oxygen, soaking up excess oxygen through cooperative binding (each new oxygen molecule changes the shape of the molecule), and releasing it as needed. gpuccio: So is the binding of Phosphate to ADP to generate ATP. ATP synthase selectively binds to ADP in order to add the phosphate group. Zachriel
Zachriel: OK, it seems that we almost agree on the following ideas: Weak binding to ATP is a function, but it is not a naturally selectable function, and certainly it is not an enzymatic activity. The original protein has low specificity. Engineered evolution increases the specificity. Regarding your last statement: "The folding was probably inefficient, but if they didn’t fold, they wouldn’t bind specifically." just a couple of comments: a) I don't think there is a clear-cut separation between "folding" as we see it in most functional proteins and "some minimal 3D structure" which is probably recognizable in many sequences which essentially do not fold in the strict sense of the word. IOWs, we usually speak of protein folding referring to the very efficient, complex and ordered folding process which transforms a very long linear sequence into a very definite 3D form, with specific functions. So, we could say that most functional proteins which we observe in the natural world have a very specific and ordered folding. Again, that is not a general principle, and there are many functional proteins which do not fold in the traditional sense. So, let's say that the original sequences in the Szostak experiment had probably "some minimal 3D structure", which you call "inefficient folding". That was enough to confer weak ATP binding, and nothing more. In no way we can assume that those sequences presented any folding comparable to that of known functional proteins, while the engineered protein derived from them certainly presented some definite ordered folding. b) I am still not sure of what you mean with "specific". Chemical bindings are often very specific. The binding of Hydrogen to Oxygen to make water is specific and strong. But is is not supported by any folding whatsoever, only chemical properties. So is the binding of Phosphate to ADP to generate ATP. Why do you think that only reactions favored by protein folding are "specific"? Moreover, many highly sophisticated reactions which involve folded proteins are not very specific. For example, the interaction between antibodies and antigens in the primary immune response is typically a low affinity and low specificity reaction, while antibody maturation enhances both affinity and specificity of the molecules. gpuccio
Dionisio: 3D folding is very important in many proteins, probably not in all. In enzymes, the specific form of the molecules allows stronger binding and specific positioning of the substrates, and helps the enzymatic activity. So, the protein acts as a machine which has a specific form, so that it can receive the substrates, bind them, change their form or biochemical status, and bind them together, or separate them. The cooperation of form and biochemistry is a very powerful tool, and biochemical reactions which would never happen spontaneously, or would happen only very very slowly, are hugely helped and accelerated. In general, it is true that the 3D structure is determined by the primary structure (the sequence of AAs). However, that is not always a fixed relationship. Moreover, the tertiary structure is not a fixed reality, and it is often flexible and constantly changing. Our models of 3D structure are only a reasonable approximation of reality. Computing the 3D structure of a protein from the primary sequence is a very hard task: it is very difficult, and it requires huge computational resources, usually higher than those we can use. However, it is often possible to approximate some structure by reasonable shortcuts, for example by comparing the sequences with others whose structure has been directly analyzed. At present, the best way to determine the 3D structure of a protein is to study it directly, through a biophysics approach. The Protein Data Bank (PDB) is a very good resource for known structures of proteins. gpuccio
EugeneS: Therefore evolution spans over chemistry as well, and who knows what else. The word "evolution" has many uses, however, the biological Theory of Evolution does not explain stellar evolution or the evolution of the works of Hemingway. Dionisio: Is that a reason why the exact 3D shape of a folded protein is so important for its intended functioning? The three-dimensional shape, including the distribution of charges is the reason why proteins can be very specific to their substrates. If it were simple chemical affinity, then they would bind indiscriminately to many different substrates. Dionisio: Is that 3D shape determined by the sequence of AAs in the polypeptide? That, and the actual process of folding. Many proteins require helpers to fold. Dionisio: IOW, given a sequence of AAs, is there a known algorithm to display the correct 3D shape of the folded protein? Protein folding is a complex process, involving thousands of atoms, and is not easy to simulate algorithmically. It can be done for some proteins, but requires large amounts of computational resources. https://en.wikipedia.org/wiki/Lattice_protein Zachriel
gpuccio: Now, as I think we have already discussed in the past, a protein which just weakly binds ATP is not an enzyme, because it does not “accelerate, or catalyze” any chemical reaction. But it is a function. gpuccio: Indeed, the engineering can contribute some specific folding which enhances and makes different the original weak binding, so that in the end some chemical reaction of the substrate may be catalyzed. That's exactly what happens. The protein has a three-dimensional structure that conforms to the substrate. The original protein has low specificity. Evolution increases the specificity. gpuccio: I maintain that there is absolutely no evidence that folding ... The folding was probably inefficient, but if they didn't fold, they wouldn't bind specifically. Zachriel
gpuccio @881
They are parts in a folded protein where chemical binding and other chemical activities are enhanced and helped by the 3D configuration of the whole molecule.
Is that a reason why the exact 3D shape of a folded protein is so important for its intended functioning? Is that 3D shape determined by the sequence of AAs in the polypeptide? IOW, given a sequence of AAs, is there a known algorithm to display the correct 3D shape of the folded protein? Dionisio
Zachriel, It means you haven't understood the theory of evolution been indoctrinated well enough. It can indeed explain everything. Motion of particles of matter is evolution, chemical reactions are natural selection. After all, there is no difference, allegedly, between life and non-life. Therefore evolution spans over chemistry as well, and who knows what else. The funny thing is all this Plato said ages ago. Darwin did not bring anything new. Nor did any other big fan of evolutionism. These fables appear new only because we all lack classical education. EugeneS
Zachriel: From Wikipedia: "A chemical bond is a lasting attraction between atoms that enables the formation of chemical compounds. The bond may result from the electrostatic force of attraction between atoms with opposite charges, or through the sharing of electrons as in the covalent bonds. The strength of chemical bonds varies considerably; there are "strong bonds" such as covalent or ionic bonds and "weak bonds" such as Dipole-dipole interaction, the London dispersion force and hydrogen bonding." From Wikipedia: "Enzymes are macromolecular biological catalysts. Enzymes accelerate, or catalyze, chemical reactions. The molecules at the beginning of the process are called substrates and the enzyme converts these into different molecules, called products." Now, as I think we have already discussed in the past, a protein which just weakly binds ATP is not an enzyme, because it does not "accelerate, or catalyze" any chemical reaction. Simply binding a substrate by some chemical bond is not an enzymatic activity. Now, if I remember well, some enzymatic activity (ATPase) was demonstrated in particular circumstances for a very late derivation of the Szostak protein. Certainly, no ATPase activity has ever been demonstrated for the original sequences in the random pool, which were never studied in detail, and certainly it would be very unlikely to assume it existed, given the weak binding of ATP by those sequences. Is it possible that a weak chemical binding may evolve into a stronger bond, and even into some enzymatic activity, by protein engineering? Sure it is. Indeed, the engineering can contribute some specific folding which enhances and makes different the original weak binding, so that in the end some chemical reaction of the substrate may be catalyzed. That's what active sites are. They are parts in a folded protein where chemical binding and other chemical activities are enhanced and helped by the 3D configuration of the whole molecule. So, I maintain that there is absolutely no evidence that folding and enzymatic activity were present in the original random sequences of Szostak's experiment. gpuccio
gpuccio: Why do you say that a simple chemical bond would not be specific? Perhaps you could explain what chemical bond you have in mind, and how this could evolve into an enzymatic affinity. Zachriel
Zachriel: Why do you say that a simple chemical bond would not be specific? I don't understand. Any bond is specific to the things that are bound. Could you explain what you mean? gpuccio
gpuccio: A weak binding of ATP is not an enzymatic activity, just a chemical bond. That is incorrect. If it were a simple chemical bond, it wouldn't be specific, and it couldn't be optimized. Zachriel
Zachriel: "The biological Theory of Evolution doesn’t explain the behavior of quantum particles, or the explosion of supernovas, among other things." Think about it. If it were really necessary... gpuccio
Zachriel: A weak binding of ATP is not an enzymatic activity, just a chemical bond. gpuccio
EugeneS: Tell us what evolution cannot explain. The biological Theory of Evolution doesn't explain the behavior of quantum particles, or the explosion of supernovas, among other things. Zachriel
Zachriel Tell us what evolution cannot explain. Theories that can explain everything are not scientific. EugeneS
gpuccio: Binding does not happen only because of folding, at lest not weak binding. An enzyme binds by conforming to the specific shape and charge of the substrate. If it doesn't conform, then it wouldn't be specific, and it couldn't evolve into a tighter fit. gpuccio: You bet! But evolution doesn't care about perfection, but differences, in this case, differences in function. Once you have a selectable function, then evolution can improve the fit. That is also shown by Keefe & Szostak. Zachriel
Zachriel: "If they didn’t fold, they wouldn’t bind." Why? Binding does not happen only because of folding, at lest not weak binding. And remember, there are functional proteins which do not fold. "What you can reasonably say is that they weren’t in a very precise configuration." You bet! :) gpuccio
EugeneS: The claim that all complexity in the biosphere can be explained as RV+NS is plain wishful thinking and has no empirical basis. Evolution can explain the origin of a vast number of complex structures in biology. However, understanding the precise history of specific structures is another matter. Appeal to extraneous and unevidenced entities is scientifically vacuous, while hypotheses concerning known mechanisms have been scientifically fruitful. Zachriel
Me_Think 868 I respect your view. EugeneS
Zachriel, "None whatsoever". Depends on the claim. The claim that all complexity in the biosphere can be explained as RV+NS is plain wishful thinking and has no empirical basis. What can be empirically demonstrated is radically different from the grand Darwinian claims. As you may remember me saying to you many times, the human ability to walk does not mean we can walk to the Moon. EugeneS
EugeneS @ 859
You raised an important issue. Which option does one prefer: 1. To continue to make believe we know the answer. 2. To honestly acknowledge fundamental problems in the current understanding of what life is
I will continue to believe that we will find the answer. A year ago majority didn't believe we can detect the incredibly faint gravitational wave, a few years ago detecting Higgs boson was just a figment of LHC scientists imagination. Yet we detected both. Biology just needs more interdisciplinary research to find answers to perplexing problems. Me_Think
Mung: So gradualism is false. That doesn't necessarily follow, however, from studies of network evolution, we would expect lots of small changes, a few big changes, and the occasional revolution. However, even the revolutions would generally take place over thousands of generations. Zachriel
Zachriel: The RV part of your equation can be very complex, including everything from point-mutations to recombination to endosymbiosis. So gradualism is false. Glad you finally admit it. Mung
EugeneS: What Darwinian evolution really claims is that all observed biological complexity with statistically significant levels of functional information can be generated by RV+NS. None whatsoever? You mean generations of scientists have never found any evidence to support their claims? The RV part of your equation can be very complex, including everything from point-mutations to recombination to endosymbiosis. gpuccio: No, the folding was shown only in the final engineered proteins. If they didn't fold, they wouldn't bind. What you can reasonably say is that they weren't in a very precise configuration. gpuccio: I am sure that your theory could explain even a fossil of a chimp dating 4 billion years ago! Um, no. Zachriel
bill cole: "Io vivo per lei", here, means "I live for her", and I suppose it means "the music". In italian, music is a feminine word. "Lei" can also mean "you" in the formal way of addressing a person. But in the friendly way, which would be used by a lover, it would be "Io vivo per te". gpuccio
Zachriel: "Of course there is. For instance, common descent implies a historical progression." I am sure that your theory could explain even a fossil of a chimp dating 4 billion years ago! You know, accelerated evolution in reproductive isolation, and some selective extinction: what could be unexpected, when we have such easy tools in our hands? :) gpuccio
Zachriel: "That means the sequences folded into a three-dimensional structure capable of binding to ATP specifically." No, the folding was shown only in the final engineered proteins. The original sequences were never studied, and there is no evidence at all that they had any significant folding. gpuccio
Zachriel, "Common descent implies a historical progression" Common descent is assumed not only by Darwinian evolution. What Darwinian evolution really claims is that all observed biological complexity with statistically significant levels of functional information can be generated by RV+NS. This claim was and is without any empirical support. EugeneS
gpuccio: Again? The data doesn't go away because it doesn't fit your narrative. gpuccio: That is simply not true.
Keefe & Szostak: Starting from a library of 6 * 10^12 proteins each containing 80 contiguous random amino acids, we selected functional proteins by enriching for those that bind to ATP. This selection yielded four new ATP binding proteins that appear to be unrelated to each other or to anything found in the current databases of biological proteins.
gpuccio: “about 1 in 10^11 random sequences have some weak binding for ATP ..." That means the sequences folded into a three-dimensional structure capable of binding to ATP specifically. gpuccio: There is nothing unexpected in evolutionary theory. Of course there is. For instance, common descent implies a historical progression. EugeneS: The real question is not biological evolution ... Which is why Charles Darwin has been forgotten in the biological sciences. Zachriel
Me_Think: You raised an important issue. Which option does one prefer: 1. To continue to make believe we know the answer. 2. To honestly acknowledge fundamental problems in the current understanding of what life is. The second option opens up grand challenges which may lead to reconsidering the philosophical foundations of contemporary science. Fine by me. The main thing is to stop lying to ourselves. EugeneS
Bill Cole # 851, Absolutely! I have been working in the area of combinatorial search and I am keen to know about the developments on the evolution/evolvability front. Since I do a bit of actual hands-on programming myself, people like Zachriel do not impress me with their stale arguments dating back to the times of evolutionist euphoria. The likes of Zachriel always conflate natural selection with intelligent search guidance. All evolution can really achieve is noise compared to the amount of instructions such information-rich systems as organisms need to self-assemble and metabolize. Biological evolution to even kick off needs intelligence. The real question is not biological evolution though but, in David Abel's words, is how the first set of instructions for a living cell came to be. And that is insurmountable for naturalism. OPs like this one easily expose the inability of naturalism to explain biology. That's what I like about them. EugeneS
seanpit @ 852
Regarding the odds of stable protein folding for a random protein sequence: In short, most mutations that affect a region or island cluster of thermodynamically stable sequences in sequence space are destabilizing in such a way that each additional mutation has an exponentially destabilizing effect. Obviously, this means that the vast majority of sequences in sequence space would not produce viably stable proteins. It also suggests that as sequence space increases in size by 20^N, the ratio of viable vs. non-viable sequences, not just systems, decreases exponentially.
So, what's your theory of protein folds? That Designer intervenes through some 5th force to fold the protein? Me_Think
seanpit: "Obviously, this means that the vast majority of sequences in sequence space would not produce viably stable proteins. It also suggests that as sequence space increases in size by 20^N, the ratio of viable vs. non-viable sequences, not just systems, decreases exponentially." Absolutely true. That's why the biases and ideological papers about protein functional space which are commonly used for darwinist propaganda, like the quoted one, are realized anyway with short protein sequences. In the case of the Szostak paper, 80 AAs. gpuccio
Zachriel: "There is nothing unexpected in evolutionary theory about such a gap." There is nothing unexpected in evolutionary theory. Period. gpuccio
Zachriel: "about 1 in 10^11 random sequences fold into a functional protein." Again? That is simply not true. That paper does not show anything like that. If you want to be honest, the most you can say is: "about 1 in 10^11 random sequences have some weak binding for ATP, and after those sequences are artificially selected for that property and artificially engineered by random mutations and intelligent selections for that property, we can get some folding which enhances the original binding, although that still does not represent a functionally naturally selectable protein." gpuccio
seanpit: Keefe and Szostak 2001 clearly show ... ... about 1 in 10^11 random sequences fold into a functional protein. Zachriel
Bill Cole and Zachriel, Regarding the odds of stable protein folding for a random protein sequence: In short, most mutations that affect a region or island cluster of thermodynamically stable sequences in sequence space are destabilizing in such a way that each additional mutation has an exponentially destabilizing effect. Obviously, this means that the vast majority of sequences in sequence space would not produce viably stable proteins. It also suggests that as sequence space increases in size by 20^N, the ratio of viable vs. non-viable sequences, not just systems, decreases exponentially. "This is the reason why "simulations (Taverna and Goldstein 2002a) and experiments (Davidson et al. 1995; Keefe and Szostak 2001) clearly show that the vast majority of protein sequences do not stably fold into any structure (meaning the least stable folded protein is still far more stable than the typical random sequence)." The number of stable/viable 1000aa sequences in sequence space is around 1e707. Given the size of sequence space at this level is 20^1000, the ratio of viable vs. non-viable is ~1e-594. And, this isn't the worst of it. This number is "further reduced by the dual requirements of stability and kinetic accessibility and the number of sequences that are biologically competent." In short, the ratio of 1e-594 potential targets vs. non-targets is being generous for 1000aa sequence space. Sean Pitman http://www.detectingdesign.com/flagellum.html#Calculation seanpit
EugeneS Thanks for your post. We are in very interesting scientific times. I remember in the 1980's when I had to re learn management in order to keep up with the Japanese companies we were competing with. People hold on to old paradigms until it affects their survival. It will be interesting to see how this plays out. bill cole
Zachriel Thank you for the paper. It will be interesting to follow the dei novo gene experiments going forward. bill cole
bill cole: As you move forward in evolution the odds of finding a new protein get longer and longer as proteins have to work together and find fit in charge and shape. Which explains the high death rate and low transcription rates of de novo genes. You might find this overview helpful: Schlötterer, Genes from scratch – the evolutionary fate of de novo genes, Trends in Genetics 2005. Zachriel
Bill Cole Thanks for sharing your arguments. Evolutionists are rarely being specific. Science though involves concrete figures, calculations, probabilities etc. That is exactly their weakest point. They can tell you stories. However these stories shatter against reality. EugeneS
bill cole: The probability depends on the length of the amino acid sequence and the specificity of the protein. Your claim concerned the evolution of any new protein. Zachriel
Zachriel: While evolution doesn’t work with random sequences, as an experiment, if we take a random sequence of amino acids, what are the odds it will fold into a functional protein? The probability depends on the length of the amino acid sequence and the specificity of the protein. For a nuclear protein that works with several other proteins like beta catenin the amino acid sequence must be specific so the odds of randomly finding this protein are less than 20^200 which is exceeding low. In general the sequence information is a great mystery given that we have no idea how to generate this data from scratch. Any process involving trial and error would fail with all the computer power in the world. This is why I am so skeptical of the current mechanisms. As you move forward in evolution the odds of finding a new protein get longer and longer as proteins have to work together and find fit in charge and shape. bill cole
bill cole: I have seen paper that say what you are claiming here and agree this is possible but a some point you need a new sequence While evolution doesn't work with random sequences, as an experiment, if we take a random sequence of amino acids, what are the odds it will fold into a functional protein? Zachriel
Zachriel Zachriel:Or if transcribed, it can increase its activity, as well as modify that activity. If you are talking about de novo genes, there are several mechanisms by which they can occur, including exon shuffling, or born from non-genic sequences. I have seen paper that say what you are claiming here and agree this is possible but a some point you need a new sequence and run into the same problem you and Sean are discussing. I think he is making strong arguments and you should ask more questions of him. bill cole
bill cole: One of my ideas of a new specie is one that has new proteins. I will concede branching is possible if a new specie does not require new proteins. New proteins are not required. For instance, many beetles speciate when their sex organs change shape. bill cole: If a gene is copied and not transcribed then it can start to mutate without affecting the animal. Or if transcribed, it can increase its activity, as well as modify that activity. If you are talking about de novo genes, there are several mechanisms by which they can occur, including exon shuffling, or born from non-genic sequences. Zachriel
You’re confusing adaptation with speciation. The evidence for branching descent generally does not depend on the evidence for adaptation.
One of my ideas of a new specie is one that has new proteins. I will concede branching is possible if a new specie does not require new proteins.
According to that argument, there can be no evolution at all. In any case, life never leaves areas of functionality, or it would cease to exist.
If a gene is copied and not transcribed then it can start to mutate without affecting the animal. This is the current thinking around the emergence of novel genes. INMHO people who believe in this hypothesis do not understand the sequential space problem. bill cole
bill cole: The sequential space problem is not easy conceptually but when you get the “a ha” moment and understand the magnitude of this problem I think you will understand my skepticism. You're confusing adaptation with speciation. The evidence for branching descent generally does not depend on the evidence for adaptation. bill cole: Once you leave the island of functionality you are lost in “space” forever. According to that argument, there can be no evolution at all. In any case, life never leaves areas of functionality, or it would cease to exist. Zachriel
Zachriel
The basic syllogism is as follows: If branching descent, then nested hierarchy, and sterility various in degree. These we observe, supporting the hypothesis. We also observe speciation, for example, in the genus Galeopsis, whereby a new polyploid species formed through hybridization. And we have many examples of recent speciation, such as has occurred in island radiations.
Very interesting, thanks. My skepticism about the mechanism is exactly shared with Sean's recent article that you were commenting on. The sequential space problem is not easy conceptually but when you get the "a ha" moment and understand the magnitude of this problem I think you will understand my skepticism. Sequential space is essentially infinity when sequences with 20 possibilities get over 100 strings long. Once you leave the island of functionality you are lost in "space" forever. bill cole
bill cole: Yes, this is the current story As supported by the evidence. • the nested hierarchy • reproductive isolation • sterility various in degree (Darwin, Origin of Species, 1872) • direct observations of changes in reproductive isolation. The basic syllogism is as follows: If branching descent, then nested hierarchy, and sterility various in degree. These we observe, supporting the hypothesis. We also observe speciation, for example, in the genus Galeopsis, whereby a new polyploid species formed through hybridization. And we have many examples of recent speciation, such as has occurred in island radiations. Zachriel
Zachriel
Speciation is due to a number of mechanisms, such as polyploidy. However, the typical process is gradual. A population becomes divided, such as due to geography, then begins to diverge, both because of selection and because of drift. As they diverge, they become more and more reproductively isolated. Sometimes, there are physical barriers to reproduction. Other times, the barriers are behavioral. Once completely separated, they continue to follow their own evolutionary path.
Yes, this is the current story I recognize, however I am very skeptical that these mechanisms can cause a new specie to form. The sequential space to the genome is simply too large. There are also complex epigenetic changes and alternative splicing changes that need to be accounted for. For instance if you asked what is the source of splicing changes no one could tell you. I think the real answer is we have no idea how speciation occurs. There are millions of unique species on this planet and we are not able to demonstrate HOW one transition occurred. You said it is a branching process and I accept that but when I ask how the branching occurs you give the above explanation which is almost certainly wrong due to the biochemical changes required. bill cole
bill cole: I am trying to work with you to understand what it really means. It means that different species share a common ancestor. bill cole: My thoughts are without a defined mechanism or cause it means common biochemical and anatomic components which in itself is real evidence. Not sure how to parse that. If there is a branching process, then traits will form a nested hierarchy. bill cole: The next step is significant, which is can we understand the cause of how speciation occurred? Is it natural variation followed by population genetics and selection or is it directed. Speciation is due to a number of mechanisms, such as polyploidy. However, the typical process is gradual. A population becomes divided, such as due to geography, then begins to diverge, both because of selection and because of drift. As they diverge, they become more and more reproductively isolated. Sometimes, there are physical barriers to reproduction. Other times, the barriers are behavioral. Once completely separated, they continue to follow their own evolutionary path. Zachriel
Zachriel
Then why not respond to the specifics. Are you rejecting common descent, or just have questions about how it occurs?
No, I am not rejecting common decent. I am trying to work with you to understand what it really means. My thoughts are without a defined mechanism or cause it means common biochemical and anatomic components which in itself is real evidence. The next step is significant, which is can we understand the cause of how speciation occurred? Is it natural variation followed by population genetics and selection or is it directed. In nature we see both occur... Lenski experiment is and example of natural variation and selection. An embryo is and of example of directed change. bill cole
gpuccio: Let’s assume for a moment that you have all those fixations, and that by some magic you lose all the intermediates. It's not magic, but population genetics. gpuccio: “if there is a direct selectable pathway” The question being addressed was the so-called "gap" that occurred during a period of a hundred million years. There is nothing unexpected in evolutionary theory about such a gap. Zachriel
Zachriel: I appreciate your answer. I would remark that the role of peripheral populations remains scarcely clear. You say that they allow for "experimentation and fixation". Well, while fixation is certainly easier in a small population, I really can't see what "experimentation" we can expect with minimal probabilistic resources. Let's go to big populations, which indeed are the only ones which are really in the game, for complex functional information. Let's assume for a moment that you have all those fixations, and that by some magic you lose all the intermediates. The biggest if remains just the same. You are well aware of that if: "if there is a direct selectable pathway" (emphasis mine). A direct selectable pathway which has never been found even for one single complex protein. A direct selectable pathway which does not exist in any other form of complex digital functional information, not in software and not in language, nor in any kind of complex machine. A direct selectable pathway which is only imagined in name of some protein functional landscape which is not supported by any facts, or by any reasonable data about proteins. IOWs, an "ad hoc" concept which has no scientific validity. gpuccio
gpuccio: I think you have never answered my point that “geographic separation” and “reproductive isolation” are factors which drastically minimize the advantage attributed to NS, because they drastically reduce the size of the population, and therefore the expansion of the selected trait, and therefore the gain in probabilistic resources. Asked and answered. Large populations allow for the growth of diversity, while peripheral populations allow for experimentation and fixation, which then overtake the parent population, often as a new species. However, even with a large population, time to fixation of a selectable trait, if fixation does occur, is typically only a few thousand generations. Consider a a simplified model, a well-mixed species of fish with a population of a million and a genome of 100 million base-pairs reproducing once a year. And assume a selectable mutation that provides a mere 0.01 selective benefit. Ninety-nine times out of a hundred, the mutation will be lost to drift. In a population of a million, we expect the mutation to occur once every couple hundred generations or so. For the one in a couple hundred that reaches fixation, it will take an average of about 3000 generations to reach fixation, or 3000 years. Now, if there is a direct selectable pathway, then 1000 mutations could fix in a few million years. This is a simplified model, but then again, your objection is based on a simplified model. What really happens is that when a selectable mutation begins to expand in the population, it is more likely to have a second selectable mutation, increasing its rate of expansion, and possibly increasing the rate of speciation. Other mutations also confer benefits to other populations, leading to diversification and speciation. This is a chaotic process that doesn't yield to simple computation, but can be simulated. Zachriel
bill cole: The tree you are talking about is a conceptual tree not one planted in the ground that you can observe… An oak tree. Your claim is that if we don't know the mechanism of branching, then we can't determine that branching has occurred. That is clearly not the case. However, we provided evidence of supporting that branching has occurred, and evidence of mechanisms of branching. bill cole: I have not ignored the evidence, I have evaluated it Then why not respond to the specifics. Are you rejecting common descent, or just have questions about how it occurs? Zachriel
Zachriel: Just a brief observation. I think you have never answered my point that "geographic separation" and "reproductive isolation" are factors which drastically minimize the advantage attributed to NS, because they drastically reduce the size of the population, and therefore the expansion of the selected trait, and therefore the gain in probabilistic resources. I notice that you recur often to those concepts when it is useful for your momentary argument, but strangely you forget them when you invoke huge numbers of fish in the old oceans to imagine enormous fixations which can give a semblance of credibility to your reasoning. Will you please make up your mind? Were the incredible non existent paths to functional complexity traversed (at least in your theory) through the help of huge fixations in huge and maximal populations, or did they take place in limited subpopulations, reproductively isolated? Just to understand... gpuccio
Zachriel
bill cole: Without knowing HOW you do not have a theory and the branching idea remains speculation. If we watch a tree grow, we can see it branches without having to know anything about the mechanism of plant growth. Nonetheless, the obvious entailment is that there is a mechanism of branching. We have pointed to support for biological branching — including direct observation — , but you have ignored that evidence. Here it is again: • the nested hierarchy • reproductive isolation • sterility various in degree (Darwin, Origin of Species, 1872) • direct observations of changes in reproductive isolation.
The tree you are talking about is a conceptual tree not one planted in the ground that you can observe....it is a man made tree. I have not ignored the evidence, I have evaluated it and don't think it supports the mechanisms including random variation natural selection population genetics and geographic separation which I believe is a subset of random variation and population genetics as the cause speciation. I don't think you created any real argument for this connection in light of the sequential space of the genome. How do you get the DNA, Splicing and epigenetic changes for speciation.
The standard is hypothetico-deduction. Darwin’s theory has led to very specific empirical predictions that have been repeatedly verified. How did you think science was done?
I have taken a brief look at this standard and agree that it is close to the inference standard Darwin originally used. As far as I am concerned based on this, the design inference and the nature inference are on a level playing field both lacking testability of a mechanism. The question is the design inference ahead with CSI? bill cole
bill cole: Without knowing HOW you do not have a theory and the branching idea remains speculation. If we watch a tree grow, we can see it branches without having to know anything about the mechanism of plant growth. Nonetheless, the obvious entailment is that there is a mechanism of branching. We have pointed to support for biological branching — including direct observation — , but you have ignored that evidence. Here it is again: • the nested hierarchy • reproductive isolation • sterility various in degree (Darwin, Origin of Species, 1872) • direct observations of changes in reproductive isolation. bill cole: Again, I agree you have evidence but only to the inference standard as Darwin argued. The standard is hypothetico-deduction. Darwin's theory has led to very specific empirical predictions that have been repeatedly verified. How did you think science was done? bill cole: I am very skeptical that we would be successful with random variation and natural selection along with population genetics as our selected mechanisms. You have to include mechanisms of speciation, such as geographic separation. Zachriel
Zachriel
It is quite possible to determine that branching has occurred without knowing the details of how the actual branching happens. Consider a tree for someone ignorant of how trees grow. They can still observe branching over time. In any case, we do have evidence of the biological branching process, which was summarized above.
Without knowing HOW you do not have a theory and the branching idea remains speculation. Again, I agree you have evidence but only to the inference standard as Darwin argued. Without the cause of the branching process again you have an untested hypothesis and are on the same playing field as those proposing intelligent causation. Could we devise an experiment that can isolate the cause of the tree branching using the scientific method? I am very skeptical that we would be successful with random variation and natural selection along with population genetics as our selected mechanisms. What about alternative splicing? bill cole
bill cole: In my world branching decent is how you organize an observation. Branching is an observable phenomenon. We can observe how organisms become reproductively isolated. A simpler case is the human y-chromosome. bill cole: The mechanism is what CAUSED the tree you are looking at. The posited mechanism is branching descent. bill cole: Yes this set of bones looks similar to the other. Did one come from the other. How do we test for this? The nested hierarchy is an entailment of branching descent, as are the existence of fossil intermediates. bill cole: How did these branching changes occur? It is quite possible to determine that branching has occurred without knowing the details of how the actual branching happens. Consider a tree for someone ignorant of how trees grow. They can still observe branching over time. In any case, we do have evidence of the biological branching process, which was summarized above. bill cole: My opinion currently is that without an identified cause of the change we observe, common decent, is just a way to organize similar fossils and common biochemistry. No. The nested hierarchy is not an artifact of classification, but an observable pattern with predictable correlations. For instance, if you find an organism with mammary glands, it will also have bellows lungs. bill cole: If you could create an experiment that showed that genetic variation caused the change form a land animal to a whale then you could move from organized fossils and biochemistry to hypothesis. No. We may not even know what a molecule is, and still find evidence for common descent. However, evidence from molecules, when it is present, has to be consistent with the theory, which it is. bill cole: Currently one of the competing hypothesis is intelligent design. The obvious entailment of Intelligent Design is the who, what, when, where, why, and how of the manufacturing process. If we investigate these entailments, what will we be able to discover? Zachriel
Zachriel Thank you for filling this out. I think our disconnect is based on the definition of a mechanism which is ultimately the cause. In my world branching decent is how you organize an observation. The tree of life is the organization of the information that is observed in the fossil record and comparative genomics. The mechanism is what CAUSED the tree you are looking at. Theory is all about the cause or the mechanism. The observation of the fossil record is data but it tells us nothing about the cause. Yes this set of bones looks similar to the other. Did one come from the other. How do we test for this? Common Decent is too high a level of concept to create a testable hypothesis without identifying what caused the change form one tree branch to the other. You need to ask the how question to move to a testable hypothesis. How did these branching changes occur? THE SCIENCE IS ABOUT DETERMINING THE CAUSE OF WHAT YOU ARE OBSERVING. My opinion currently is that without an identified cause of the change we observe, common decent, is just a way to organize similar fossils and common biochemistry. If you could create an experiment that showed that genetic variation caused the change form a land animal to a whale then you could move from organized fossils and biochemistry to hypothesis. This is required if you want to use the scientific method. Inference as a lesser standard can be used by looking at the evidence and comparing it to a competing hypothesis. Currently one of the competing hypothesis is intelligent design. According to the paper I cited the competing hypothesis for Darwin was creationism when he argued to use the inference standard for evolution. bill cole
bill cole: 1... 2... 3... 4... 5... How do you test a hypothesis? A more precise formulation is hypothetico-deduction. A hypothesis is a tentative claim. From the claim, we deduce its empirical implications. Then we test for those entailments. bill cole: 3.Construct a Hypothesis Common descent. bill cole: 4.Test Your Hypothesis by Doing an Experiment Predict an intermediate and find a fossil. bill cole: I agree there are testable theories inside the grand theory but the missing link is a testable mechanism for a speciation event. Speciation is the process of reproductive isolation, which is supported by a variety of evidence: • the nested hierarchy • reproductive isolation • sterility various in degree (Darwin, Origin of Species, 1872) • direct observations of changes in reproductive isolation. bill cole: I think you are telling me is the mechanism for common decent is random variation and then branching descent. No. The mechanism is branching descent, a topological structure called a tree. Branching descent with heritable variation leads to a nested hierarchy at the leaves. Random variation and extinction is a simplified model so that you can more readily understand the mathematical pattern. This is strict deduction. Branching descent --> Tree Branching descent & variation --> Nested hierarchy Zachriel
1.Ask a Question 2.Do Background Research 3.Construct a Hypothesis 4.Test Your Hypothesis by Doing an Experiment 5.Analyze Your Data and Draw a Conclusion 6.Communicate Your Results bill cole
Not at all. For instance, common descent predicts the existence of intermediate organisms, which can often be found as fossils.
This is not the scientific method. I will post the scientific method in the next comment.
Huh? A good theory will produce many testable hypotheses. A great theory will spawn entire new fields of study. By this measure, Darwin’s Theory of Evolution is a great theory.
I agree there are testable theories inside the grand theory but the missing link is a testable mechanism for a speciation event. Without this there is no Grand theory, just a collection of smaller theories and inference. Did you read the paper I cited on inference? I think you are telling me is the mechanism for common decent is random variation and then branching descent. Is that right? bill cole
bill cole: Yes, I agree but in this case you are not using the process of the scientific method just a piece of it. Not at all. For instance, common descent predicts the existence of intermediate organisms, which can often be found as fossils. bill cole: Darwin was criticized for using the lesser standard of inference. Huh? A good theory will produce many testable hypotheses. A great theory will spawn entire new fields of study. By this measure, Darwin's Theory of Evolution is a great theory. bill cole: What other mechanisms are can substitute for natural selection? Think you missed the point. If we have random variation and branching descent, then it will form a nested hierarchy at the leaves. With random extinction, we will typically see gaps between the leaves. This simple model doesn't include selection. bill cole: What is he process that causes a branching event? Reproductive isolation, that is, speciation. Zachriel
Thanks Virgil. bill cole
Natural selection is gradual evolution and gradual evolution produces transitional forms. However no one knows if natural selection can do anything other than stabilize an already population. That means NS reigns in the fringe and makes everything the norm. Those that do manage to break free are freaks that lead to their own evolutionary dead-end. Virgil Cain
Virgil
Natural selection cannot produce a nested hierarchy.
Can you explain this? bill cole
Zachriel
Inference is part of the scientific method; the deduction part of hypothetico-deduction.
Yes, I agree but in this case you are not using the process of the scientific method just a piece of it. The scientific method directly tests your hypothesis.
In isolation, no particular data can “prove” evolution
Yes, I agree this is the state of the science at this point but more then "prove" you cannot create a testable hypothesis based on the standard of the process of the scientific method. Usually a 5 step process.Darwin was criticized for using the lesser standard of inference. Here is a paper. Van Fraassen’s Critique of Inference to the Best Explanation Samir Okasha*
Natural selection isn’t required to produce a nested hierarchy. Indeed, natural selection often confounds the nested hierarchy. To create a tree just requires a branching process. To create the nested hierarchy requires a branching process and variation.
What other mechanisms are can substitute for natural selection? Can a supernatural(one we cannot currently explain) mechanism be a part of common decent? What is he process that causes a branching event? Sorry :-( NT mean Means neutral theory bill cole
Zachriel:
Natural selection isn’t required to produce a nested hierarchy.
Natural selection cannot produce a nested hierarchy.
To create the nested hierarchy requires a branching process and variation.
That is incorrect and demonstrates complete ignorance of nested hierarchies. Just because a nested hierarchy can be depicted as a branching pattern does not mean all branching patterns form a nested hierarchy. A family tree is not a nested hierarchy and Common Descent is just a family tree writ large.
This is the posited pattern.
That is an imagined pattern. Each point along each line could be filled by an asterisk denoting the real pattern that easily could have come about. Virgil Cain
bill cole: So inference is the scientific standard. Inference is part of the scientific method; the deduction part of hypothetico-deduction. bill cole: I am admittedly skeptical that a 100AA bacterial protein showing nominal bonding capability is an adequate simulation to infer complex multicellular evolutionary change, although inference to this is a valid competing hypothesis. In isolation, no particular data can "prove" evolution. Rather, it is the consilience of evidence that lends confidence to the theory. It starts with common descent, which this thread takes for granted. bill cole: On Common Decent: Can you have a theory of common decent without an identified mechanism on how phyla move through the tree of life? Don't know what that means. A phyla is just a large limb of the tree of life. bill cole: What is common decent without the mechanism of RMNS and NT? Natural selection isn't required to produce a nested hierarchy. Indeed, natural selection often confounds the nested hierarchy. To create a tree just requires a branching process. To create the nested hierarchy requires a branching process and variation. What is NT? A nested hierarchy? A nested tree would be redundant. bill cole: Gradual descent with modification would produce numerous transitional forms making a classification scheme very messy and almost impossible. This is the posited pattern. http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Zachriel
Got it. Thanks Virgil bill cole
bill cole- a nested hierarchy requires distinct character sets. Linnaean taxonomy is the observed nested hierarchy and it doesn't have anything to do with Common Descent. Transitional forms are a blend of characteristics. With gradual evolution we would expect to see a smooth blending of traits and not distinct and separate classes. Virgil Cain
Hi Virgil
Actually a nested hierarchy would refute common descent. Gradual descent with modification would produce numerous transitional forms making a classification scheme very messy and almost impossible. I am not sure what you mean by this. Can you elaborate? bill cole
Zachriel:
We have evidence from fossils, such as the evolution of the mammalian middle ear.
We have no way to test the claim that the mammalian middle ear evolved from a reptilian ear and jaw. All the fossils show are organisms with different ears and hearing adaptations. Zachriel is just another gullible fool who thinks he can read the bones like some mystic. Virgil Cain
Zachriel:
They’re inferred from a consilience of the evidence, from fossils to molecules to mathematics.
And a common design is inferred from a consilience of evidence, from fossils to molecules to mathematics to chemistry to physics.
It’s not a mere similarity, but the nested hierarchy which implies common descent.
Actually a nested hierarchy would refute common descent. Gradual descent with modification would produce numerous transitional forms making a classification scheme very messy and almost impossible. Virgil Cain
Zachriel
They’re inferred from a consilience of the evidence, from fossils to molecules to mathematics.
So inference is the scientific standard. We then agree on the rest of the points regarding proteins. I am admittedly skeptical that a 100AA bacterial protein showing nominal bonding capability is an adequate simulation to infer complex multicellular evolutionary change, although inference to this is a valid competing hypothesis. On Common Decent: Can you have a theory of common decent without an identified mechanism on how phyla move through the tree of life? I am skeptical of the position that evolution is both theory and fact. What is common decent without the mechanism of RMNS and NT? bill cole
bill cole: Can you give me an example of a test that validates large scale evolutionary change or are these changes inferred from small scale evolutionary tests? They're inferred from a consilience of the evidence, from fossils to molecules to mathematics. bill cole: What type of proteins? The typical experiment looks for binding to a specific substrate. This requires, of course, that the protein fold into a specific three-dimensional shape. bill cole: How many AA’s in the sequence? The typical experiment works with sequence of length 80-100. bill cole: How about nuclear proteins that have to interact with other nuclear proteins thus requiring a great deal of specificity? How about multi protein complexs that also require specific sequences for shape and charge fit? Experiments have been done with bacteria, wherein certain protein sequences have been replaced with random sequences, and the bacteria have to re-evolve a working protein. We'll remind you that scientists don't have to build a star in order to understand how they work, or how they formed. bill cole: I have heard of common decent but really do not understand the definitions given. If it means common biochemistry among living creatures I understand that and agree that there is strong evidence. It's not a mere similarity, but the nested hierarchy which implies common descent. Zachriel
Zachriel I have heard of common decent but really do not understand the definitions given. If it means common biochemistry among living creatures I understand that and agree that there is strong evidence. bill cole
Zachriel
Biological evolution is a very well tested hypothesis.
Can you give me an example of a test that validates large scale evolutionary change or are these changes inferred from small scale evolutionary tests?
We can make novel proteins from random sequences, so we know that proteins are not that rare in protein-space.
What type of proteins? How many AA's in the sequence? How about nuclear proteins that have to interact with other nuclear proteins thus requiring a great deal of specificity? How about multi protein complexs that also require specific sequences for shape and charge fit? bill cole
bill cole: I am not sure from your answer if you agree that evolution is an inference and not a tested hypothesis. Biological evolution is a very well tested hypothesis. bill cole: A less than equivalent test for evolution would be to create a complex novel protein in the lab by the selected mechanism followed by a protein complex. We can make novel proteins from random sequences, so we know that proteins are not that rare in protein-space. bill cole: As current evolutionary theory proposes stochastic processes and large sequences, the lab verification is very difficult. Start with common descent... Zachriel
Zachriel I am not sure from your answer if you agree that evolution is an inference and not a tested hypothesis. I am not being critical of the concept because I think the other argument(design) is on the same playing field. I am just trying to baseline in my mind the status of the science.
One doesn’t have to build a star in the laboratory in order to test theories of how stars work, or their history of formation.
I agree but in this case we can directly test the mechanism (gravity fusion) against the hypothesis. A less than equivalent test for evolution would be to create a complex novel protein in the lab by the selected mechanism followed by a protein complex. As current evolutionary theory proposes stochastic processes and large sequences, the lab verification is very difficult. bill cole
Zachriel: evolution is capable of building up complex structures incrementally, such as when there is a selectable pathway. bill cole: Has that evidence lead to the inference you concluded or is there experimental data that directly supports it? We have evidence from fossils, such as the evolution of the mammalian middle ear. We have theoretical evidence, such as models that show evolution is effective on fitness landscapes that exhibit certain kinds of order. bill cole: If the answer is inference without experimental data then I would classify it as an untested hypothesis, One doesn't have to build a star in the laboratory in order to test theories of how stars work, or their history of formation. Zachriel
Zachriel I should not have included the first statement...sorry. The second statement is supported by evidence. Has that evidence lead to the inference you concluded or is there experimental data that directly supports it? If the answer is inference without experimental data then I would classify it as an untested hypothesis, which I believe that evolution( with defined mechanism) of all major transitions ( i.e.reptile to mammal) are at this point. The inference standard (untested hypothesis) has brought the design hypothesis into the game because you can infer design but it is harder to test and certainly does not describe a direct mechanism. Thoughts? bill cole
bill cole: How would you classify this statement. There were two connected statements. The first statement is a profession of ignorance. If someone provides evidence of the history of manufacture, then we'll be happy to take a look at it. The second statement is a summary of what is supported by evolutionary science, both theoretical and evidential. Zachriel
Zachriel
Have no idea about Prickle 1, nor has any IDer provided any evidence of the manufacturing process. However, evolution is capable of building up complex structures incrementally, such as when there is a selectable pathway.
How would you classify this statement. -An idea -An untested hypothesis -A tested hypothesis -theory(tested with a mathematical model) -fact (directly observed measured) bill cole
Dionosio My first foreign language was Spanish but after a year in Italy it was difficult for me to speak both languages because the are so similar. I live in a town across from San Francisco. I attended the University of California in Berkeley. If you ever return to California please let me know. Thanks again for you're interesting insight and debate:-) bill cole
Dionosio Io vivo per lei= I live for you Io vivo per la musica=I live for the music quite a love song :-) The italian language is quite beautiful bill cole
Dionisio: Aren’t they still birds? D: Is that “Cit+. E. coli” also a bacteria? Z: Of course. Are humans also mammals? Notably, you didn't answer our question @734. Have you ever seen a tree? Consider a limb (aves) of that tree. A branch (passerine) grows on that limb, a twig (finch) appears on that branch. On what limb is the twig associated? Zachriel
bill cole I should stop the 'off topic' digression. The teacher could come back to the classroom any moment. I don't know how long he stepped out for. :) But one more thing: Here is the Italian song text I referred to @794 (second paragraph). Note the word 'lei' repeated in the lyrics. Does it refer to music or to a lady? Vivo per lei da quando sai La prima volta l'ho incontrata, Non mi ricordo come ma Mi entrata dentro e c' restata. Vivo per lei perché mi fa Vibrare forte l'anima, Vivo per lei e non é un peso. Vivo per lei anch'io lo sai E tu non esserne geloso, Lei é di tutti quelli che Hanno un bisogno sempre acceso, Come uno stereo in camera, Di chi da solo e adesso sa, Che anche per lui, per questo Io vivo per lei. è una musa che ci invita A sfiorarla con le dita, Attraverso un pianoforte La morte lontana, Io vivo per lei. Vivo per lei che spesso sa Essere dolce e sensuale, A volte picchia in testa ma ha un pugno che non fa mai male. Vivo per lei lo so mi fa Girare di citta in citta, Soffrire un po' ma almeno io vivo. è un dolore quando parte. Vivo per lei dentro gli hotels. Con piacere estremo cresce. Vivo per lei nel vortice. Attraverso la mia voce Si espande e amore produce. Vivo per lei nient'altro ho E quanti altri incontrer Che come me hanno scritto in viso: Io vivo per lei. Io vivo per lei Sopra un palco o contro ad un muro... Vivo per lei al limite. ... anche in un domani duro. Vivo per lei al margine. Ogni giorno Una conquista, La protagonista Sará sempre lei. Vivo per lei perché oramai Io non ho altra via d'uscita, Perché la musica lo sai Davvero non l'ho mai tradita. Vivo per lei perché mi da Pause e notte in liberta` Ci fosse un'altra vita la vivo, La vivo per lei. Vivo per lei la musica. Io vivo per lei. Vivo per lei unica. Io vivo per lei. Io vivo per lei. Io vivo Per lei. http://www.tekstowo.pl/piosenka,andrea_bocelli,vivo_per_lei.html Dionisio
bill cole @794 (second paragraph) where it reads 'she' it probably should say 'her' instead, but gpuccio may clarify this later. Dionisio
bill Cole @789
Thanks for the very interesting discussion.
Well, you may want to thank the author of the OP and maybe some of his persistent interlocutors, but not me. I have just asked simple questions. Don't have much (if any) scientific knowledge to share here. But perhaps my questions could motivate those who do have it to delight us with interesting information, as "nostro caro dottore" has usually done here. Some folks who apparently don't have the knowledge but think they do may jump into the discussion too every once in a while. :( But my Maker asked me to love others, regardless of what they think, because my Master loves them. Sometimes that's not an easy task for me to do, but I've got to do what I've got to do, because I love my King and want to please Him. Os deseo que paséis un buen domingo. Dionisio
bill cole Yes, you've got it exactly right - io non sono italiano. But what would make you think that I could be Italian? My native language is Spanish. When I read your question, it did not make sense to me, because I thought 'lei' meant 'she' as in Andrea Bocelli's song 'Vivo per lei'. Shouldn't the question be "sei Italiano?" or something like that? We should ask "nostro caro dottore" gpuccio to teach us. :) That's interesting that you've been most your life in California but a year in Italy. A year is sufficient time to learn at least some basic Italian language. I like that language, but have not made an effort to learn it (I'm kind of lazy). Sometimes that language sounds funny to me, though. BTW, why did you go there for one year? [you don't have to answer]. My wife and I visited Italy first time a couple years ago and toured part of that interesting country. We still plan to go back there (D m)*, to visit other areas we didn't see on our firth visit. But that might never happen. We don't know the future. BTW, regarding your state, my wife and I visited San Francisco years ago to celebrate our anniversary. Rented a car and drove around that area. North to Sausalito and Muir Beach. Obviously drove on the Golden Gate bridge both ways and even took pictures! :) South as far as Monterey, Pebble Beach, Carmel. Stopped by my wife's childhood friends in San Jose too. That's all I've seen in California. That's the only time I've been there. One of my children and two cousins travel to the headquarters of their respective employers in that area. A cousin works at the University of California. Have a good Sunday. Dionisio
Dionisio You answered my question. It asked, are you Italian? Although I lived most my life in California the exception was a year in Italy. bill cole
bill Cole @789 What does the last phrase mean? I don't understand it. I don't know Italian language. Thank you. Dionisio
Zachriel @788
In any case, by saying “14 different species of birds? Aren’t they still birds?” you seem to be suggesting that the differences are insignificant. Try to be precise in your position.
Did you miss answering a simple yes/no question? Did you see the question in bold characters? Why didn't you answer it? Let me use the positive format: Are they still birds? Yes or no? Dionisio
[...] the very words that explain what the authors believe explain the adaptability of E. coli.
What they believe is irrelevant unless it's true. Dionisio
Zachriel Dionisio Thanks for the very interesting discussion. I think a definition of a new specie would be very helpful although it is difficult. This post brought about a very interesting discussion because no one is able to model large protein changes. Some maybe DNA changes some splicing changes but how these new species with very different proteins remains a mystery. Mathematically you can make very few mutational changes successfully because of the size of the sequential space of the genome. The 2010 Lynch paper is limited to a maximum of 6 changes to a given gene. This works for an epigenetic change like Lenski's result but does not create a novel protein. So the appearance of new species with novel proteins is beyond science at this point. At least if your standard is the scientific method. BTW Dionisio lei Italiano? bill cole
Dionisio: But birds are birds, flowers are flowers, seeds are seeds, fish are fish. That's not quite correct, as a close look at Archaeopteryx or other such intermediate species would reveal. https://upload.wikimedia.org/wikipedia/commons/e/e8/Archaeopteryx_fossil.jpg In any case, by saying "14 different species of birds? Aren’t they still birds?" you seem to be suggesting that the differences are insignificant. Try to be precise in your position. Zachriel
Zachriel @786
Turns out that not all birds [...] are the same.
Duh! Of course! Did you just realize that? :) Not all flowers are the same, not all seeds are the same, not all fish are the same,... But birds are birds, flowers are flowers, seeds are seeds, fish are fish. The wide diversity is beautiful! I celebrate it! The biological systems are designed for wide diversification. Dionisio
Dionisio: 14 different species of birds? Aren’t they still birds? Different species of Hominids? Aren't humans still Hominids? Turns out that not all birds, or Hominids, are the same. Zachriel
Zachriel @781
As for the finches on Galápagos, they have diversified enough to be considered macroevolution, including specializations for eating nuts, insects, flowers, and even blood, forming fourteen different species.
Macro-what? C'mon! You're making me laugh out loud. :) 14 different species of birds? Aren't they still birds? Bacteria remained bacteria, birds remained birds. Where's the beef? Show me the money! :) Dionisio
Zachriel @781
We did answer, but will do so again.
Why did your write 'we'? Are you more than one person? Dionisio
EugeneS: I thought that you would be able to explain the concrete observed difference, instead of telling another just so story. We are not aware of the exact history. The claim was that the history is inconsistent with evolution, which is not the case. Zachriel
Zachriel. I thought that you would be able to explain the concrete observed difference, instead of telling another just so story. EugeneS
EugeneS: Organisms do go extinct. Didn't think it was controversial. Extinction doesn't just apply on the species level, but entire families may go extinct. EugeneS: The evolutionary gradualism attempts to attribute its appearance in sharks to unguided gradual information increase due to consistent positive natural selection up to sharks. But this is contrary to what is actually observed and reported in the OP. No. The original post points to an evolutionary gap of a hundred million years. This certainly isn't inconsistent with positive selection occurring during that long interval. EugeneS: However, nowhere in your comments did I see an attempt to explain how it came to be that the red sequence shows no significant stepwise information gains while at the same time the blue sequence does. Have no idea why you consider the different evolutionary history of the "red" and "blue" sequences to be a conundrum for evolution. Some structures evolve, reach fixation, then stabilize. Other structures evolve and continue to diversify. EugeneS: In particular explain why you think that the extinction argument should apply only to the blue sequence and not the red one. If a structure continues to branch and leaves many descendants, then you will find many extant intermediates. If a structure evolves, then reaches fixation, and none of the intermediate species survive, then you will only see extant beginning and end structures. There will be a gap. It's important to note the general congruence between morphological and molecular trees, so if we were to find fossil intermediates, that would support that there were molecular intermediates. Dionisio: So much hype from an experiment that so far doesn’t even hint to a future new species? That's directly contrary to the statement above. The results do hint at speciation. Cit- is one of the defining characteristics of E. Coli, so the fact that it evolved Cit+ would mean it would not pass the standard test for E. coli. The authors are not claiming it's a new species, species being an ambiguous term with regards to bacteria. Dionisio: Or is it more comparable to the difference between a cat and a dog? We did answer, but will do so again. Species is an ambiguous term with regards to bacteria, so the comparison is not particularly useful. In any case, E. coli Cit+ is not considered a new species. If you want to stretch the point, it might be comparable to the difference between a wolf and a dog — different enough to distinguish, but not so different that they are different species. Dionisio: Doesn’t the text that was omitted -for being irrelevant to that given context- refer to ‘microevolution’, which is a grandiose way to call the ubiquitous adaptation processes seen all around us -like the famous finch beak adaptation process Darwin observed in the G alapagos and later grossly extrapolated to a fictitious ‘macroevolution’ that seems to exist only like a figment in some human minds? You snipped out just three words, the very words that explain what the authors believe explain the adaptability of E. coli. There are theoretical reasons for how historical memory can lead to evolvability in genomes. As for the finches on Galápagos, they have diversified enough to be considered macroevolution, including specializations for eating nuts, insects, flowers, and even blood, forming fourteen different species. Zachriel
All: since the teacher (OP author/moderator) of this thread left the classroom for a moment, anyone else is welcome to comment on the questions posted @778 & @779. Thank you. :) Dionisio
gpuccio #778 addendum: Any information about the phenotypic functional effect of the Prickle1 2nd part (blue) big jump from Tunicata to Shark? How did that change affected the developmental/reproductive processes (regulatory networks, signaling pathways, etc) between those two biological systems? Thank you PS. perhaps this question has been answered (at least partially) in this thread. If this is the case, please just point at the post(s) where this was explained. Dionisio
gpuccio Here I go with another uneducated (dumb) question: what was the phenotypic functional effect of the first part (red) small jumps from prokaryotes to fungi, from fungi to C. Elegans, from C. Elegans to Drosophila, etc? IOW, what do those small jumps affected in the developmental or reproductive processes (regulatory networks, signaling pathways, etc) that led to the evolution from prokaryotes to fungi, from fungi to C. Elegans, from C. Elegans to Drosophila, and so on? Thank you. PS. perhaps this question has been answered (at least partially) in this thread. If this is the case, please just point at the post(s) where this was explained. Dionisio
Organisms go extinct. Therefore we have an acceptable excuse for the absence of any transitional protein sequences. Mung
Zachriel @771
Dionisio: Are they referring to biological systems with built-in adaptation mechanisms? Zachriel: The answer was in the part that was snipped out.
Doesn't the text that was omitted -for being irrelevant to that given context- refer to 'microevolution', which is a grandiose way to call the ubiquitous adaptation processes seen all around us -like the famous finch beak adaptation process Darwin observed in the Galapagos and later grossly extrapolated to a fictitious 'macroevolution' that seems to exist only like a figment in some human minds? Dionisio
Zachriel:
The question concerned whether so-called gaps were consistent with evolution theory. Here’s the basic pattern posited by evolutionary theory:
No, Zachriel, that is from Darwin's imagination. It is not part of any theory as there isn't any evolutionary theory.
Or given common descent, do you understand that gaps are a natural consequence of divergence and extinction?
Gaps are not a natural consequence of mere divergence and extinction. Gaps are a normal consequence of intelligent design, however. Virgil Cain
Zachriel @771
Dionisio @750: Are Cit+. E. coli as different from other bacteria as a whale is from a cow (both mammals)? Zachriel: It’s not something that makes for very useful comparison, however, Cit+ is not a new species.
Ok, maybe it would help to refresh our memory a little:
Zachriel @734
Dionisio: Is that “Cit+. E. coli” also a bacteria? Zachriel: Of course. Are humans also mammals? Dionisio: IOW, have bacteria remained bacteria so far in that famous experiment? Zachriel: Yes, just like humans are still mammals.
So much hype from an experiment that so far doesn't even hint to a future new species? Where's the beef? Show me the money! :) BTW, there was another question @750 that apparently you did not answer: Or is it more comparable to the difference between a cat and a dog? Perhaps the cat vs. dog comparison within mammals is close to the Cit+. E coli vs. another bacteria ? Dionisio
Zachriel @771
Dionisio: Are they referring to biological systems with built-in adaptation mechanisms? Zachriel: The answer was in the part that was snipped out.
Are you sure that's correct? :) Dionisio
Zachriel, I will take the liberty of answering your questions in #766. "Are you saying you don’t think organisms go extinct?" Organisms do go extinct. "Or given common descent, do you understand that gaps are a natural consequence of divergence and extinction?" Yes, I understand the implications. We observe a considerable increase in the functional information (the blue sequence in sharks and afterwards). The evolutionary gradualism attempts to attribute its appearance in sharks to unguided gradual information increase due to consistent positive natural selection up to sharks. But this is contrary to what is actually observed and reported in the OP. Your general response is that all intermediates relevant to the blue sequence must have gone extinct. However, nowhere in your comments did I see an attempt to explain how it came to be that the red sequence shows no significant stepwise information gains while at the same time the blue sequence does. The blue sequence appears as late as in sharks and remains highly conserved afterwards. At the same time, the red one is a lot more gradual across different taxa. I may have missed your detailed explanation of that particular problem. Kindly explain how your understanding of the theory of evolution explains that particular example in the OP. Please be specific and stick to this example. In particular explain why you think that the extinction argument should apply only to the blue sequence and not the red one. EugeneS
Origenes: And all those lancelets precursors, which have been expanded to the whole planet for hundreds of time, have all gone extinct? When there are extant intermediates, the genomes support phylogeny. When there are no extant intermediates, we can often find fossil intermediates. Evolution has been shown, both theoretically and experimentally, capable of incremental adaptations. Origenes: 10^12 fish for each of the 350 fixations? We are unaware of the exact history, however, fixation often occurs in smaller populations, and the trillions of fishes comprise thousands of species. Take a look at the posited pattern: http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Dionisio: You commented on my post @761 but did not answer the question I asked you @761 about previous questions @750 & @751 which apparently you have not answered (at least I don’t recall seeing your answers). Notably, you don't seem to have absorbed the previous answers. Dionisio: Are they referring to biological systems with built-in adaptation mechanisms? The answer was in the part that was snipped out.
The components of an organism’s metabolic, regulatory, and developmental networks have evolved to interact in complex ways that are attuned to its current niche. Yet, these networks are also poised such that they can be dynamically reorganized toward new purposes by only a few mutations in key enzymes and regulatory proteins.
Dionisio @750: Are Cit+. E. coli as different from other bacteria as a whale is from a cow (both mammals)? It's not something that makes for very useful comparison, however, Cit+ is not a new species. Dionisio: Why is the referenced paper ‘poorly reasoned’? Start with the first sentence, "The isolation of aerobic citrate-utilizing Escherichia coli (Cit+) in long term evolution 13 experiments (LTEE) has been termed a rare, innovative, presumptive speciation event." It wasn't termed that by LTEE. Indeed, they specifically ask "Will the Cit+ and Cit- lineages eventually become distinct species?" We already pointed out the problem with their statement that “No new genetic information” evolved. Of course there's new genetic information. A new function evolved. So, let's skip to the last sentence, "A more accurate, albeit controversial, interpretation of the LTEE is that E. coli’s capacity to evolve is more limited than currently assumed." They showed that Cit+ can evolve faster than it did in LTEE. That shows that evolution is less limited, not more limited. (By the way LTEE also showed the rapid evolution of Cit+ when they were looking for potentiated populations.) So there are problems from start to middle to end. Will you respond to these specifics? Zachriel
Zachriel @762
Dionisio: You may enjoy reading this: Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA Zachriel: Seems to be interesting research, but a poorly reasoned paper.
Why is the referenced paper 'poorly reasoned'? Dionisio
Zachriel @762 You commented on my post @761 but did not answer the question I asked you @761 about previous questions @750 & @751 which apparently you have not answered (at least I don't recall seeing your answers). I give you the benefit of the doubt, thinking that perhaps you simply missed seeing those questions. Please, keep in mind that you don't have to answer any questions. However, I'm bringing up the issue of the unanswered questions because the current discussion thread seems to be among the most visited within this site lately, hence anonymous readers should have a clear information about the way every commentator here approaches this discussion. Dionisio
Origenes @767
[...] asked you some excellent questions, which you refuse to answer.
That's an interesting observation. Thank you for bringing it up here so timely. :) Off the OP topic -the teacher (our dear OP author and discussion moderator) left the classroom for a moment :) Have you ever heard of selective reading, selective listening, selective answering? Please, note that I don't know much about that (or anything else). However, some people say that it all seems to relate to preconceived agendas or bias based on personal worldview positions, but maybe the jury is not back for the conclusive verdict yet. :) Perhaps some folks attribute it all to short attention span associated with some kind of dyslexic reading, or the side effect of sleep deprivation, or simply lack of time associated with chronic procrastination. Some controversial opinions go as far as to suggest that a breakfast heavy on vinegar might be at the root of the problem. But that kind of opinion seems to belong in the 'bzdura'* category. :) In every case, it may just reflect the state of our human condition that requires serious treatment before it's too late. The problem is that there isn't any effective natural remedy for that malady, which I myself suffered for a substantial part of my earthly life. The only known effective cure is rejected by many, though it's available to all. C'est la vie, mon ami! :) (*) a word in Polish language Dionisio
Zachriel #766, In post #726 Gpuccio's has asked you some excellent questions, which you refuse to answer. The following question deals with your terribly incoherent extinction scenario.
Gpuccio: And all those lancelets precursors, which have been expanded to the whole planet for hundreds of time, have all gone extinct? 10^12 fish for each of the 350 fixations? While we still have, only, lancelets and sharks? Is that, more or less, your idea?
Well? Is that your idea? Origenes
Origenes: Well, do tell where evolutionary theory predicts that there will be a gap for the blue sequence between vertebrates and pre-vertebrates and no gap for the red sequence. The question concerned whether so-called gaps were consistent with evolution theory. Here's the basic pattern posited by evolutionary theory: http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Are you saying you don't think organisms go extinct? Or given common descent, do you understand that gaps are a natural consequence of divergence and extinction? Zachriel
Zachriel: Good thing evolutionary theory doesn’t do that then.
Excellent news! Well, do tell where evolutionary theory predicts that there will be a gap for the blue sequence between vertebrates and pre-vertebrates and no gap for the red sequence. Origenes
Origenes: Meteorology which predicts that there will be “hot and cold, wet and dry” without any attempt to specify where and when would be just as useless as the “predictions” of evolutionary theory. Good thing evolutionary theory doesn't do that then. Extinction is a well-researched topic. Take a look again at the basic pattern. http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Zachriel
Zachriel,
Origenes: And if the theory predicts gaps and no-gaps, then the theory predicts nothing at all.
Zachriel: Sort of like meteorology. It predicts both hot and cold, wet and dry.
Meteorology which predicts that there will be "hot and cold, wet and dry" without any attempt to specify where and when would be just as useless as the "predictions" of evolutionary theory. Origenes
Dionisio: You may enjoy reading this: Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA Seems to be interesting research, but a poorly reasoned paper. Dionisio: The replaced text is irrelevant in the given context. The phrase "have evolved to" is obviously relevant in context. Let's take a guess. You used a secondary source and the ellipses came along for the ride. Zachriel
Zachriel @756
Why did you use ellipses at that point?
That's a valid question. The replaced text is irrelevant in the given context. BTW, did you answer the questions @750 & @751? Thank you. Dionisio
Zachriel You may enjoy reading this: :)
[...] because this adaptation did not generate any new genetic information and only required expanded expressions of two existing transporters (citT and dctA), generation of E. coli Cit+ phenotypes in our estimation do not warrant consideration as a speciation event. In fact, mutations in these two loci are sufficient for the LTEE Cit+ phenotype (10).
Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA Dustin J. Van Hofwegen, Carolyn J. Hovde and Scott A. Minnich doi: 10.1128/JB.00831-15 http://jb.asm.org/content/early/2016/01/28/JB.00831-15.abstract
Dionisio
Me Thinks
Andreas Wagner in ‘Arrival of the Fittest’ shows how Hyperdimensions can reduce the search space drastically. IIRC, there were a whole bunch of posts about it here. So, no, there is no ‘probabilistic problem’ in search space.
I have recently read his book and don't agree that he has solved the search space problem. He has interesting ideas and I do agree that he described the search space problem very well. bill cole
bill cole @ 575
So your idea is the environment is explorable by evolutionary search but you are not describing a mechanism at this point. It appears you understand the probabilistic problems with the genome as a sequence...
Andreas Wagner in 'Arrival of the Fittest' shows how Hyperdimensions can reduce the search space drastically. IIRC, there were a whole bunch of posts about it here. So, no, there is no 'probabilistic problem' in search space. Me_Think
Zachriel
Not sure we would call the environment a mechanism, but it is certainly an important component of the process. Turns out the physical landscape, both on the molecular and morphological level, are explorable by evolutionary search. Otherwise, the random mutation in Lenski’s bacteria would have been very unlikely to increase fitness, or in the case of Cit+, to have made multiple sequential steps in fitness.
So your idea is the environment is explorable by evolutionary search but you are not describing a mechanism at this point. It appears you understand the probabilistic problems with the genome as a sequence. In the Lenski experiment the enzyme to process citrate was already in the bacteria. It is not surprising to me that after 60000 generations that this enzyme was transcribed in an aerobic environment but I have not recently looked at all the mutations required to do this. Do you think it was random mutations or as you say the environment was enabling the evolutionary process by some mechanism we don't yet understand? bill cole
bill cole: So how do you explain 10^12 population and 60000 generations fixing only 100 mutations and chimp man split with 44million with 10^10 population and 300000 generations? The rate of fixation of neutral mutations is generally the same as the mutation rate — regardless of population size. The neutral mutation rate is about 10^-10. The genome of E. coli is about 10^7 bases, so we expect a new mutation with every thousand replications or so. After 60000 that's about 60 mutations, which is in the ballpark. Mutations in humans works a bit differently. The human gamete is the result of many replications. The human genome is about 3*10^9 base-pairs, so there are about 0.3 mutations per replication of the gamete. It takes about 30 replications to make an egg, which introduces 10 mutations average. The number of replications to make a male gamete varies with age, but about 400 replications is typical. That introduces about 120 mutations. So we have about 1.3*10^2 mutations per generation times 3*10^5 generations which equals about 4*10^7 mutations, which is in the ballpark of 44 million. The rate of fixation of selectable mutations depends on the fitness landscape. bill cole: You are describing a mechanism other then random mutation or the phone example should translate directly. Not sure we would call the environment a mechanism, but it is certainly an important component of the process. Turns out the physical landscape, both on the molecular and morphological level, are explorable by evolutionary search. Otherwise, the random mutation in Lenski's bacteria would have been very unlikely to increase fitness, or in the case of Cit+, to have made multiple sequential steps in fitness. Origenes: that if evolution predicts gaps this wide, then why is there no such gap wrt to the red sequence? The gaps are formed by extinction, which are contingent. Compare a10 to f10 to m10: http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Origenes: And if the theory predicts gaps and no-gaps, then the theory predicts nothing at all. Sort of like meteorology. It predicts both hot and cold, wet and dry. Dionisio: Can you point to what seems wrong or inaccurate in the above quoted comments? It oversimplifies what happened. There were potentiating mutations, a tandem copy, then amplification and optimizing mutations. They ask "Does any of this resemble natural, undirected Darwinian evolution?" The answer is yes. The mutations were consistent with random distributions, and the selection was consistent with population genetics. Dionisio (quoting): "The components of an organism’s metabolic, regulatory, and developmental networks […] interact in complex ways that are attuned to its current niche." Why did you use ellipses at that point? Let's read the entire quote:
The components of an organism's metabolic, regulatory, and developmental networks have evolved to interact in complex ways that are attuned to its current niche. Yet, these networks are also poised such that they can be dynamically reorganized toward new purposes by only a few mutations in key enzymes and regulatory proteins.
Now, you should be able to make sense of the researchers comments. Dionisio (quoting): "No new genetic information (novel gene function) evolved." Again, the mangling of language. New genetic information certainly did evolve. It should simply read "No novel gene evolved." Zachriel
Zachriel:
That’s was the argument presented, but evolutionary divergence predicts “gaps” in extant organisms,
Reference please. Your say-so is neither an argument nor valid Virgil Cain
Origenes @784
If evolutionary theory predicts gaps, then it cannot explain the red sequence. If the theory predicts no-gaps, then it cannot explain the blue sequence. And if the theory predicts gaps and no-gaps, then the theory predicts nothing at all.
Quite on the contrary, that theory does predict anything and everything. Head? They win. Tail? We lose. The problem is that we just don't understand it. We should start from learning biology 101. There are free courses online. Then -and only then- maybe we should understand how it all works. :) Dionisio
Zachriel @734
Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There’s no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn’t have a tendency towards complexity. Rather, it’s opportunistic and fills available niches. IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior.
Ok. Thank you. Can you comment on the below quoted text?
Van Hofwegen et al. demonstrate that E. coli rapidly evolves ability to use citrate when long selective periods are provided. This contrasts with the extreme delay (15 years of daily transfers) seen in the long-term evolution experiments of Lenski and coworkers. Their idea of “historical contingency” may require reinterpretation. Rapid evolution seems to involve selection for duplications of whole cit locus that are too unstable to contribute when selection is provided in short pulses.
Re-interpreting long-term evolution experiments — Is delayed adaptation an example of historical contingency or a consequence of intermittent selection? John Roth* and Sophie Maisnier-Patin doi: 10.1128/JB.00110-16 http://jb.asm.org/content/early/2016/02/10/JB.00110-16.abstract
Reinterpretation of Lenski's LTEE? :) [emphasis mine] Dionisio
Zachriel @734
Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There’s no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn’t have a tendency towards complexity. Rather, it’s opportunistic and fills available niches. IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior.
Ok. Thank you. Can you comment on the below quoted text?
The isolation of aerobic citrate-utilizing Escherichia coli (Cit+) in long term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. [...] direct selection would rapidly yield the same class of E. coli Cit+ mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. [...] the rarity of the LTEE mutant was an artifact of the experimental conditions, not a unique evolutionary event. No new genetic information (novel gene function) evolved.
Rapid evolution of citrate utilization by Escherichia coli by direct selection requires citT and dctA Dustin J. Van Hofwegen, Carolyn J. Hovde and Scott A. Minnich doi: 10.1128/JB.00831-15 http://jb.asm.org/content/early/2016/01/28/JB.00831-15.short?rss=1&ssource=mfr
No new genetic information (novel gene function) evolved. ? :) [emphasis mine] Dionisio
Zachriel @734
Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There’s no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn’t have a tendency towards complexity. Rather, it’s opportunistic and fills available niches. IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior.
Ok. Thank you. Can you comment on the below quoted text?
[...] mutations in the gltA gene encoding citrate synthase (CS) were critical for both potentiating the evolution of aerobic citrate utilization in the Lenski LTEE and for the subsequent refinement of this new metabolic capability. [...] complexity in both the resource environment and in the genetic architecture of the cell conspired to make this metabolic innovation possible. [...] innovations may rely [...] on the inherent malleability of core cellular processes. The components of an organism's metabolic, regulatory, and developmental networks [...] interact in complex ways that are attuned to its current niche. Yet, these networks are also poised such that they can be dynamically reorganized toward new purposes by only a few mutations in key enzymes and regulatory proteins.
Fine-tuning citrate synthase flux potentiates and refines metabolic innovation in the Lenski evolution experiment Erik M Quandt, Jimmy Gollihar, Zachary D Blount, Andrew D Ellington, George Georgiou, Jeffrey E Barrick DOI: http://dx.doi.org/10.7554/eLife.09696 eLife 2015;4:e09696 http://elifesciences.org/content/4/e09696v2
Are they referring to biological systems with built-in adaptation mechanisms? :) [emphasis mine] Dionisio
Zachriel @734
Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There’s no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn’t have a tendency towards complexity. Rather, it’s opportunistic and fills available niches. IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior.
Ok. Thank you. Are Cit+. E. coli as different from other bacteria as a whale is from a cow (both mammals)? Or is it more comparable to the difference between a cat and a dog? My children have a cat and a dog that coexist in full harmony. :) Dionisio
Zachriel @734
Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There’s no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn’t have a tendency towards complexity. Rather, it’s opportunistic and fills available niches. IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior.
Ok. Thank you. In a (3+ years old) non-academic article* they wrote the below comments on this "Cit+. E. Coli" topic:
In Lenski's experiment, the bacteria (both Cit+ and wild-type) already possessed a gene named citT. It encodes a protein that transports a range of citrate-like chemicals. The recent results showed that the bacteria made extra copies of citT and a neighboring sequence—a process called gene amplification. More copies of the gene should translate to higher amounts of the transporter protein that it encodes. With enough transporters, the bacteria could access enough citrate. But oxygen deactivates citT, and having many copies of a gene that is turned off is not very useful! But the bacteria solved this problem when the amplification event also moved the gene sequence to a different place in the bacterial chromosome, where a different but pre-existing promoter could regulate it. Unlike the original one, it appears that the new promoter does not have an "oxygen off" switching mode. Instead, it allowed expression of citT in the presence of oxygen so that the bacteria successfully imported enough citrate to grow. The study authors wrote, "The structure of the cit amplification led us to propose that the Cit+ trait arose from an amplification-mediated promoter capture."1 Further investigation confirmed the proposal. References 1. Blount, Z. D. et al. 2012. Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature. 489 (7417): 513-518.
Can you point to what seems wrong or inaccurate in the above quoted comments? Thank you. (*) http://www.icr.org/article/7083/ Dionisio
Zachriel,
Origenes: One reason is, that if evolutionary processes were responsible, then we would have found homologies in pre-vertebrates — similar to homologies found wrt the red sequence.
Zachriel: That’s was the argument presented, but evolutionary divergence predicts “gaps” in extant organisms, so such gaps are consistent with evolution.
The problem for your position is, that if evolution predicts gaps this wide, then why is there no such gap wrt to the red sequence? If evolutionary theory predicts gaps, then it cannot explain the red sequence. If the theory predicts no-gaps, then it cannot explain the blue sequence. And if the theory predicts gaps and no-gaps, then the theory predicts nothing at all. Origenes
A special thank you to Zachriel, who has with patience and intellectual honesty defended his views. Even if I don’t agree with him, I certainly appreciate his effort. I believe that we have touched some very interesting aspects of the debate here.
I agree with this. I am interested in the science returning to a discipline of testing. Zachriel discusses the issues with integrity. bill cole
Zachriel
We observe mutations, and can determine their rate. We can calculate the rate of accumulation of neutral mutations. We can then compare this to the differences between species for confirmation. That’s not circular, but independent lines of evidence supporting the same conclusion.
So how do you explain 10^12 population and 60000 generations fixing only 100 mutations and chimp man split with 44million with 10^10 population and 300000 generations? How do you explain the difference without a circular argument? In the lab large populations and 20% of human generations are producing .0004% fixed mutations. The math does not work.
You just said to duplicate the number, so the original number is still there, as well as many other discovered numbers that may be of interest. In any case, phone numbers don’t generally form a landscape suitable for evolutionary search. Compare this to Lenski’s experiment, where the bacteria evolved to their laboratory environment through mutations.
You are describing a mechanism other then random mutation or the phone example should translate directly. What is the mechanism you are describing that caused genome change in the Lenski experiment? You may say there is more proteins that can fold but this is small compared to the amount of added sequences in proteins compared to phone numbers. The protein problem is orders of magnitude larger then the phone problem with 10^500 sequential space units. I think this issues kills the current theory(random change plus selection and drift) and we should search immediately for and alternative mechanism. I hope you have ideas. Have you thought about alternative splicing as a mechanism? bill cole
Origenes: Thank you for admitting that you have no idea how the blue sequence of the Prickle 1 protein came about from an evolutionary standpoint. Well, everything else is evolution, so we can reasonably suppose evolution in this case also, but we are not knowledgeable as to the specific pathways. Origenes: One reason is, that if evolutionary processes were responsible, then we would have found homologies in pre-vertebrates That's was the argument presented, but evolutionary divergence predicts "gaps" in extant organisms, so such gaps are consistent with evolution. Zachriel
@743 +1 mike1962
To all: I will be away for a few days, so I will not be able to go on with this very good discussion for some time. I want to really thank all those who have contributed. It has been great fun! A special thank you to Zachriel, who has with patience and intellectual honesty defended his views. Even if I don't agree with him, I certainly appreciate his effort. I believe that we have touched some very interesting aspects of the debate here. So, for the moment, many greetings to all! :) gpuccio
Zachriel:
We expect millions of neutral mutations to fix (the rate of fixation of neutral mutations is generally equal to the rate of mutation)...
Unfortunately no one has ever validated the math of neutral evolution. That means Zachriel is spewing pure propaganda and trying to pass it off as a fact. Virgil Cain
Zachriel,
Origenes: There is simply no coherent evolutionary explanation for the sudden appearance of 600 bits of specific functional information in the “blue sequence” of Prickle 1
Zachriel: Have no idea about Prickle 1,
Thank you for admitting that you have no idea how the blue sequence of the Prickle 1 protein came about from an evolutionary standpoint.
Zachriel: (...) nor has any IDer provided any evidence of the manufacturing process.
Incorrect. Thanks to Gpuccio's argument we know that intelligent design must be involved.
However, evolution is capable of building up complex structures incrementally, such as when there is a selectable pathway.
That is the Darwinian hypothesis. However, as you have admitted, this doesn't explain the blue sequence of the Prickle 1 protein. One reason is, that if evolutionary processes were responsible, then we would have found homologies in pre-vertebrates — similar to homologies found wrt the red sequence. Origenes
bill cole: So evolution is a circular argument. We look at history and assume random mutations created what we see and then determine mutation rate. We observe mutations, and can determine their rate. We can calculate the rate of accumulation of neutral mutations. We can then compare this to the differences between species for confirmation. That's not circular, but independent lines of evidence supporting the same conclusion. bill cole: If we had 1000000 people do this for a year. Would anyone have added a new number without destroying the rest of their numbers? You just said to duplicate the number, so the original number is still there, as well as many other discovered numbers that may be of interest. In any case, phone numbers don't generally form a landscape suitable for evolutionary search. Compare this to Lenski's experiment, where the bacteria evolved to their laboratory environment through mutations. Zachriel
Zachriel So evolution is a circular argument. We look at history and assume random mutations created what we see and then determine mutation rate. Don't you think 100 fixed mutations over 30 years and populations 0f 10^12 we would need to see more than 100 fixed mutations or does this rule out random mutation and selection as the driver of lifes diversity? Again the sequential space of the genome is 4^3.2 billion. Imagine taking your cell phone and copying one of the numbers you have on direct dial(simulate gene duplication). Now change a number randomly from one of your direct dial numbers every hour. Do you ever expect your direct dial numbers to improve? If we had 1000000 people do this for a year. Would anyone have added a new number without destroying the rest of their numbers? Sequences and random mutation are like oil and water. Your computer password in an example how we use sequences to block random search. bill cole
"None of this tells us whether we should see a new protein in Lenski’s experiment." Pathetic. EugeneS
bill cole: With so many more populations and generations how do you expect so few fixed mutations? We expect millions of neutral mutations to fix (the rate of fixation of neutral mutations is generally equal to the rate of mutation), but the amount of fixation due to selection depends on the fitness landscape. The number fixed due to selection could be few or many. Only a look at the actual history can answer this question. Zachriel
Zachriel
That would be the rate of fixation of neutral fixation, but does not include fixation of alleles under selection. More important, forty-four million is the number of mutations that have become fixed — not the total number of mutations, while you compare it to the total number of mutations in Lenski’s experiment. About 100 mutations were fixed in Lenski’s experiment, most of them neutral.
A good point thanks. With so many more populations and generations how do you expect so few fixed mutations? It seems like the difference between man and chimps could not be caused by mutations if an experiment like Lenski's only created 100 mostly neutral mutations. bill cole
Zachriel the grand equivocator:
However, evolution is capable of building up complex structures incrementally, such as when there is a selectable pathway.
There isn't any evidence that evolution by natural selection, drift and/ or neutral construction can produce complex adaptations. No one knows how to test the claim. Virgil Cain
bill cole: The 44 million is based on 130 mutations per generation, a number proposed by Dr Moran. That would be the rate of fixation of neutral fixation, but does not include fixation of alleles under selection. More important, forty-four million is the number of mutations that have become fixed — not the total number of mutations, while you compare it to the total number of mutations in Lenski's experiment. About 100 mutations were fixed in Lenski's experiment, most of them neutral. bill cole: If the evolutionary story were true I would expect the Lenski experiment to produce multiple functioning proteins with the populations and generations involved. Ignoring the gross error in your argument just detailed, again, new folds may or may not have been found by bacteria in Lenski's experiment, but they won't become observable unless they become populous. Bacteria have highly optimized genomes, so we wouldn't expect radical changes in a short period of time. Indeed, Cit+ is beyond what most biologists would have expected. Its support for evolutionary contingency makes it all the more interesting. Dionisio: Is that “Cit+. E. coli” also a bacteria? Of course. Are humans also mammals? By the way, the inability of E. coli to metabolize citrate in aerobic conditions is generally considered a distinguishing characteristic of the species. Dionisio: How many generations of RM+NS+HGT+… did it take to get that Cit+. E. coli? There's no horizontal gene transfer in this strain of bacteria. It took about 31000 generations for Cit+ to be discovered, but potentiating mutations occurred much earlier. Dionisio: Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? Why would they? Bacteria have evolved to be fast reproducers, so they have highly optimized genomes. Evolution doesn't have a tendency towards complexity. Rather, it's opportunistic and fills available niches. Dionisio: IOW, have bacteria remained bacteria so far in that famous experiment? Yes, just like humans are still mammals. Dionisio: How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let’s say multicellular? Bacteria can exhibit primitive colonial behavior. Origenes: There is simply no coherent evolutionary explanation for the sudden appearance of 600 bits of specific functional information in the “blue sequence” of Prickle 1 Have no idea about Prickle 1, nor has any IDer provided any evidence of the manufacturing process. However, evolution is capable of building up complex structures incrementally, such as when there is a selectable pathway. Zachriel
Gpuccio @726,
Gpuccio: Let’s try to understand well what your theory seems to be. (...)
It's very telling that after so many posts, you are the one who has to take on the task to piece together an evolutionary "explanation", because Zachriel is unable/unwilling. I take it that this is his way of conceding the argument. There is simply no coherent evolutionary explanation for the sudden appearance of 600 bits of specific functional information in the "blue sequence" of Prickle 1 — and other proteins. Even a vague broad evolutionary sketch is amiss. Gpuccio, you have presented a very strong argument. Thank you very much! Origenes
Zachriel @719
Dionisio: what’s the name of the new biological system that has resulted from this experiment? It’s called Cit+. E. coli have the ability to metabolize citrate in anaerobic conditions. Cit+ is the trait that allows the strain to metabolize citrate in aerobic conditions. Dionisio: Where is that new biological system located in the so called “tree of life”? It’s obviously a branch of E. coli.
Thank you for the information. Is that "Cit+. E. coli" also a bacteria? How many generations of RM+NS+HGT+... did it take to get that Cit+. E. coli? Have those results provided any hint pointing to the possibility of getting a higher complexity system above the bacteria in the tree of life? IOW, have bacteria remained bacteria so far in that famous experiment? BTW, how could we convert the bacteria into something of higher complexity in the bio ladder? How can we at least theoretically propose a step-by-step process to move from bacteria up to the next level, let's say multicellular? Thank you in advance for answering my laughable, naïve, uneducated questions. :) Dionisio
gpuccio @724
No new complex functional information was generated in Lenski’s experiment. There was one significant result in the acquisition of the Cit+ phenotype which, as explained, is the result of a few mutations, maybe three. The only one which has been well identified, as far as I understand, is a duplication/inversion event, which results in the reactivation of a citrate transporter, which usually is active only in anaerobic conditions. Essentially, it is the activation of a new promoter, similar to the translocation in Burkitt’s lymphoma which I have mentioned in my post #713. One point which has not been stressed enough is that Lenski’s experiment creates very hard selecting conditions. Those very local and strong conditions can easily select simple variation events which can be useful in that context. The situation is very similar to simple forms of antibiotic resistance, well know for a long time.
Very interesting. Thank you. Dionisio
Zachriel
Where did you get that there were 44 million mutations? None of this tells us whether we should see a new protein in Lenski’s experiment. As noted, there may have been new folds involved, but they probably didn’t provide a selectable advantage so never entered the population.
The 44 million is based on 130 mutations per generation, a number proposed by Dr Moran. My skepticism of evolution or Modern evolutionary theory is that I don't see any way for mutation to find working proteins based on the sequential space of the genome. Lenski experiment just confirmed my thoughts. For the evolutionary story to be true we need to create 20000 proteins to get to us. We know that order matters the question is how much. This was part of the Hunt paper. Statistically when the genome mutates it is much more likely to be delirious then not. How in the world do you form 20000 proteins with this process when you are randomly changing 10^3.2 billion possible sequences. This thesis is nonsense. I am not saying there is not a possible natural solution, I am just saying that there is not a credible proposal yet. If the evolutionary story were true I would expect the Lenski experiment to produce multiple functioning proteins with the populations and generations involved. If no new proteins occurred how do you explain other evolutionary events with orders of magnitude of smaller populations and generations that required multiple novel proteins. bill cole
bill cole: There were billions of mutations in this experiment. Most being point mutations. bill cole: Compare that to a more modern evolutionary event like man’s where 50 novel proteins emerged with 44 million mutations. Where did you get that there were 44 million mutations? None of this tells us whether we should see a new protein in Lenski's experiment. As noted, there may have been new folds involved, but they probably didn't provide a selectable advantage so never entered the population. Zachriel
Zachriel
One in 10^10 doesn’t indicate protein space is flat, but somewhat rugged. That doesn’t mean it is not traversable by evolution. In any case, perhaps a new protein fold was discovered, but it’s not likely to become fixed if it doesn’t provide an advantage somehow.
There were billions of mutations in this experiment. Compare that to a more modern evolutionary event like man's where 50 novel proteins emerged with 44 million mutations. Plus a 50% change in splicing sequences. Do you see the problem with the proposed mechanism of random change? If we don't see a new protein emerge in the largest evolutionary experiment on the planet how do we explain anything through a random process? bill cole
gpuccio: Therefore, I maintain that the Lenski experiment does not help you in any way to support your theory of how complex functional sequence information is generated in proteins, like in the examples I have offered. If there are selectable pathways, there is no particular limit to the size of the structure that can evolve. gpuccio: No new complex functional information was generated in Lenski’s experiment. However you want to characterize it, significant changes to the genome evolved that were far beyond what would be expected of random change alone. gpuccio: The only one which has been well identified, as far as I understand, is a duplication/inversion event, which results in the reactivation of a citrate transporter, which usually is active only in anaerobic conditions. We know there was a potentiating event, probably consisting of more than one mutation. We know that the tandem repeat was followed by copying of the module, then additional optimizing mutations. bill cole: If the protein coding space was flat i.e. many possible proteins that fold and function I would expect one to form with a gene duplication if Art Hunts probability numbers of 10^10 probability of finding a protein with 100 AA length. One in 10^10 doesn't indicate protein space is flat, but somewhat rugged. That doesn't mean it is not traversable by evolution. In any case, perhaps a new protein fold was discovered, but it's not likely to become fixed if it doesn't provide an advantage somehow. Zachriel
Zachriel: Let's try to understand well what your theory seems to be. Let's go back to our blue sequence of the Prickle 1 protein. Now, as we have spoken of "fish", let's refer to the most likely fish-like ancestor of vertebrates, or to be more precise modern descendante of such an ancestor: the lancelet. Now, as I have tried to argue in my follow-up post, the blue sequences of this protein are strictly taxonomically restricted. Here is the blue sequence of the lancelet blue sequence in the lancelet homologue of Prickle 1: SKQSPPAQSSGSPY DTGFDTLTRGDGSQESDNNSTRSRKRDRRSRSMENLKREFYARKPGWGQSKLRMESARNLQKYDLSSDGS PDVNVQPRRVKHRSRSMTRMSSDARRATDYSDPRSDTENQSVASGTSGKQSPWVPRDGFTKENLERISPP NGFESAPQNMLPQWQSTPQEARYWNIQGGVTQGGFPSAVQADVKDPDAQYDTSQGYDSGGHECESDRQSQ ASGWTAPQDLPLPVPENGPRYEERTVPYTTQEYLPHDRRNVYIPQEPEIEYSSTSELPPPRGILRNASDT QLAEKFRKMKLRDEYYTSSSSSDSEDDDWLIPQRRVRVRYVDTDFTGGGRHGSMPPGAERPRGKKSKHCT IS This one, instead, is the blue sequence in Callhorincus milii: ASDSSDSAFQSARSRESRRSVRMGKSSKSADQCRQSL LLSPTINYKCPDGSIKGDDPLSQQMDVLSLNSQTTSLSSDHFWKGRMDPDAPEHEEWAEHDDYMTQLLLK FGDRGIFQQSNEGNRQCDPWMSDSEVKSKSELKSHHQGLASKKYQSNMYWAQSQDNLGDSAYGSHPGPAS SRKIQELDIEHGATSYKHEQNPWYEGSLECLTNQSKPAEESVRDSVDSLALSNITGASIDGESQSQQRSS MFALQDFQEMENDCEKMSTMGTMNSSMRHRSTESLKSLTSELCQVVVPEEKQKPLYLPILRRSESQSRSQ QVKFSDDVIDNRNYEEIEIRRPPMSERARRRAYNFDGHSNRHHHRRRRSRKSRSDNALHLATERRGQRER PRLCSPEDYDKLMQAKSSQEVQTYIQNQEMYRQYTPSTPDYALQNQVVDKFLGLYGDDDDSWCSTCSSSS SDSEEEGYFLGQPIPQPKAQRYQCYTDDLSEPSSVLSTSIVGPRTSKPTKKKGHKSKNCIIS OK, some points: 1) These two sequences have absolutely no homology one with the other. 2) The lancelet sequence has absolutely no homology with the human sequence. 3) The callorhincus milii sequence, instead, has almost 600 bits of homology and 350 identities with the human sequence. Now, in my follow-up post, I have argued, with motivations, that the blue sequences are an integral and functional part in all Prickle proteins in all species, but that they are taxonomically restricted. Therefore, let's accept for this discussion that: 4) Both the sequence in Lancelet and the sequence in Callorhincus are functional. And completely different. Because, reasonably, they do different things in the two different species. Now, what would be your scenario? Let's say that, more than 400 million years ago, our oceans were filled with the common ancestor of lancelet and shark, ad that it was more similar to a fish, let's say to lancelet. Let's say that this ancestor had about 100 million years to split into cephalochordata and cartilaginous fish. These, with great generosity, are your: "10^12 fish-duplications/year * 10^8 years = 10^20 fish-duplications." OK, so this common ancestor had Prickle 1, with its red sequence and... what kind of blue sequence? Let's suppose that it was similar to the lancelet blue sequence. Now, the mutations have apparently the result to transform the functional sequence in lancelet (or some homologue of it) into a completely new sequence, the one which will be largely conserved in vertebrates. IOWs, those mutations must generate 600 bits of specific functional information, for a new function. With about 350 AAs which will be conserved as identities for 400 million years. So what? Let's say that there is a path of 350 steps of 1 AA, such that each step will be fixed (in the planet's oceans!), one at a time, because each of them brings a significant reproductive advantage. One with a big s, for each AA mutation, so that those precious mutations are not lost by drift. Is that what you believe? That single AA steps from the sequence in lancelet, or some equivalent of it, each conferred strong reproductive advantage? In a precursor which is very much like a lancelet? And which is going to become like a shark? While a lot of other proteins undergo similar "magical" innovations? And all those lancelets precursors, which have been expanded to the whole planet for hundreds of time, have all gone extinct? 10^12 fish for each of the 350 fixations? While we still have, only, lancelets and sharks? Is that, more or less, your idea? And of course, if the steps are "bigger" (say 2-3 AAs at a time), they are less numerous, yes, but each of them is also much more unlikely. I doubt that using bigger steps helps you in any way. OK, you will probably mention recombination again. I can't imagine how, but I am sure you will! gpuccio
Zachriel If the protein coding space was flat i.e. many possible proteins that fold and function I would expect one to form with a gene duplication if Art Hunts probability numbers of 10^10 probability of finding a protein with 100 AA length. It appears that the protein coding space is not a flat as Art thought. bill cole
Dionisio: No new complex functional information was generated in Lenski's experiment. There was one significant result in the acquisition of the Cit+ phenotype which, as explained, is the result of a few mutations, maybe three. The only one which has been well identified, as far as I understand, is a duplication/inversion event, which results in the reactivation of a citrate transporter, which usually is active only in anaerobic conditions. Essentially, it is the activation of a new promoter, similar to the translocation in Burkitt's lymphoma which I have mentioned in my post #713. One point which has not been stressed enough is that Lenski's experiment creates very hard selecting conditions. Those very local and strong conditions can easily select simple variation events which can be useful in that context. The situation is very similar to simple forms of antibiotic resistance, well know for a long time. gpuccio
Zachriel: Thank you for the references. I hoped there was something more precise, but I appreciate your information. By the way, I acknowledge that you have not commented on my last statements, relative to the problem of combinatorial probabilities: "Therefore, I maintain that the Lenski experiment does not help you in any way to support your theory of how complex functional sequence information is generated in proteins, like in the examples I have offered. Is it necessary for me to remind that 1300 bits of information are not the sum of smaller chunks of, say, 1-16 bits? Or, IOWs, that a specific sequence of 906 AAs is definitely not the sum of 906 variations of 1 AA?" gpuccio
bill cole: With billions of mutations over 30 years to demonstrate large scale evolutionary change we would expect de novo protein coding genes if the protein gene sequence space was flat. Why would you expect de novo proteins? Zachriel
Virgil
However Lenski has demonstrated the severe limitations of evolutionary processes.
I agree with this. The Lenski experiment did demonstrate adaption with the citrate enzyme turning on however the sequence already existed. With billions of mutations over 30 years to demonstrate large scale evolutionary change we would expect de novo protein coding genes if the protein gene sequence space was flat. This experiment showed that protein coding space is indeed rare. bill cole
Zachriel:
The rate of mutation was such that if the potentiating mutations had a significant benefit, they probably would have appeared in other populations.
Not necessarily and not an argument. The fact that the only gene capable of transporting citrate through the membrane was duplicated and put under the control of an existing promoter suggests this was not a random change. However Lenski has demonstrated the severe limitations of evolutionary processes. Virgil Cain
Dionisio: what’s the name of the new biological system that has resulted from this experiment? It's called Cit+. E. coli have the ability to metabolize citrate in anaerobic conditions. Cit+ is the trait that allows the strain to metabolize citrate in aerobic conditions. Dionisio: Where is that new biological system located in the so called “tree of life”? It's obviously a branch of E. coli. Zachriel
gpuccio: How do you know? Have they been identified? The rate of mutation was such that if the potentiating mutations had a significant benefit, they probably would have appeared in other populations. The rnk-citT module itself was only slightly advantageous, and was subject to clonal interference. Statistical tests indicate that the potentiating mutations were unlikely to have conferred a benefit. By the way, even if the potentiating mutations were beneficial, that just means the chain of selectable events was even longer. gpuccio: “multiple duplications of the rnk-citT module, then additional optimizing mutations.” The fact that the early versions of Cit+ were very weak compared to later versions indicates a process of optimization. See Blount et al., Genomic Analysis of a Key Innovation in an Experimental E. coli Population, Nature 2012: "These early Cit+ genomes also show increases in cit copy number. ... Amplifications tend to be unstable, and further refinement may have favored stable mutations. The evolution of the mutator phenotype in the Cit+ lineage complicates efforts to identify these later refining mutations, but some interesting candidates include SNPs in citT itself ..." Zachriel
gpuccio I highly appreciate that many times you've been kind enough to answer my embarrassing dumb questions gracefully, setting a nice precedent in this forum for others to imitate (though unfortunately some folks don't). Taking advantage of your proven patience and tolerance, I'll dare to ask a few questions related to the Lenski's experiment that has been mentioned recently in this discussion, hoping that at least they make some sense, even if this makes most readers laugh at my deep ignorance of this subject: After gazillion evolutionary generations with so many accumulated random mutations (perhaps many of them beneficial) and the powerful natural selection operating on the fittest individuals and moving forward toward higher complexity, what's the name of the new biological system that has resulted from this experiment? Where is that new biological system located in the so called "tree of life"? Which branch? Does it resemble another known biological system of higher complexity than the bacteria or it is a 'de novo' entity? Thank you. Dionisio
Zachriel: "The potentiating mutations were neutral mutations." How do you know? Have they been identified? "multiple duplications of the rnk-citT module, then additional optimizing mutations." Could you provide the source of these last statements' gpuccio
Right the only gene that could provide a protein capable of transporting citrate through the membrane was magically duplicated and magically put under the control of a promoter that was on in the presence of O2. Sounds like an example of Dr Spetner’s non-random evolution via built-in responses to environmental cues. Lenski has shown the world how very limited evolutionary processes are. By continuing to use his experiment as some example it proves that evolutionists really do have nothing to offer. Virgil Cain
gpuccio: Neutral mutations, even if fixed, have no relevance for the probabilistic problem, as many times discussed. gpuccio: The two supposed potentiating mutations for Cit+ occurred apparently in the first 20000 generations. The potentiating mutations were neutral mutations. gpuccio: It is better to refer ro the number of genome duplications. 10^12 fish-duplications/year * 10^8 years = 10^20 fish-duplications. gpuccio: The only example of “coordinated” events seems to be the evolution of Cit+, which apparently implies three interacting single events. There was at least one potentiating mutation (probably two or more), a tandem duplication forming the rnk-citT module, multiple duplications of the rnk-citT module, then additional optimizing mutations. In other words, a lot of sequential changes providing increasing degrees of fitness for the environment. Zachriel
Zachriel: By the way, the abnormal activation of a promoter as a result of gross genomic variation is a well known event. In humans, we have a good example in Burkitt's lymphoma and B cell leukemia, where some B cell precursor becomes neoplastic because of a chromosomal translocation, 8 - 14, which moves the gene of an important transcription factor, c-myc, implied in cell reproduction regulation, near the promoter of the immunoglobulin heavy chain, which in the B lineage is obviously very active. As a result, c-myc is overexpressed, and the mutated cell line acquires a reproductive advantage (becomes neoplastic). Therefore, Lenski's results are no news at all. gpuccio
Zachriel: First of all, the concept of generations is confounding in Lenski's experiment, because we are dealing with a constantly expanding population. It is better to refer ro the number of genome duplications. Beneficial mutations, therefore, would be approximately 1 in 10^11 genome duplications. Neutral mutations, even if fixed, have no relevance for the probabilistic problem, as many times discussed. The two supposed potentiating mutations for Cit+ occurred apparently in the first 20000 generations. We must also remember that in Lenski experiment many mutations were not beneficial at all, and that one of the results was an increase in genomic variation rate. From Wikipedia: "Of the 12 populations, four developed defects in their ability to repair DNA, greatly increasing the rate of additional mutations in those strains." And: "All twelve of the experimental populations show an increase in cell size, and in many of the populations, a more rounded cell shape.[9] This change was partly the result of a mutation that changed the expression of a gene for a penicillin-binding protein, which allowed the mutant bacteria to outcompete ancestral bacteria under the conditions in the long-term evolution experiment. However, although this mutation increased fitness under these conditions, it also increased the bacteria's sensitivity to osmotic stress and decreased their ability to survive long periods in stationary phase cultures." OK, to sum up, let's say that 10 - 20 "beneficial" (under the circumstances) mutations were fixed in 10^12 - 10^13 genome duplications. Still, they are apparently single independent mutations. The only example of "coordinated" events seems to be the evolution of Cit+, which apparently implies three interacting single events. Even if that is true, and even if it is not in any way facilitated by some adaptive response, as Virgil Cain suggested, we are still left with a rather simple variation. Moreover, in no way it seems to be "helped" by any particular functional landscape of proteins, because apparently the important final event is a duplication-inversion which simply activates a promoter activity: IOWs, a simple switch activation, which has nothing to do with protein sequence-structure-function landscape. Therefore, I maintain that the Lenski experiment does not help you in any way to support your theory of how complex functional sequence information is generated in proteins, like in the examples I have offered. Is it necessary for me to remind that 1300 bits of information are not the sum of smaller chunks of, say, 1-16 bits? Or, IOWs, that a specific sequence of 906 AAs is definitely not the sum of 906 variations of 1 AA? gpuccio
Zachriel:
This was before the Cit+ trait evolved, which entailed both potentiating mutations and optimizing mutations.
Right the only gene that could provide a protein capable of transporting citrate through the membrane was magically duplicated and magically put under the control of a promoter that was on in the presence of O2. Sounds like an example of Dr Spetner's non-random evolution via built-in responses to environmental cues. Lenski has shown the world how very limited evolutionary processes are. By continuing to use his experiment as some example it proves that evolutionists really do have nothing to offer. Virgil Cain
gpuccio: In general, mutations with only weak beneficial effects, even those lucky enough to escape drift loss, require a very long time to become fixed or even numerically dominant, and thus a clone bearing a weakly beneficial mutation will usually be out-competed by some more beneficial mutation that appears on another background. A hundred mutations were fixed in the first 20,000 generations, 10-20 of them with beneficial effect, which is consistent with clonal interference. This was before the Cit+ trait evolved, which entailed both potentiating mutations and optimizing mutations. gpuccio: Zachriel will say that we don’t take into account recombination! Lenski's statement takes into account the lack of recombination, which results in clonal interference of weakly selective mutations. With recombination, the chance of fixation of independent, beneficial mutations remains 2s. The time to fixation, which is also relevant, depends on the selection coefficient, and somewhat on the size of the population. Even in Lenski's asexual bacteria exhibiting clonal interference, beneficial mutations were fixed at an average rate of one per thousand generations. The rate was faster at the beginning of the experiment, slowed, then accelerated again during the evolution of Cit+. Over millions of years, in organisms that reproduce a several times a years, that still allows for vast changes to the genome to occur. Zachriel
Virgil Cain: "Unless, of course, there is a competing advantageous trait, which there usually is." And, of course, Lenski is well aware of that. From his paper: "The situation is made even more complicated, and the fixation probabilities further reduced, by the fact that the populations studied here are asexual, which leads to a phenomenon called clonal interference. In essence, clonal interference occurs because beneficial mutations may arise in two or more different clones but, in the absence of recombination, only one of them can ultimately go to fixation. In general, mutations with only weak beneficial effects, even those lucky enough to escape drift loss, require a very long time to become fixed or even numerically dominant, and thus a clone bearing a weakly beneficial mutation will usually be out-competed by some more beneficial mutation that appears on another background. Thus, the 2s probability of fixation calculated by Haldane is, in fact, an upper limit." Now, Zachriel will say that we don't take into account recombination! Recombination is, together with extinction his pet argument. :) gpuccio
Zachriel:
So if a particular trait provides a 10% advantage, there is a 20% chance of fixation.
Unless, of course, there is a competing advantageous trait, which there usually is. Virgil Cain
gpuccio: The important point is that each selectable step must expand to the whole population, or almost, if it must be a reasonable place where the successive step can take place. The chance of fixation is 2s, where s is the selection coefficient. So if a particular trait provides a 10% advantage, there is a 20% chance of fixation. Zachriel
Zachriel: Your last post is senseless. The important point is that each selectable step must expand to the whole population, or almost, if it must be a reasonable place where the successive step can take place. That is true for any possible path to complex functional information, even those which don't exist (practically all). Now, it is irrelevant if the step is fixed in a small population, if after it has to expand to the whole population. It is still one step. One intermediate. And it must expand to the whole population. And that is true of each step, of each intermediate. Therefore, local fixation in a small population does not help. If fixation there must be, it must be in the big population. Therefore, each intermediate must expand, and those many expanded intermediate must be erased, for your dream to come true. gpuccio
gpuccio: A small expansion is irrelevant. Consider a large population with significant genetic diversity. Edges of the population adapt to local conditions through natural selection, often becoming reproductively isolated. This child population then overtakes the parent population. gpuccio: If you have 10^12 fish, and one gets a useful mutation, the probability of a second useful mutation which contributes to the final result (if ever there is such a path!) are completely negligible, if the first mutation remains confined to that fish and to its descendants. That doesn't add up. Let's say there are 10^8 fish of a given species, and a genome of 10^8. That means every mutation is being tried in every generation on average. Such a population is going to have a wide number of types, with distinct geographical variations. gpuccio: But if the mutation expands to a limited population, for some reason reproductively isolated, say of 10^4 fish, then the second mutation will have to occur in that limited population. No, because the child population with the beneficial mutation will tend to overtake the niche of the parent population. This will frequently be accompanied by reproductive isolation. Zachriel
Mung the Internet Prig and Stalker @680
Hi Troll!
A poster responds to another post and is called a "troll." I don't think the word means what Internet epithet hurler Mung thinks it means. Has it ever thought of getting a life? Or saying something intelligent? Daniel King
Zachriel: "It expands in a smaller population" But that's exactly the point! A small expansion is irrelevant. The probabilistic resources of a small population are small. If you have 10^12 fish, and one gets a useful mutation, the probability of a second useful mutation which contributes to the final result (if ever there is such a path!) are completely negligible, if the first mutation remains confined to that fish and to its descendants. Now, if after time t the mutation has become expanded to 10^12 fish again (or even almost to that), then the probabilities of the second mutation will be comparable to those of the first mutation. And that is certainly some help, not negligible. But if the mutation expands to a limited population, for some reason reproductively isolated, say of 10^4 fish, then the second mutation will have to occur in that limited population. OK, 10^4 is better than 1, but only slightly better, for the informational complexity levels we are discussing. Certainly, it is very different from 10^12 organisms. IOWs, the size of the population is the most relevant component of the probabilistic resources of the system, if populations are big enough. And if populations are not big enopugh, there is absolutely no game. gpuccio
Zachriel seems to think there is only ever one population of a given species. Mung
gpuccio: So, one thing is if some beneficial mutation step is expanded to a population of 2^30, all another thing if it is expanded only to a population of 2^10. It expands in a smaller population, which then crowds out sister species. Rinse and repeat. Zachriel
Zachriel: "It means that the history of transitions are lost." That does not seem at all an answer to my quoted comment: "Yes, but fixation in a small population means low probabilistic gain." You realize, I suppose, that the only way positive NS really helps in probabilistic problems is by the quantitative expansion of some trait, don't you? So, one thing is if some beneficial mutation step is expanded to a population of 2^30, all another thing if it is expanded only to a population of 2^10. That was my comment. Which was in answer to your comment that: "Reproductive isolation allows for rapid fixation, especially when the pace of evolution is increased, such as during adaptive radiation." Usually, I try to offer pertinent comments. :) gpuccio
gpuccio: Yes, but fixation in a small population means low probabilistic gain. It means that the history of transitions are lost. Again, this is easy to simulate. If you have divergence, then the leaves will appear to have gaps between them, even if extinction if random. Zachriel
gpuccio: Isn’t that amazing? Well, it's interesting, but not sure why you think it is inconsistent with evolution. Insects diverged from other arthropods and the intermediates are extinct. Zachriel
Zachriel: "Reproductive isolation allows for rapid fixation, especially when the pace of evolution is increased, such as during adaptive radiation." Yes, but fixation in a small population means low probabilistic gain. gpuccio
Zachriel: OK, I suppose we are at a standstill again. Old arguments come back. However, I appreciate the original aspects in the discussion here. I suppose that: "No, that is not correct. If the components were random, then that would be true, but the components aren’t random, but usually the parts of other components, or the detritus of obsolete components." is an appeal to recombination again. But you see, recombination is detected by sequence blasting. Take the case of the 26 AAs segment (post #590 here, and #13 in the other thread). I quote myself: "A 26 AAs sequence is already so specific in the search space of proteins (after all, it corresponds to a search space of 20^26, which is about 112 bits of information) that it is a signature, a fingerprint. Just blast the above sequence and you will get only Prickle proteins in insects. Isn’t that amazing?" So, modules are recognizable. Recombination is detectable. What a pity, when all you need is undetectables, which can remain in the kingdom of fancy! gpuccio
gpuccio: OK, let’s say 10^20 fish-replications. In the whole planet, with all the objections about fixations in a widespread population. Reproductive isolation allows for rapid fixation, especially when the pace of evolution is increased, such as during adaptive radiation. Zachriel
gpuccio: You brought Lenski’s experiment as an example (the only one) of fixation in a biological context, so I commented on it. It shows fixation, and how evolution causes jumps in extant genomes occur. gpuccio: Now, take into account all the other objections which I have made, especially those about combinatorial complexity in a single sequence. As long as there a selectable pathways, then any manner of complex structure can evolve. That's a question of the landscape, however, there are vast numbers of dimensions, and small changes in sequence can often result in small changes in structure, meaning there are selectable pathways, such as with optimizing selection. gpuccio: 1) That observed gaps are too large for evolution to cross. That is the argument from complex functional information, you know. When only looking at the leaves, the gaps will appear larger than they do from a historical perspective. gpuccio: 2) That if the neo darwinian explanation were true, you would have hundreds or thousands of molecular intermediates which were fixed and then disappeared. This is the argument of the missing intermediates. Yes, and it turns out that extinction is rampant in the history of life. We end up with something like this (compare a10 to f10 to m10): http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg gpuccio: But remember, the longer the sequence which builds a single step which will go to fixation, the higher the improbability of having that specific variation. Combinatorial principles always apply. No, that is not correct. If the components were random, then that would be true, but the components aren't random, but usually the parts of other components, or the detritus of obsolete components. Mung: You are aware of the existence of protein superfamilies within the human species, aren’t you? Yes. And? Zachriel
Zachriel:
In any case, now your argument has drifted. It was that historical vestiges would have to be extant in the very same strain. Now, it’s that the gap it too large for evolution to cross.
You are aware of the existence of protein superfamilies within the human species, aren't you? Mung
Zachriel: My argument has not drifted at all. I am just answering your comments. You brought Lenski's experiment as an example (the only one) of fixation in a biological context, so I commented on it. It's the discussion which drifts, not my arguments. OK, let's say 10^20 fish-replications. In the whole planet, with all the objections about fixations in a widespread population. And so? Now, take into account all the other objections which I have made, especially those about combinatorial complexity in a single sequence. You say: "if there is a selectable pathway, then it is well-within the resources described." A very big if, indeed. And are you aware of how many different functional sequences arise in vertebrates from pre-vertebrates? Remember, I have only given a few examples. My argument has always been: 1) That observed gaps are too large for evolution to cross. That is the argument from complex functional information, you know. 2) That if the neo darwinian explanation were true, you would have hundreds or thousands of molecular intermediates which were fixed and then disappeared. This is the argument of the missing intermediates. Both arguments are strong and valid, ad they are complementary. Regarding the possibility that the path is not made of simple mutations, it is obviously a possibility. But remember, the longer the sequence which builds a single step which will go to fixation, the higher the improbability of having that specific variation. Combinatorial principles always apply. gpuccio
gpuccio: That’s 1500 billion divisions {10^12}. Are you sure that we are so distant from the number of replications in a pre-vertebrate population? There are, say, about a trillion fish in the ocean, and say they replicate only once each year. That's 10^12 fish-replications per year * 10^8 years = 10^20 fish-replications. gpuccio: And however, we have 10 – 20 fixations in the whole genome, that is 5×10^6 bp. There were about 100 fixed mutations, though only 10-20 provided a known benefit. gpuccio: In my example, what you need is a sequence of at least 906 coordinated mutations which build a specific sequence in one single protein! That's assuming it was built one point-mutation at a time, which is unlikely. However, even then, if there is a selectable pathway, then it is well-within the resources described. gpuccio: The case of the protein could be treated like the case of Lenski’s fixations only if each single aminoacid of the sequence were capable of giving a strong reproductive advantage to the organism. What Lenski's experiment showed was that functional structures can be contingent on potentiating mutations. In any case, now your argument has drifted. It was that historical vestiges would have to be extant in the very same strain. Now, it's that the gap it too large for evolution to cross. Zachriel
Origenes: The point is: Lenski's events are one more example of what we can call "molecular microevolution". IOWs, very simple mutations which, in a context of extremely strong selection, confer some advantage. Essentially, like simple cases of antibiotic resistance. In no way they are examples of generation of complex functional information. If a new protein which could metabolize citrate had been generated, with an original long and complex sequence which generated a new structure and biochemical activity, then it would be all another thing. But that is not what happened. The sequences which I have brought as examples in this discussion, instead, are true example of complex functional information. In each case, there is an informational gain of many hundreds of bits at stake. There is one reason why neo darwinists always try to use molecular microevolution as though it were complex functional information: it's because it's all that they have. You just spend what you have. Zachriel, with all his ability, cannot do anything different. gpuccio
Zachriel: About Cit+. From Wikipedia:
In 2012, Lenski and his team reported the results of a genomic analysis of the Cit+ trait that shed light on the genetic basis and evolutionary history of the trait. The researchers had sequenced the entire genomes of twenty-nine clones isolated from various time points in the Ara-3 population's history. They used these sequences to reconstruct the phylogenetic history of the population, which showed that the population had diversified into three clades by 20,000 generations. The Cit+ variants had evolved in one of these, which they called Clade 3. Clones that had been found to be potentiated in earlier research were distributed among all three clades, but were over-represented in Clade 3. This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution.[5] The researchers also found that all Cit+ clones had duplication mutations of a 2933 base pair segment that were involved in the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem and resulted in two copies that were head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by altering the regulation in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activated the expression of the citrate transporter when oxygen was present, and thereby enabled aerobic growth on citrate.[5]
So, "two potentiating mutations" (in the first 20000 generations, therefore, I suppose, to be counted among the 10 -20 already discussed), plus a single duplication event. It really does not seem that the Cit+ mutation is in any way different from what we have already discussed. gpuccio
Zachriel: The fact remains that only 10 - 20 positive mutations achieved fixation in 20000 generations, according to Lenski. "Twenty thousand generations vs. hundreds of million of generations." 20000 generations in an expanding population of bacteria, according to the described methodology, corresponds to about 1,49E+12 divisions. That's 1500 billion divisions. Are you sure that we are so distant from the number of replications in a pre-vertebrate population? And however, we have 10 - 20 fixations in the whole genome, that is 5x10^6 bp. In my last example, we need at least 906 fixations in a genetic sequence corresponding to 1589 AAs, therefore in 4767 bp! Moreover, the most important point: the mutations which are fixed in Lenski's experiment are, as far as we know, point mutations, and are unrelated to each other. IOWs, those 10 - 20 mutations are fixed because each of them gives some reproductive advantage in the conditions of the experiment, but in no way they build a sequence of 10 - 20 AAs in a protein! In my example, what you need is a sequence of at least 906 coordinated mutations which build a specific sequence in one single protein! As you certainly understand, the combinatorial analysis of the two cases is completely different. The case of the protein could be treated like the case of Lenski's fixations only if each single aminoacid of the sequence were capable of giving a strong reproductive advantage to the organism. IOWs, the functional sequence should be deconstructable into at least 906 intermediates, each of them capable of complete positive expansion and therefore fixation. We are no more in the boundaries of myth. This is complete folly. gpuccio
There are two possibilities. Either Zachriel doesn't grasp the problem at hand or he is playing dumb as a debating tactic. Whatever the case may be, he is becoming more and more unresponsive. Origenes
Me_Think: "Shouldn’t that convince you that protein sequence has nothing to do with conservation? I also notice that both in red and blue sequence, we have essential amino acids. ‘essential’ means the body cannot synthesize it and thus it must be obtained from the diet. Eg W- Tryptophan, M-Methionine,T-Threonine, I-Isoleucine,D- aspartate etc. How can something which can’t be produced by body be conserved in a sequence?" I really don't understand if it's just that you really do not understand the basics of biology. You say things which are beyond any reasonable understanding. Even Zachriel pointed to your error. What is conserved, obviously, is the information in the protein coding gene. And all organisms use the 20 AAs for their proteins, essential or not. How can you say that "protein sequence has nothing to do with conservation"? We have been discussing conservation of sequences here. Your statement is senseless! Of course, we can have conservation of structure with low conservation of sequence, but conservation of sequence can only be explained by functional constraints, as any book of biology will tell you. gpuccio
gpuccio: So, only 10 – 20 mutations achieve fixation by positive selection in 20000 generations in the whole bacterial genome! By the way, that was before the evolution of Cit+. The organisms were still evolving! For Cit+, there was at least one potentiating mutation (probably more), a tandem copy, then a series of incremental optimizations which became dominant in the population, leaving gaps or jumps in the extant population. If they hadn't kept clones of previous generations, then they would not have been able to determine the sequence of events just from the extant population. While Cit- persisted in the population, much of the history between Cit- and Cit+ had been lost to extinction. Zachriel
Me_Think: How can something which can’t be produced by body be conserved in a sequence? All animals consume other organisms for nourishment. Also, many animals can synthesize those amino acids which humans must consume. Zachriel
gpuccio: Lenski’s experiment is certainly very artificial: a constantly expanding bacterial population subject to strong and constant environmental pressure, in a homogeneous and connected space. That's right. So is dropping stones from the Tower of Pisa. It simplifies some parameters in order to study others. gpuccio: So, only 10 – 20 mutations achieve fixation by positive selection in 20000 generations in the whole bacterial genome! That's right. The intermediates were lost from the extant population. Fortunately, they did keep samples (fossils) of earlier generations so they could unravel the lines of descent. gpuccio: I have mentioned, and in all those which I could still mention, and all of this happened in the population of the common precursors of cephalochordata, tunicata and cartilaginous fishes, in a population of quasi-fishes or quasi-cionas or what else, spread in the oceans of the whole planet, in a 100 million years time (more or less)? Twenty thousand generations vs. hundreds of million of generations. Origenes: Zachriel is arguing that evolutionary theory somehow explains that no detectable precursors of the blue sequence are to be found. Don't know about the "blue sequence", but gaps between extant forms are the expected pattern from evolutionary divergence and extinction (Darwin 1859). Consequently, pointing to such gaps doesn't constitute an argument against evolution. Zachriel
gpuccio @ 677
So, how can Zachriel explain the different behavior? Why do those selective extinctions, and exceptional fixations/expansions, erase the imagined evolutionary history of the blue sequence, while they apparently have no effect on the red sequence? After all, we are talking the same protein here!
Shouldn't that convince you that protein sequence has nothing to do with conservation? I also notice that both in red and blue sequence, we have essential amino acids. 'essential' means the body cannot synthesize it and thus it must be obtained from the diet. Eg W- Tryptophan, M-Methionine,T-Threonine, I-Isoleucine,D- aspartate etc. How can something which can't be produced by body be conserved in a sequence? Me_Think
Mung: Indeed, Daniel King is shameless. I often wonder what motivates people like him to waste their time (and dignity) here. Are they feeling as participating to some crusade? Is it simply goliardic arrogance? Just a way of killing time, for lack of better chores to be done? gpuccio
Hi Troll! Mung
Dionisio:
Sorry to see someone giving up on trying to understand something as simple as this. Did you have problems opening the provided links? Did you try and read the referenced papers, at least the text where the word ‘design’ (or a variation of it) is used within serious scientific research reports? Did you encounter difficulties trying to locate where in the referenced papers that keyword was written in? If that was the case, just let me know, and I gladly could try to quote the specific text explicitly here for you. Perhaps the indicated links take too long to open on certain mobile devices? I’ve noticed very different speed between my laptop and my Surface tablet, though both run on W8.1. I haven’t tested this on my wife’s iPad or iPhone. If that’s what kept you from looking into those papers from the beginning of our mini-discussion, please let me know and I will certainly try my best to make the referenced text visible to you here. Your obvious mistake has been clearly identified and described here, but still you have not been able (or maybe willing?) to see it? The anonymous visitors in this discussion can read this and draw their own conclusions. Could it be that your apparent unwillingness to accept your error is revealing the real motives behind some of your comments in this discussion thread and perhaps even in the whole site? You still may come back later and admit your mistake. I’m sure many folks here will welcome you gladly. Please, think about it. Don’t quit so easily. I encourage you to reconsider this once more. Thank you. I look forward to reading more positive comments from you in the days ahead. Be more open-minded, think out of the box. And read carefully any text that you read. You’ll see the difference that makes. Have a good weekend.
So Dionisio can't (or won't) tell me what my error is, but he's happy to condescend at great length. It's like trying to nail Jello to a wall. That's ID in a nutshell. Daniel King
Gpuccio @677, Zachriel is arguing that evolutionary theory somehow explains that no detectable precursors of the blue sequence are to be found. The problem for Zachriel is that the stronger his case wrt the blue sequence, the greater a conundrum the red sequence becomes — and vice versa. The red sequence behaves in perfect accord with evolution — from fungi to mammals. And guess what? Evolutionary theory treats it like a persona non grata and claims that it cannot explain it. One cannot help but feeling sorry for the red sequence :) Origenes
Origenes at #675: "Zachriel, Can you explain why the blue sequence of the Prickle 1 protein seems (?) to jump into existence with the advent of vertebrates, unlike the red sequence, which (more or less) has a step-by-step evolutionary history from fungi to mammals?" A very good question! A point which has not been discussed as it deserves is the different behaviour of the two halves of the Prickle 1 molecule. So, how can Zachriel explain the different behaviour? Why do those selective extinctions, and exceptional fixations/expansions, erase the imagined evolutionary history of the blue sequence, while they apparently have no effect on the red sequence? After all, we are talking the same protein here! Thank you for stressing this point. :) gpuccio
Zachriel: So, let me understand. Your example of fixation in a real biological model is Lenski's experiment. Now, Lenski's experiment is certainly very artificial: a constantly expanding bacterial population subject to strong and constant environmental pressure, in a homogeneous and connected space. However, let's see how fixation works there. We will refer to the paper which analyzes the 20000 generations results: https://www.researchgate.net/publication/228017441_Phenotypic_and_Genomic_Evolution_during_a_20000-Generation_Experiment_with_the_Bacterium_Escherichia_coli Wikipedia sums up Lenski's considerations as follows: "Although the bacteria in each population are thought to have generated hundreds of millions of mutations over the first 20,000 generations, Lenski has estimated that within this time frame, only 10 to 20 beneficial mutations achieved fixation in each population, with fewer than 100 total point mutations (including neutral mutations) reaching fixation in each population." This, with a total number of mutations per population which is evaluated by Lenski at 3E08 - 1.5E09 mutations. So, only 10 - 20 mutations achieve fixation by positive selection in 20000 generations in the whole bacterial genome! OK, this is your model. Now, you want that we believe that, for example, the 906 identities which appear in sharks and are conserved up to humans in the sequence of ARI1b (first part) all occurred and reached fixation in a single gene, together with all the other positive mutations which are present in the other proteins which I have mentioned, and in all those which I could still mention, and all of this happened in the population of the common precursors of cephalochordata, tunicata and cartilaginous fishes, in a population of quasi-fishes or quasi-cionas or what else, spread in the oceans of the whole planet, in a 100 million years time (more or less)? Thousands and thousands of fixations by positive selection? When in Lenski's experiment we have only 10 - 20 for the whole bacterial genome? And more: Lenski's mutations are point mutations. They are fixed individually. In our last quoted protein, what you need is at least 906 AAs in a single sequence, which will remain fixed up to humans. Do you really believe that each of those 906 mutations conferred some reproductive advantage, big enough to make the mutation fixed? Zachriel, do you really believe this staff? Seriously? gpuccio
Zachriel, Can you explain why the blue sequence of the Prickle 1 protein seems (?) to jump into existence with the advent of vertebrates, unlike the red sequence, which (more or less) has a step-by-step evolutionary history from fungi to mammals? Origenes
gpuccio: the import point is that we agree that “perfect positive expansion” and fixation mean the same thing, in our discussion. So there's no need for the new term which incorporates the confusing notion of perfection. gpuccio: What models are you considering? Antibiotic resistance? So, only resistant bacteria survive today? In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) to a situation where only one of the alleles remains. https://en.wikipedia.org/wiki/Fixation_(population_genetics) Gene pool refers to a population. So when Lenski says he observed fixation that means fixation within the experimental population. Because you seemed to have either missed it, or misunderstood, let's review: In the presence of antibiotics, bacterial resistance in a population can reach fixation. In more complex organisms, those that undergo speciation, selection can result in the loss of the original form in those lines. Another simple example is due to a population bottleneck where the effects of drift can be substantial. This results in a permanent loss of genetic diversity, that is, the permanent extinction of alleles. gpuccio: So, at some time we have two contrasting expansions in A: A1 and A1b And you end up with something like this (compare a10 to f10 to m10): http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg gpuccio: You need a lot of intermediates, and each one of them must undergo big expansions to big populations. And there is evidence that the vast majority or organisms never leave fossils, while the fossils we do find support the existence of intermediates. Zachriel
Zachriel,
“Perfect positive expansion” seems to me like an apt term for Zachriel’s fantasy of worldwide fixation of the entire blue sequence of Prickle 1 protein and apparently many other sequences (see GPuccio 616 and 661) in vertebrate proteins. [Origenes]
It isn’t worldwide, in the sense of being universal. It’s limited to only certain lineages. [Zachriel]
Aha, so, the blue sequence is limited to certain lineages of vertebrates. Can you provide some examples of vertebrates who lack this blue sequence? Origenes
Origenes: I am happy that you have appreciated my example at #661. More than Zachriel, probably! :) Yes, 1300 bits are really something. I love these long functional proteins. gpuccio
Zachriel: OK, the import point is that we agree that "perfect positive expansion" and fixation mean the same thing, in our discussion. Again, I ask you: "Typical? What models are you considering? Antibiotic resistance? So, only resistant bacteria survive today? I never realized that. I don’t see the “problem” with my argument. Please, give us a real biological model where what you describe happens, and there are intermediate selectable and selected states which are fully erased." You say: "It isn’t worldwide, in the sense of being universal. It’s limited to only certain lineages." But the problem is: you need big expansions if you want to overcome the probability barriers for hundreds or thousands of bits of information. You need a lot of intermediates, and each one of them must undergo big expansions to big populations. "Certain lineages" will be completely insufficient to change anything in the probability game. IOWs, you need the whole world, and the whole world many times. gpuccio
Zachriel:
In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) to a situation where only one of the alleles remains.
And that will only happen by design or in very small populations. Virgil Cain
Origenes: “Perfect positive expansion” seems to me like an apt term for Zachriel’s fantasy of worldwide fixation of the entire blue sequence of Prickle 1 protein and apparently many other sequences It isn't worldwide, in the sense of being universal. It's limited to only certain lineages. Zachriel
"Perfect positive expansion" seems to me like an apt term for Zachriel's fantasy of worldwide fixation of the entire blue sequence of Prickle 1 protein and apparently many other sequences (see GPuccio 616 and 661) in vertebrate proteins. Origenes
gpuccio: I just meant expansion to 100% of the population. The term is fixation. https://en.wikipedia.org/wiki/Fixation_(population_genetics) Zachriel
Zachriel: No, I just meant expansion to 100% of the population. gpuccio
gpuccio: So, what is the difference with “perfect positive expansion”? Never heard the term before, but presumably you mean the expansion is monotonic and inevitable, both of which are inconsistent with population genetics. Zachriel
Zachriel: So, what is the difference with "perfect positive expansion"? I suppose we mean the same thing here. The concept of expansion is important, for my reasoning, because it emphasizes that only positive expansion has some effect on probabilistic resources. gpuccio
gpuccio: And, if possible, define with precision what you mean by “fixation”. With precision. We are using the conventional definition. In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) to a situation where only one of the alleles remains. https://en.wikipedia.org/wiki/Fixation_(population_genetics) Zachriel
Zachriel: "There’s a congruence between molecules and morphology. Hence, if there are morphological intermediates between humans and chimpanzees, those intermediates should exhibit intermediate molecular traits. Indeed, when we do salvage fossil molecules, they support phylogeny." I have no doubts that molecular data from extinct species would support philogeny. But I must remind you that here the point is not to support philogeny. The red part of the Prickle molecule supports philogeny (which does not mean that it is explained by philogeny). The point here is how to explain new sequences, like the blue part of Prickle 1 in vertebrates, which appear as de novo sequences, without detectable precursors. Nobody is denying that philogeny would be supported. It's you who have been arguing, out of mere imagination, that molecular data from extinct species not only would support philogeny (a trivial, expected result), but also would explain de novo sequences without any known precursor (a whole jump of reasoning, logics and methodology). gpuccio
Zachriel: In the meantime, just to help you relax, I will give you another jump to consider. ARI1b: "AT-rich interactive domain-containing protein 1B" Length: 2236 AAs (human form). A few words from Uniprot about the function:
Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth (By similarity). Binds DNA non-specifically.
Wow! Now, the least conserved part of the protein is the first part, let's say AAs 1 - 1589. Let's remember, however, that this part includes a short but well defined domain, a BR domain, AAs 1053 - 1144 (91 AAs). So, let's blast this sequence (1589 AAs). In fungi, we can recognize a weak homology limited to the BR domain (56 - 84 bits) In Protostomia, we find again some homology limited to the BR domain (134 - 154 bits) In Deuterostomia, excluding Vertebrates and including Lancelets and Tunicata, we find again 81 - 129 bits of homology, always driven by the BR domain. IOWs, only the short BR domain has recognizable homologies in all pre-vertebrates. Let's go to our beloved cartilaginous fishes: the first vertebrates. Guess what? 1447 bits of homology, obviously regarding the whole sequence (906 identities). So, let me see... how big is this jump? About 1300 bits, if I remember well how to do subtractions. Ah, those busy oceans, 400 million years ago! :) gpuccio
Zachriel: "You basically made up that selection will only result in 90% predominance — and then stop." "Huh? Who said anything about “perfect positive expansion”. However, over hundreds of generations, selection will tend to drive fixation." Try to make up your mind, please. And, if possible, define with precision what you mean by "fixation". With precision. Perfect positive expansion means 100% expansion, with no remains of the previous trait. 90% expansion is not perfect expansion. When you say "fixation", do you mean perfect positive expansion, whatever the necessary time? Just to understand. By the way, I must have missed the "real biological models" in your answer. gpuccio
Not all variations are lost. (...) There also remain vast reservoirs of variation that are not under significant selection, as well as new variation due to mutational mechanisms. [Zachriel]
Ok. So, do tell us, where are these "vast reservoirs of variation" that lead to the blue sequence of Prickle 1 in vertebrates? Origenes
Zachriel:
There’s a congruence between molecules and morphology.
Is there? Do you have anything but your say so?
There are no extant intermediates between chimpanzees and humans. By your argument, they never existed. But we know that is false.
How do we know that is false? No one can test the claim tat chimps and humans shared a common ancestor so you claim is BS Virgil Cain
Mung: We have fossil intermediates and this ought to demonstrate that there may be no evidence left of intermediate proteins. There's a congruence between molecules and morphology. Hence, if there are morphological intermediates between humans and chimpanzees, those intermediates should exhibit intermediate molecular traits. Indeed, when we do salvage fossil molecules, they support phylogeny. Zachriel
gpuccio: Antibiotic resistance? In the presence of antibiotics, bacterial resistance in a population can reach fixation. In more complex organisms, those that undergo speciation, selection can result in the loss of the original form in those lines. Another simple example is due to a population bottleneck where the effects of drift can be substantial. This results in a permanent loss of genetic diversity, that is, the permanent extinction of alleles. gpuccio: Please, give us a real biological model where what you describe happens, and there are intermediate selectable and selected states which are fully erased. You're the one claiming there should be residue after millions of generations. You provided a simplified model @606 using population genetics, but one that is contrary to how population genetics actually works. You basically made up that selection will only result in 90% predominance — and then stop. Origenes: Suppose that Zachriel proposal is right and countless original/intermediate gene sequences disappear swiftly and without leaving any trace, then what is left for evolution to “experiment” with? Not all variations are lost. The common ancestor may leave daughter groups that continue to evolve. However, in the case of chimpanzees and humans, the sister groups have all gone extinct. There also remain vast reservoirs of variation that are not under significant selection, as well as new variation due to mutational mechanisms. gpuccio: Zachriel has apparently gone back to the “perfect positive expansion” argument Huh? Who said anything about "perfect positive expansion". However, over hundreds of generations, selection will tend to drive fixation. If selection is weak, or traits are linked, then fixation may not occur. However, we're talking about millions of generations, so fixation will often occur due to stochastic mechanisms alone, especially in a population, such as humans, that experienced at least one significant bottleneck. gpuccio: Most cases of supposed positive selection could not certainly be as drastic. Most selection is not very strong, but in cases where there are multiple steps, such as in optimizing selection, then the drive towards fixation can be very significant. Lenski's experiment found 10-20 mutations that reached fixation, including the Cit+ complex that required multiple mutations. gpuccio: Neo darwinists make a great use of the concept of “niche”, when it is useful to their reasonings, and promptly forget the various landscape of our planet, with countless different niches, as soon ad they have to argue that all intermediates go extinct. There are no extant intermediates between chimpanzees and humans. By your argument, they never existed. But we know that is false. There may be many different niches, but there is less room in the present than in the sum of all the presents during the history of life. Consequently, there is far more variation over the history of life than is expressed in extant biology. Apply the pigeonhole principle. gpuccio: So, A1 starts its expansion, in times which we really don’t know, but certainly are not instantaneous. The chance of fixation is 2s, while the time to fixation for those lines that reach fixation are typically in the hundreds of generations, inversely proportional to the magnitude of selection. It's easy to model. Just assume each mutation allows on average one extra surviving child out of ten or twenty. Or even have zero selection and random extinction, you will still see that the history of many transitions is lost @537. gpuccio: So, at some time we have two contrasting expansions in A: A1 and A1b That's right. And you end up with something like this (compare a10 to f10 to m10): http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Zachriel
It's truly hilarious that Zachriel thinks pointing to fossil intermediates somehow refutes gpuccio when in fact it does the exact opposite. We have fossil intermediates and this ought to demonstrate that there may be no evidence left of intermediate proteins. Are you serious? Mung
Me_Think: They may, and they may not. The problem with you neo darwinists is that you don't accept that, when many different things can happen, it will not always be the thing that you want that will happen. IOWs, you treat probabilistic system as though they were guided by design. A clear example of that is how a lot of defenders of neo darwinism, even illustrious ones, are ready to invoke genetic drift as a powerful tool to generate functional information, while it should be clear even to a baby that genetic drift, being a random process which can interest any variation, has absolutely no effect on the probabilistic barriers. But no, neo darwinists are always ready to believe that genetic drift will produce exactly the events that theory theory badly needs! Magical thinking at its best. gpuccio
So, at some time we have two contrasting expansions in A: A1 and A1b, which are two separate positive mutations in the population. Not a favourable scenario for a perfect expansion of either.
A1 and A1b, can interact (Epistasis) to form a better phenotype. The combine may take on the expansion rate of faster gene Me_Think
Origenes: Zachriel has apparently gone back to the "perfect positive expansion" argument, leaving aside for the moment convenient extinctions (although I am sure they will come back as soon as it is comfortable again). But perfectly erasing expansion is an even more extreme myth. First of all, we have clear models of positive biological selection only in extreme contexts where the selective pressure is strong and generalized, like in the case on antibiotic resistance. Even in those cases, the selection is not perfect. Most cases of supposed positive selection could not certainly be as drastic. Moreover, populations are not homogeneous and relegated to a homogeneous space and context. Neo darwinists make a great use of the concept of "niche", when it is useful to their reasonings, and promptly forget the various landscape of our planet, with countless different niches, as soon ad they have to argue that all intermediates go extinct. In real biological populations, the spread of the population in dishomogeneous contexts, the effect of drift and other stochastic factors, the partial nature of most reproductive advantages (if and when they exist, at all, as the result of random variation), and especially the possible contrasting effect for different "positive" variations, certainly exclude a perfect positive selection of one trait in practically all cases. The last point deserves better clarification. Let's say that in a population A becomes A1 for some random mutation, and that A1 confers some reproductive advantage. So, A1 starts its expansion, in times which we really don't know, but certainly are not instantaneous. At the same time, it is perfectly possible that in organism A, another member of the population undergoes some positive mutation in another gene, which confers an advantage too. After all darwinists believe that positive mutations are so common! So, let's call that A1b. Now, A1b starts in a different member of A and starts its expansion. So, at some time we have two contrasting expansions in A: A1 and A1b, which are two separate positive mutations in the population. Not a favourable scenario for a perfect expansion of either. gpuccio
Origenes In combinatorial optimization there is a colloquial term, the divine heuristic, that means a perfect heuristic that always makes the right choices. What Zachriel proposes is only good when the divine heuristic is used. The obvious question is, where does the knowledge come from?! Evolutionists are solipsists and reality deniers. EugeneS
Suppose that Zachriel proposal is right and countless original/intermediate gene sequences disappear swiftly and without leaving any trace, then what is left for evolution to "experiment" with? Clearly Zachriel's version of evolution as a search is extremely limited. Origenes
Zachriel: "The problem with this argument is that fixation under selection usually occurs fairly rapidly, and when there are a sequence of selectable steps, this only increases pressure towards fixation. It’s typical in experimental evolution to observe, once a pathway is found, for the population to quickly optimize, with the original form going extinct." Typical? What models are you considering? Antibiotic resistance? So, only resistant bacteria survive today? I never realized that. I don't see the "problem" with my argument. Please, give us a real biological model where what you describe happens, and there are intermediate selectable and selected states which are fully erased. gpuccio
Popular Posts (Last 30 Days) [March 2, 2016 at 5:51 am] A world-famous chemist tells the truth: there’s no… (15,655) Homologies, differences and information jumps (2,657) Durston and Craig on an infinite temporal past . . . (2,583) Larry Moran needs to do some more reading (1,700) A Little Timeline on the Second Law Argument (1,635) +++++++++++++++++++++++++++++++++ Popular Posts (Last 30 Days) [March 4, 2016 at 2:00 am] A world-famous chemist tells the truth: there’s no… (15,778) Homologies, differences and information jumps (2,603) Durston and Craig on an infinite temporal past . . . (2,320) Larry Moran needs to do some more reading (1,708) A Little Timeline on the Second Law Argument (1,663)
:) Dionisio
Daniel King @646
Thank you for all your efforts, but I guess that I’m too stupid to follow your arguments. Maybe for the record it would be useful for you to simply state where I am in error when I ask about Creation ex nihilo. You have my permission to say that publicly.
Sorry to see someone giving up on trying to understand something as simple as this. Did you have problems opening the provided links? Did you try and read the referenced papers, at least the text where the word 'design' (or a variation of it) is used within serious scientific research reports? Did you encounter difficulties trying to locate where in the referenced papers that keyword was written in? If that was the case, just let me know, and I gladly could try to quote the specific text explicitly here for you. Perhaps the indicated links take too long to open on certain mobile devices? I've noticed very different speed between my laptop and my Surface tablet, though both run on W8.1. I haven't tested this on my wife's iPad or iPhone. If that's what kept you from looking into those papers from the beginning of our mini-discussion, please let me know and I will certainly try my best to make the referenced text visible to you here. Your obvious mistake has been clearly identified and described here, but still you have not been able (or maybe willing?) to see it? The anonymous visitors in this discussion can read this and draw their own conclusions. Could it be that your apparent unwillingness to accept your error is revealing the real motives behind some of your comments in this discussion thread and perhaps even in the whole site? You still may come back later and admit your mistake. I'm sure many folks here will welcome you gladly. Please, think about it. Don't quit so easily. I encourage you to reconsider this once more. Thank you. I look forward to reading more positive comments from you in the days ahead. Be more open-minded, think out of the box. And read carefully any text that you read. You'll see the difference that makes. Have a good weekend. Dionisio
Dionisio:
Apparently you’ve misunderstood this again. It’s not a matter of disagreeing, it’s simply that your comment @510 is wrong. Unlike gpuccio, who has corrected your error directly and clearly, I first tried to help you see your own error yourself, so I did not have to publicly point at your mistake. Well, as everybody can see, you still don’t understand it.
Thank you for all your efforts, but I guess that I'm too stupid to follow your arguments. Maybe for the record it would be useful for you to simply state where I am in error when I ask about Creation ex nihilo. You have my permission to say that publicly. In doing so, you might describe the tools that the Designer uses to create and modify living things and how you know what those tools are. Thank you, and best wishes. Daniel King
GP @ 640
Again, I can’t follow your line of thought.
You can't !!.... because this final para was not pasted from my notepad:
None of the aforementioned details is given by ncbi BLAST (which is what I presume you use).It brings into question the algorithm used for search by ncbi. I don't see the more refined Compositional matrix adjust method of search.
I will try 3d model search. If that too doesn't bring up anything useful, it means there is no reason for intermediary protein sequence to be preserved or-as zac says- the intermediaries are extinct. Me_Think
Zachriel:
The problem with this argument is that fixation under selection usually occurs fairly rapidly...
Your opinion is neither an argument nor evidence.
It’s typical in experimental evolution to observe, once a pathway is found, for the population to quickly optimize, ...
Except natural selection doesn't optimize... Virgil Cain
gpuccio: I am afraid that our discussion is not any more stimulating. You repeat your ideas, and what can I do if not repeat mine? You could address the argument. Originally, we thought the existence of fossil intermediates directly refuted your position. Now we understand that you think molecular intermediates would survive even if all the sister branches went extinct because the original sequences would never be completely purged from any of the populations. So, we have made progress. The problem with this argument is that fixation under selection usually occurs fairly rapidly, and when there are a sequence of selectable steps, this only increases pressure towards fixation. It's typical in experimental evolution to observe, once a pathway is found, for the population to quickly optimize, with the original form going extinct. Also, with neutral evolution, alleles are often lost just by happenstance. There's an interesting sidenote with regards to diploid evolution. If a new dominant allele is destined to reach fixation, it will quickly rise in the population, then only slowly reach fixation, because at that point the recessive allele will be rarely expressed. If a new recessive allele is destined to reach fixation, it will only slowly rise in the population, then once it becomes predominant, it will be commonly expressed, and reach fixation quickly. In either case, the new allele, if it is destined to reach fixation, will become fixed in about the same amount of time. Zachriel
Zachriel: I am afraid that our discussion is not any more stimulating. You repeat your ideas, and what can I do if not repeat mine? Which is something I hate doing. gpuccio
Zachriel:
Even if not perfect, though, even random mutation and extinction results in “gaps” between extant organisms, as shown above.
1- It doesn't have to be so 2- Neither random variation nor extinctions can account for the organisms in the first place.
Pointing out that they consistent with evolution is certainly relevant to the topic.
It seems that pretty much anything and everything is consistent with the equivocal evolution. Virgil Cain
Me_Think: Again, I can't follow your line of thought. You "did an evolutionary trace of part of the Blue sequence" (that is, the vertebrate blue sequence, the human form), and found... that it is present in vertebrates!!! Excuse me, is that an argument of some kind? Please, explain. gpuccio
gpuccio: So, you are saying that positive selection is either a failure or a perfect process, with each fixed gene causing the complete extinction of the original gene? Is that your point of view? Nothing in biology is ever that simple, but it is a more accurate model than what you had posted. Even if not perfect, though, even random mutation and extinction results in "gaps" between extant organisms, as shown above. EugeneS: Sticking to the point of discussion is indeed rare The point gpuccio raised was that intermediates should be found in the extant proteome. We pointed to fossil data to show how intermediates may go extinct. That was to the point. Origenes: “Even without selection, jumps will still be observed in extant organisms due to extinction” is irrelevant to the topic at hand. The claim is that "jumps" are not consistent with evolution. Pointing out that they consistent with evolution is certainly relevant to the topic. Zachriel
Zachriel,
Turns out that cometary impacts have had a large effect on the history of life. (...) megadinosaurs (...). [Zachriel]
However, cometary impacts bear no relevance to the "intelligent extinction" being discussed — see Gpuccio's post 616 — and which is in desperate need of an explanation. Which brings me (again) to the conclusion that your statement “Even without selection, jumps will still be observed in extant organisms due to extinction” is irrelevant to the topic at hand. Origenes
Zachriel, Me: The OP discusses molecular issues. Let’s stick to this. You: The morphological data doesn’t go away just because you wave your hands. No, it doesn't. But I must say you have a strange definition of hand-waving. Sticking to the point of discussion is indeed rare ) "With your particular use of “inanimate” and “symbol”, there are no known examples." Thank you for being honest. I have no further questions. Let them be my particular definitions. EugeneS
Gp @ 631
Please, look again at the graph in the OP. You will find there the homology bit score of both the domain part and the “blue” part of huamn Prickle 1 with different organisms. The homology bit score of the whole protein is simply the sum of the two values.
I did an evolutionary trace of part of the Blue sequence RVEQETPEDPEEWADHEDYMTQLLLKFGDKSLFQPQPNEMDIRASEHWISDNMVKSKTEL at Baylor College of Medicine The Sequence identity tree is shown here The tree shows that the species which have the above sequence are:
Monodelphis domestica (F7CAA2-1) Sarcophilus harrisii (G3VFF7-1) Ornithorhynchus anatinus(F6U3C0-1) Xenopus (Q28FG2-1) ...etc.
Similarly the following sequences (part of Blue sequence) too also show Evolutionary Trace: KQNNQSLASKKYQSDMYWAQSQDGLGDSAYGSHPGPASSRRLQELELDHGASGYNHDETQ WYEDSLECLSDLKPEQSVRDSMDSLALSNITGASVDGENKPRPSLYSLQNFEEMETEDCE KMSNMGTLNSSMLHR..........KILPEEKPVHLPVLRRSKSQSRPQQVKFSD DVIDNGNYDIEIRQPPMSERTRRRVYNFEE..........DNALNLVTERKY Me_Think
Zachriel: So, you are saying that positive selection is either a failure or a perfect process, with each fixed gene causing the complete extinction of the original gene? Is that your point of view? gpuccio
Zachriel:
Within a single population, if a trait is under positive selection with a selection coefficient of s, then it will reach fixation with a probability of 2s. If it doesn’t reach fixation, it usually goes extinct while it is still a small portion of the population. If it reaches fixation, it typically does so in a few hundred generations.
It's your view that this is how protein evolution works? Mung
gpuccio: A -> A1 -> A2 -> B1 -> B2 -> B where each step is positively expanded. We have: 1000 A 900 A1 + 100 A 810 A2 + 90 A1 +100 A 729 B1 + 81 A2 + 90 A1 +100 A 656 B2 + 73 B1 + 81 A2 + 90 A1 +100 A 590 B + 66 B2 + 73 B1 + 81 A2 + 90 A1 +100 A Within a single population, if a trait is under positive selection with a selection coefficient of s, then it will reach fixation with a probability of 2s. If it doesn't reach fixation, it usually goes extinct while it is still a small portion of the population. If it reaches fixation, it typically does so in a few hundred generations. Furthermore, we are talking about a progressive adaptation, with each step providing an advantage. If each step is defined with s = 0.1, then the second mutation will provide about s = 0.2 advantage, driving the extinction of the original gene even faster. EugeneS: The OP discusses molecular issues. Let’s stick to this. The morphological data doesn't go away just because you wave your hands. Origenes: I took it that you hold this statement to be relevant to the topic at hand. Turns out that cometary impacts have had a large effect on the history of life. In particular, by wiping out the megadinosaurs, they wiped out many of the sister taxa of birds. EugeneS: I am still waiting for your response on examples of inanimate nature using symbolic representations. We answered a similar question @420. With your particular use of "inanimate" and "symbol", there are no known examples. Zachriel
#624 addendum 510 Daniel King February 26, 2016 at 7:33 pm
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
512 Dionisio February 26, 2016 at 11:04 pm
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the papers referenced in the comments posted @1553, @1583 in the below links are saying when they used that same term? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597094 https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-598657
513 Dionisio February 26, 2016 at 11:33 pm
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the paper referenced in the comment posted @1562 in the below link are saying when using the word ‘designing’? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597764
516 gpuccio February 27, 2016 at 5:03 am
Daniel King:
“When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?”
Absolutely not. Is Windows Vista a creation ex nihilo?
523 Dionisio February 27, 2016 at 10:46 am
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the paper referenced in the comment posted @31 in the below linked thread are saying when they use that same term (in past tense) twice in their abstract? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-538316
531 Daniel King February 27, 2016 at 7:19 pm
Daniel King:
“When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?”
gpuccio:
Absolutely not. Is Windows Vista a creation ex nihilo?
There is a difference between “Design,” which refers to the belief system of the Intelligent Design community, and “design,” which refers to the actions of human designers of things like Windows Vista. What does computer programming (by human beings) have to do with Intelligent Design (by who, what, when, and how)? Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo?
532 Dionisio February 28, 2016 at 2:42 am
Daniel King @531
My reading comprehension is quite poor. But now I see that I’m not alone on this struggle. :) It’s written that we (humans) all have reading comprehension difficulties. However, apparently the seriousness of the problem varies among people. :) Don’t get discouraged. There’s hope. BTW, would you mind answering the questions posted @512, @513 and @523? There are many similar examples in the biology literature, but those three should suffice for now. Thank you in advance for taking a look at those posts. Also, communicating ideas clearly doesn’t seem like an easy task for us humans. Please, note that @510 you referred to ‘people’ in general. Generalizing may render sentences inaccurate. Sometimes even on the borderline with senseless hogwash. You may want to review your comment @510 and consider rewriting it? Have a good day!
533 gpuccio February 28, 2016 at 5:29 am
Daniel King:
“Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo?”
Again: absolutely not! And computer programming (by human beings) has everything to do with Intelligent Design. About the who, what, when, and how, look for a start at my post #381 here.
535 Dionisio February 28, 2016 at 8:15 am
Daniel King @531
“Does Intelligent Design of biological entities involve creation ex nihilo?”
As far as I’m aware of, the (intelligent) designing activity originates in the mind, hence the resulting (intelligent) design comes out of the mind, not out of nothing. Consciousness and mind are something. We can (at least partially) detect their effect, even though we can’t characterize them precisely. I think someone said that ‘nothing’ is what rocks dream about, but I don’t recall the exact phrase. In any case, always verify and double check whatever I write here (or anywhere else).
547 Daniel King February 28, 2016 at 7:17 pm
Daniel King: “Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo?” gpuccio: Again: absolutely not!
How not? Is this how you practice medicine: by making unsupported assertions (with exclamation points)?
548 Daniel King February 28, 2016 at 7:20 pm
gpuccio: And computer programming (by human beings) has everything to do with Intelligent Design.
Everything? How so? Have you really thought this through?
563 Dionisio February 29, 2016 at 4:10 pm
Daniel King @547 & @548
Any problem responding 532? :)
566 Daniel King February 29, 2016 at 7:29 pm
Dionisio:
Daniel King @547 & @548 Any problem responding 532?
Hi Dionisio. There are references in that post to several other posts and I honestly don’t understand what you’re asking. My time on this planet is limited. Kindly get to the point before the hearse comes: What is your question?
567 Daniel King February 29, 2016 at 7:33 pm
Hi Troll!
A prig (/?pr??/), sometimes spelled prigg, is a person who shows an inordinately zealous approach to matters of form and propriety—especially where the prig has the ability to show superior knowledge to those who do not know the protocol in question. They see little need to consider the feelings or intentions of others, relying instead on established order and rigid rules to resolve all questions. The prig approaches social interactions with a strong sense of self-righteousness.
576 Dionisio March 1, 2016 at 1:46 pm
Daniel King @566
Hi Dionisio. There are references in that post to several other posts and I honestly don’t understand what you’re asking. My time on this planet is limited. Kindly get to the point before the hearse comes: What is your question?
Everybody’s time on this planet is limited. No exceptions. Gpuccio has used a substantial amount of his limited time explaining things very clearly over and over again. So clearly, that even I have understood his point. :) Certain things are so obvious, that even I get them right away. :) However, still some folks here don’t seem to get it. Why? Don’t know. Do they really want to understand it? BTW, understanding someone else’s explanation does not mean agreeing with it. Not at all. Now, let’s review/summarize my questions, as per your request: My questions @512, @513 and @523 were related to your comments @510, where you wrote a general statement in this format: “When people say ‘X’ they are saying ‘Y'” (emphasis mine). Well, I found several apparently serious papers where the authors also say ‘design’ or ‘designing’ or ‘designed’ but they don’t seem to mean what you suggested, hence they render your comment @510 very inaccurate (to say it in mild terms). Bottom line, those few referenced papers show that your generalized statement @510 is totally incorrect. I wanted to let you arrive to that obvious conclusion yourself, so I did not have to say it publicly here. But since you don’t have time to answer my questions, I don’t mind answering them for you, to the benefit of the many visitors of this thread. Although some interlocutors here don’t seem to see it clearly, UD is an “eintopf” of philosophical and theological worldviews. Unlike some ID-proponents in this blog, I strongly believe that Jesus made you, me and this whole universe we are in. However, when I say “design” I’m just saying “design”. Words have meaning. Intelligent design is related to consciousness and mind, which are not ‘nihilo’. The engineering design software I worked on for years existed first as an idea in the mind of my brilliant project leader and director of development, who was an engineer. He could visualize it clearly before we even got the technical specifications to implement it as a software. My boss mind was not “nihilo” but something serious. His ideas came out of his mind, not out of “nihilo”. Consciousness and mind are difficult mysterious concepts we still don’t understand well, but they are not “nihilo”. We cannot characterize them but we can detect their effect, or at least some of it. FTR: Here is your incorrect statement @510 and my easy questions @512, 513 and 523: [...] Should I quote the specific text from the referenced papers?
579 Dionisio March 1, 2016 at 2:08 pm
#576 error correction where it reads: “…arrive to that obvious conclusion…” it should read: “…arrive at that obvious conclusion…” Sorry for the mistake. My fault.
592 Dionisio March 2, 2016 at 5:51 am
Daniel King FYI – Regarding your comment @566, I posted my response @576 (+ grammar error correction @579). Maybe this time it’s easier for you to understand it better. :) However, given an allegedly busy schedule, which can limit spare time, it’s understandable that one can’t read certain things. But that’s fine, because this thread seems to receive a relatively significant number of visitors who could read the posted comments and arrive at their own conclusions. :)
Popular Posts (Last 30 Days) A world-famous chemist tells the truth: there’s no… (15,655) Homologies, differences and information jumps (2,657) Durston and Craig on an infinite temporal past . . . (2,583) Larry Moran needs to do some more reading (1,700) A Little Timeline on the Second Law Argument (1,635)
622 Daniel King March 2, 2016 at 8:50 pm
Hi Dionisio, I’m sorry, but I can’t figure out what you’re driving at. Apparently, I said something that you disagree with. Can you state in a single sentence what you’re asking me? I’m baffled when you say, “When people say ‘X’ they are saying ‘Y’” What do mean by that? If you have evidence for how a designer operates when it creates or modifies life on this planet other than by making something out of nothing, please provide it.
624 Dionisio March 3, 2016 at 12:49 am
Daniel King @622
Hi Dionisio, I’m sorry, but I can’t figure out what you’re driving at. Apparently, I said something that you disagree with. Can you state in a single sentence what you’re asking me?
Apparently you’ve misunderstood this again. It’s not a matter of disagreeing, it’s simply that your comment @510 is wrong. Unlike gpuccio, who has corrected your error directly and clearly, I first tried to help you see your own error yourself, so I did not have to publicly point at your mistake. Well, as everybody can see, you still don’t understand it. OK, let’s try one more time: in this discussion thread, most posts addressed to you -after post #510- have been -directly or indirectly- in reference to -or associated with- your comment posted @510. Here it is, so you don’t have to scroll up this long discussion thread:
510 Daniel King February 26, 2016 at 7:33 pm When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Please, make another effort to understand this. Thank you.
Dionisio
Me_Think: Please, look again at the graph in the OP. You will find there the homology bit score of both the domain part and the "blue" part of huamn Prickle 1 with different organisms. The homology bit score of the whole protein is simply the sum of the two values. For example, the bit score of the whole protein with shark is 1189 bits, which is the sum of the bit scores of the two parts. Is that clear? Another important point, which I have highlighted in the follow-up post, is that the different blue sequences are different in different animal groups. Each of them is restricted to some group, like I have shown for Hymenoptera. And, reasonably, conserved in the group to which it is restricted. gpuccio
Zachriel, A gentle reminder. Also I am still waiting for your response on examples of inanimate nature using symbolic representations. The only example that you have managed to present so far being life itself cannot be accepted because life is the case in point. I asked you to kindly provide empirical evidence in support of your claims about life. Merely stating is not a way to deal with scientific issues. So far in this thread I can agree with you on one point only. It is that evidence should not be ignored. EugeneS
Zachriel,
I really don’t see how cometary impact is relevant to the specific gaps in protein evolution which are being discussed here. [Origenes]
You asked about random causes of extinction. [Zachriel]
When you wrote in post 603 that “Even without selection, jumps will still be observed in extant organisms due to extinction”, I took it that you hold this statement to be relevant to the topic at hand. Now I understand that bringing it up was an irrelevancy on your part. Ok. Thank you for clearing that up. You provided an equally irrelevant example when you mentioned selectively neutral mutations, since if such were available for the second sequence of the Prickle 1 protein in vertebrates, then surely nature would have found them in abundance and we would not be here attempting to explain its extreme conservation. Origenes
GP @ 625
Why do you think that we cannot search for part of a sequence? It is simply not true.
I am not saying we can't search for part of sequence. We can, but since you didn't get any result, I suggested the alternate method, as an 'unbroken' polypeptide is more likely to be conserved than a broken segment. I am sure some species should have part of the 'blue' sequence, although I am not sure what it means in terms of being conserved. If we find part of blue sequence in some species, what will that prove? Me_Think
Zachriel, " Again, consider humans and chimpanzees. " The OP discusses molecular issues. Let's stick to this. You are constantly changing the subject. There are no molecular intermediates now. How can you explain that without referring to chimpanzees and humans? And how, in the statistical sense, is now different from the past? EugeneS
Zachriel: "Why?" Because molecule are much more pervading than organisms. I will try to explain. In my gross example in post #606, we have in the last stage 2 organisms (A and B) and 6 types of molecules (A, A1, A2, B2, B1, B). The intermediates are present in both organisms, and your extinction should selectively target only those organisms carrying the intermediate forms, and avoid those carrying the initial form and the final form of the ladder. Believe me, only invoking perfect positive selection at each step can explain what we observe. But, as you know, perfect positive selection is a myth. So, you are invoking two different myths here: 1) The existence of functional selectable intermediates which are nowhere observable. 2) The occurring of perfect positive expansion at each single step. Good science, isn't it? Very empirical indeed! :) gpuccio
Me_Think: Why do you think that we cannot search for part of a sequence? It is simply not true. In all my activities here, I have searched first for the whole sequence, and then for the separated parts: the alignments are the same, but searching for the parts allows me to get from the blast software the bit scores and other values for that part only. The blast software even has an option for searching only part of a sequence, you just specify from which to which aminoacid you want the search to be done. I have used that tool many times in this searches. Please, look again at my post #590, and to the pertinent post #13 in the other thread: https://uncommondesc.wpengine.com/intelligent-design/information-jumps-again-some-more-facts-and-thoughts-about-prickle-1-and-taxonomically-restricted-genes/ How do you think that I got my results for the 26 AAs sequences (part of a part of a longer sequence)? LPPRRAYGGVRISYVPNDAVACARKR That sequence is neither at the N terminal nor at the C terminal, just in the middle (indeed, nearer to the C terminal). And it is perfectly blasted, and it finds all its homologues, many of them at the level of perfect identity, in Prickle proteins in insects. In particular, the first 46 hits, in Hymenoptera, are of absolute identity. I hoe this answers your question. gpuccio
Daniel King @622
Hi Dionisio, I’m sorry, but I can’t figure out what you’re driving at. Apparently, I said something that you disagree with. Can you state in a single sentence what you’re asking me?
Apparently you've misunderstood this again. It's not a matter of disagreeing, it's simply that your comment @510 is wrong. Unlike gpuccio, who has corrected your error directly and clearly, I first tried to help you see your own error yourself, so I did not have to publicly point at your mistake. Well, as everybody can see, you still don't understand it. OK, let's try one more time: in this discussion thread, most posts addressed to you -after post #510- have been -directly or indirectly- in reference to -or associated with- your comment posted @510. Here it is, so you don't have to scroll up this long discussion thread:
510 Daniel King February 26, 2016 at 7:33 pm When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Please, make another effort to understand this. Thank you. Dionisio
GP @ 594
What do you mean? It’s really obscure.
Let's take the sequence Valine-Glycine-Serine-Alanine. Every polypeptide has to start with N-Terminus amino acid. Here Valine is the such an acid. Every polypeptid ends with C-terminus. Here Alanine is such an acid. Now if you search for 'Glycine-Serine' sequence instead of 'Valine-Glycine-Serine-Alanine', you are in essence breaking the whole polypetide and searching for only part of it. A broken polypetide can't be conserved. May be if you search for entire ploypetide sequence starting from N-Termius and ending in C-Terminus, you will get conserved sequence. IOW search for sequence which starts with N-Terminus and ends with C-Terminus. Me_Think
Hi Dionisio, I'm sorry, but I can't figure out what you're driving at. Apparently, I said something that you disagree with. Can you state in a single sentence what you're asking me? I'm baffled when you say, “When people say ‘X’ they are saying ‘Y'” What do mean by that? If you have evidence for how a designer operates when it creates or modifies life on this planet other than by making something out of nothing, please provide it. Daniel King
gpuccio: “if there were the naturally selectable molecular intermediates which are necessary for your theory to work, we should find detectable traces of them in the proteome” Why? Zachriel
Zachriel: "you base that on your assertion that if there were intermediates, they would still be extant." Why do you say that? I have never said such a thing. I have said, as repeated many times, that "if there were the naturally selectable molecular intermediates which are necessary for your theory to work, we should find detectable traces of them in the proteome". I am speaking of the molecules, not of organisms. Why do you conflate what I say of molecules with what you say of organisms? gpuccio
Origenes: I really don’t see how cometary impact is relevant to the specific gaps in protein evolution that are being discussed here. You asked about random causes of extinction. Origenes: The laws of arithmetic? What exactly do you mean? And how is that unrelated to natural selection? Consider a simple case: a selectively neutral mutation in a haploid population. The chance of this new mutation fixing in the population, and the original form reaching extinction is the inverse of the population size. gpuccio: I only claim that, if there were the naturally selectable molecular intermediates which are necessary for your theory to work, we should find detectable traces of them in the proteome. Yes, and you base that on your assertion that if there were intermediates, they would still be extant. That has been shown to be false. Zachriel
Zachriel:
1. If humans and chimpanzees evolved from a common ancestor, there must have been intermediates.
Even if they didn't share a common ancestor phenotypic plasticity and normal variation could easily make it look like intermediates existed. Virgil Cain
"Intelligent extinction"! Thank you Gpuccio, that one is priceless. You have made my day :) Origenes
Zachriel: Just a couple of accessory points which have not been mentioned in the discussion: 1) Given the nature and historical location of the jump we are discussing, it can be helpful to remember that we are not dealing with huge populations like bacteria or fungi, here. We are dealing with pre-vertebrates. Now, I have no idea of how big a population of proto-chordates could be at the times we are considering, but certainly it was not huge. I have found estimates of the total mass of fishes today which could be compatible with a number of living fishes, today, in the maximum range of 2^50. Just to give a very generous number. We are dealing, with the Prickle 1 blue chain only, with a jump of 600 bits. Which is certainly greatly "out of range" for a population which, in the whole planet, did not probably exceed 2^50, and whose reproduction rate is certainly not comparable to that of bacteria. That makes the probabilistic resources even smaller. 2) A second important point is that the blue sequence of Prickle 1 is only an example, but its 600 bits are not certainly the only original functional information which appears in vertebrates. At the same time, in the same process, hundreds, probably thousands of similar informational jumps took place. That makes your theory of RV + NS + mass extinction even more irrational, if possible. For just a second example, look at my post #14 in the new follow-up thread, here: https://uncommondesc.wpengine.com/intelligent-design/information-jumps-again-some-more-facts-and-thoughts-about-prickle-1-and-taxonomically-restricted-genes/ about HDAC4, which shows another 600+ jump between pre-vertebrates and vertebrates. I could easily quote many other examples, but that would probably be boring. I hate repetitions. So, what tremendous scenario of lucky random variation and intelligent extinction was taking place in the oceans of our planet, a few million years ago? gpuccio
Origenes: Thank you for your very helpful comments. gpuccio
Gpuccio @284,
But to invoke selective and total extinction of all the intermediate forms of a sequence in natural history is folly. Sequences, as a rule, are conserved and leave detectable traces in the existing proteome. We are speaking of huge numbers of sequences still represented in the existing proteome, which are very good samples of the processes which took place at the molecular level. To argue that thousands, maybe millions, of intermediate sequences which are absolutely necessary for your theory to be credible simply were lost because of hyperselective extinction of all the species which had some testimony of them is taking cognitive bias to new and unprecedented levels of excellence. [Gpuccio]
Extremely clear! And here we are — about 300 posts later — discussing cometary impact as an explanation for Zachriel's "surgical" extinction story. Origenes
Zachriel: "Gpuccio claims that if there were intermediates, intermediates should still be extant." Sorry to contradict you, but I only claim that, if there were the naturally selectable molecular intermediates which are necessary for your theory to work, we should find detectable traces of them in the proteome. It's not the same as what you make me say. However, if you can't meet my real argument, and must still restate a weak and wrong argument, it's fine with me. I take it as a compliment. gpuccio
Zachriel @611, I really don't see how cometary impact is relevant to the specific gaps in protein evolution that are being discussed here.
Another example would be two populations with negligible differences inhabiting the same niche, and over time one strain eventually going extinct simply by the laws of arithmetic. [Zachriel]
The laws of arithmetic? What exactly do you mean? And how is that unrelated to natural selection? Origenes
gpuccio: Not very likely, I would say. Great argument, except for the part about it being contradicted by the facts. 1. If humans and chimpanzees evolved from a common ancestor, there must have been intermediates. 2. Gpuccio claims that if there were intermediates, intermediates should still be extant. 3. If there are no extant intermediates, then there were probably never any intermediates, and it represents an unevolvable jump. 4. There are no extant intermediates between humans and chimpanzees. Therefore it represents an unevolvable jump. Gpuccio's argment is contradicted by fossil intermediates, not just in the case of humans and chimpanzees, but between many other taxonomic groupings. EugeneS: There must be evidence of this process at the molecular level, which is not there, if I understand the OP correctly. It doesn't require molecular evidence to demonstrate that extinction is rampant in the fossil record, or that intermediate forms exist between otherwise disconnected leaves on the tree. EugeneS: The only thing you have is the fossil record, which is very inconclusive and scanty, if nothing else. The fossil record clearly shows extinction. EugeneS: There must be plenty of intermediate forms. There are plenty of intermediate forms, as Darwin pointed out. But some organisms represent the leaves at the end of their branch, so there may not be extant intermediates. Again, consider humans and chimpanzees. According to gpuccio's argument, as there are no extant intermediates, there never were intermediates. But from the fossils, we know this isn't true. Origenes: So, extinction on its own causes jumps — no need for natural selection. It's easy to show that even random variation and extinction results in wide "jumps" between the leaves of the tree. See @537. Origenes: Since just about anything can be considered being part of “natural selection”, Not all evolution is due to natural selection. Origenes: what kind of extinction is unrelated to natural selection and causes jumps? Your species being wiped out by a cometary impact would be an extreme example of random extinction. Another example would be two populations with negligible differences inhabiting the same niche, and over time one strain eventually going extinct simply by the laws of arithmetic. Zachriel
There must be plenty of intermediate forms. Even Darwin knew this. Mung
Even without selection, jumps will still be observed in extant organisms due to extinction. [Zachriel]
So, extinction on its own causes jumps — no need for natural selection. Can you help me out here? Since just about anything can be considered being part of "natural selection", what kind of extinction is unrelated to natural selection and causes jumps? Origenes
Zachriel:
This is because selection will tend to weed out intermediate forms.
Intermediates usually exist in an environment conducive to their form. For example Tiktaalik is an alleged intermediate yet it existed many millions of years after the tetrapods arrived because it existed in an environment that was better suited to its form than that of fish and tetrapods. NS weeds out the less fit. Virgil Cain
"This is because selection will tend to weed out intermediate forms." There must be evidence of this process at the molecular level, which is not there, if I understand the OP correctly. You don't have this evidence. The only thing you have is the fossil record, which is very inconclusive and scanty, if nothing else. You and wd400 do not appear to understand that the past is no different from the present in the statistical sense. This means that on average in a population you always tend to see intermediate forms. There must be plenty of intermediate forms. Extinction is irrelevant. EugeneS
Zachriel: You seem not to understand. Let's make a very gross example, just to explain what I mena, with a fixed population of 1000, and a NS 90% efficient, and a transition like that: A -> A1 -> A2 -> B1 -> B2 -> B where each step is positively expanded. We have: 1000 A 900 A1 + 100 A 810 A2 + 90 A1 +100 A 729 B1 + 81 A2 + 90 A1 +100 A 656 B2 + 73 B1 + 81 A2 + 90 A1 +100 A 590 B + 66 B2 + 73 B1 + 81 A2 + 90 A1 +100 A Very grossly. Just to discuss. Now, you say that your extinction targets all the: 66 B2 + 73 B1 + 81 A2 + 90 A1 leaving only A and B. Not very likely, I would say. gpuccio
Zachriel:
Darwin’s tree represents divergence due to natural selection.
No, it represents his imagination.
It turns out, however, that there are fossil intermediates,
Not really. Only opinion based on necessity says that. Virgil Cain
Again, your claim is that because there are jumps between the extant taxa of humans and chimps, and because there are no extant intermediates, then the jump is real, rather than an artifact of extinction. It turns out, however, that there are fossil intermediates, which directly contradicts your claim. Zachriel
gpuccio: You continue to ignore the necessity of huge positive selection, for your theory to work. Even without selection, jumps will still be observed in extant organisms due to extinction. However, in the case of functional novelty requiring selection, the apparent jumps will be more common, not less. This is because selection will tend to weed out intermediate forms. gpuccio: Your trees and examples show nothing like that. Darwin's tree represents divergence due to natural selection. Zachriel
Zachriel:
Despite what gpuccio has claimed, the absence of extant transitionals for many taxa is an inevitable consequence of biological evolution.
Especially given that said transitional forms never existed.
Gene duplication is an important mechanism of variation.
Gene duplication followed by protein function altering mutations plus the addition of a new binding site is out of the reach of stochastic processes. See Durrett and Schmidt, Waiting for Two Mutations
A gene duplication occurs in one, and one of those copies evolves stepwise into a novel form;
That may work in imaginationland but reality tells a different story. Virgil Cain
Zachriel: You continue to ignore the necessity of huge positive selection, for your theory to work. Your trees and examples show nothing like that. gpuccio
Mung: Zachriel continues to deny that protein evolution occurs by gene duplication. Where in Heavens did you get that from? Gene duplication is an important mechanism of variation. Mung: where both the ancestral sequence and the new sequence are both there. No extinction required. No magically missing intermediates required. Not everything goes extinct, if that is what you mean. Let's consider two lineages that diverge, and there are no extant sister groups (such as the case with humans and chimpanzees). A gene duplication occurs in one, and one of those copies evolves stepwise into a novel form; A ——> A-A0 ——> A-A1 ——> A-A2 ——> A-A3. The result is still going to be an apparent jump, from A0 to A3, when looking at only the extant organisms. Zachriel
Meanwhile, Zachriel continues to deny that protein evolution occurs by gene duplication. you know, where both the ancestral sequence and the new sequence are both there. No extinction required. No magically missing intermediates required. Mung
Origenes: How unfortunate for your position! And now — even worse — Gpuccio has eloquently pointed out that transitional (protein) forms are also missing at the molecular level. Despite what gpuccio has claimed, the absence of extant transitionals for many taxa is an inevitable consequence of biological evolution. Consider a standard tree. Compare a10 to f10 to m10: http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Zachriel
Zachriel @596, How unfortunate for your position! And now — even worse — Gpuccio has eloquently pointed out that transitional (protein) forms are also missing at the molecular level. And this time one cannot posit the incompleteness of the fossil record as an excuse. Origenes
Origenes: If we assume the existence of innumerable transitional forms as posited by Darwinian evolution, then the fossil record clearly shows that extinction without leaving a single trace is the prevalent pattern. Indeed. If we assume the existence of the last twenty generations of your ancestors, then the record of remains is probably very incomplete as well. Preservation is the exception, not the rule. Zachriel
Dionisio: Yes, the discussion here has been rather satisfying. gpuccio
Me_Think: "Are you breaking at the start of N-terminus ? May be we can’t find a conversed sequence if the break is not correct." What do you mean? It's really obscure. gpuccio
MT:
The entire amino acid sequence determines the 3D structure and the way the protein folds.
That is refuted by prions, silent mutations that cause the polypeptide to misfold and chaperones that allow polypeptides to fold into their functional shapes.
Long sequence of protein are nothing but shorter polypeptides strung together.
That is only your opinion and not backed by science. Virgil Cain
Daniel King FYI - Regarding your comment @566, I posted my response @576 (+ grammar error correction @579). Maybe this time it's easier for you to understand it better. :) However, given an allegedly busy schedule, which can limit spare time, it's understandable that one can't read certain things. But that's fine, because this thread seems to receive a relatively significant number of visitors who could read the posted comments and arrive at their own conclusions. :)
Popular Posts (Last 30 Days) A world-famous chemist tells the truth: there’s no… (15,655) Homologies, differences and information jumps (2,657) Durston and Craig on an infinite temporal past . . . (2,583) Larry Moran needs to do some more reading (1,700) A Little Timeline on the Second Law Argument (1,635)
Dionisio
GP @ 590
I am not sure that I understand. Some parts of a protein are modular, others definitely are not. What do you mean?... and you will see that even a relatively short sequence: LPPRRAYGGVRISYVPNDAVACARKR can be extremely conserved, and easily detected by BLAST, if it is a functional module in longer sequences which are extremely different in all the rest.
The entire amino acid sequence determines the 3D structure and the way the protein folds. If we break the sequence , we are in essence breaking the protien. A polypeptide chain has two ends - N-terminus (an amine group), and the C-terminus (carboxyl group)- Are you breaking at the start of N-terminus ? May be we can't find a conversed sequence if the break is not correct.
Isn’t that amazing?
Yes,It is. Me_Think
Me_Think: "Long sequence of protein are nothing but shorter polypeptides strung together." I am not sure that I understand. Some parts of a protein are modular, others definitely are not. What do you mean? "Why should all the intermediary polypeptide chain be conserved ?" Please, look at my post #13 in my new thread: https://uncommondesc.wpengine.com/intelligent-design/information-jumps-again-some-more-facts-and-thoughts-about-prickle-1-and-taxonomically-restricted-genes/ and you will see that even a relatively short sequence: LPPRRAYGGVRISYVPNDAVACARKR can be extremely conserved, and easily detected by BLAST, if it is a functional module in longer sequences which are extremely different in all the rest. A 26 AAs sequence is already so specific in the search space of proteins (after all, it corresponds to a search space of 20^26, which is about 112 bits of information) that it is a signature, a fingerprint. Just blast the above sequence and you will get only Prickle proteins in insects. Isn't that amazing? gpuccio
Origenes: Thank you for the kind help. :) gpuccio
GP @ 569
We look for intermediaries of protein functional information in the sequences of protein coding genes. Prudent or not, it is certainly reasonable.
Long sequence of protein are nothing but shorter polypeptides strung together. Why should all the intermediary polypeptide chain be conserved ? Me_Think
(...) the fossil record clearly shows that extinction is the prevalent pattern. [Zachriel]
Correction: If we assume the existence of innumerable transitional forms as posited by Darwinian evolution, then the fossil record clearly shows that extinction without leaving a single trace is the prevalent pattern. Origenes
gpuccio: You argue from fossils that such molecular intermediates existed, and that they are extinct. Yes. Your claim is that such intermediates are expected to survive in most cases, when the fossil record clearly shows that extinction is the prevalent pattern. Zachriel
Zachriel: I understand your logic, but it is really weak: you conflate, as usual, fossils with molecular data. My claim is that molecular intermediates should be extant, in most cases, if they really existed in great abundance, as your theory "posits". You argue from fossils that such molecular intermediates existed, and that they are extinct. Maybe I should try a new OP about "thought jumps". :) gpuccio
gpuccio: the gap between humans and chimps, the true gap, is the result of design. An evolutionary biologist, such as Darwin, would posit that there were once species that exhibited intermediate characteristics. Your claim was that intermediates should normally be extant. Fossil finds support the existence of extinct intermediates, contradicting your claim. Zachriel
mike1962: "Is Zach the best they have to offer?" Yes, he is. (No irony, Zachriel. This is a sincere compliment). :) gpuccio
Zachriel: No conundrum at all: the gap between humans and chimps, the true gap, is the result of design. Obviously. gpuccio
gpuccio: They can also never have existed, which is my point. So, we have 1. The gap between humans and chimpanzees too large to plausibly be a single evolutionary step. 2. No extant intermediates. 3. Gpuccio says intermediates, if they ever existed, should in all probability still exist. What a conundrum! Zachriel
Guppucio continues to flatten Zachriel Is Zach the best they have to offer? mike1962
#576 error correction where it reads: "...arrive to that obvious conclusion..." it should read: "...arrive at that obvious conclusion..." Sorry for the mistake. My fault. Dionisio
Mung: Have you never seen those magic ladders, maybe made of smoke, which come out of nothing, step by step, in Disney like movies? Ah, you obstinate magics denier! :) gpuccio
Zachriel: "Keep in mind that your claim at issue is that intermediates should be extant." Yes, if they exist. They can also never have existed, which is my point. gpuccio
Daniel King @566
Hi Dionisio. There are references in that post to several other posts and I honestly don’t understand what you’re asking. My time on this planet is limited. Kindly get to the point before the hearse comes: What is your question?
Everybody's time on this planet is limited. No exceptions. Gpuccio has used a substantial amount of his limited time explaining things very clearly over and over again. So clearly, that even I have understood his point. :) Certain things are so obvious, that even I get them right away. :) However, still some folks here don't seem to get it. Why? Don't know. Do they really want to understand it? BTW, understanding someone else's explanation does not mean agreeing with it. Not at all. Now, let's review/summarize my questions, as per your request: My questions @512, @513 and @523 were related to your comments @510, where you wrote a general statement in this format: "When people say 'X' they are saying 'Y'" (emphasis mine). Well, I found several apparently serious papers where the authors also say 'design' or 'designing' or 'designed' but they don't seem to mean what you suggested, hence they render your comment @510 very inaccurate (to say it in mild terms). Bottom line, those few referenced papers show that your generalized statement @510 is totally incorrect. I wanted to let you arrive to that obvious conclusion yourself, so I did not have to say it publicly here. But since you don't have time to answer my questions, I don't mind answering them for you, to the benefit of the many visitors of this thread. Although some interlocutors here don't seem to see it clearly, UD is an "eintopf" of philosophical and theological worldviews. Unlike some ID-proponents in this blog, I strongly believe that Jesus made you, me and this whole universe we are in. However, when I say "design" I'm just saying "design". Words have meaning. Intelligent design is related to consciousness and mind, which are not 'nihilo'. The engineering design software I worked on for years existed first as an idea in the mind of my brilliant project leader and director of development, who was an engineer. He could visualize it clearly before we even got the technical specifications to implement it as a software. My boss mind was not "nihilo" but something serious. His ideas came out of his mind, not out of "nihilo". Consciousness and mind are difficult mysterious concepts we still don't understand well, but they are not "nihilo". We cannot characterize them but we can detect their effect, or at least some of it. FTR: Here is your incorrect statement @510 and my easy questions @512, 513 and 523:
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Dionisio @512
Is that what the authors of the papers referenced in the comments posted @1553, @1583 in the below links are saying when they used that same term [i.e. design]? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597094 https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-598657
Dionisio @513
Is that what the authors of the paper referenced in the comment posted @1562 in the below link are saying when using the word ‘designing’? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597764
Dionisio @523
Is that what the authors of the paper referenced in the comment posted @31 in the below linked thread are saying when they use that same term (in past tense) [i.e. designed] twice in their abstract? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-538316
Should I quote the specific text from the referenced papers? Dionisio
gpuccio: The only molecular example in your post is HARs. So? The principle is the same. There are large gaps between extant taxa. In any case, HARs are multiple. gpuccio: but if they are functional thy are examples of molecular changes with complex functional specification, and they are probably designed. They represent gaps that can't be explained by single evolutionary jumps. Evolutionary biologists would posit intermediate species, even though there are no extant intermediates. Keep in mind that your claim at issue is that intermediates should be extant. Zachriel
Zachriel: The only molecular example in your post is HARs. Well, the function of HARs is not well understood, but if they are functional thy are examples of molecular changes with complex functional specification, and they are probably designed. However, they are not very long sequences, and their functional information should be re-evaluated as soon as function will be better documented. What in your "argument" can make us believe that molecular intermediates of HARs have existed in extinct ancestor, and therefore HARs evolved by gradual RV + NS? You are really begging the question. gpuccio
The missing rung theory of protein evolution. It's like a ladder, where when the protein moves up to the next rung of the ladder the previous rung of the ladder disappears and leaves behind no trace it ever existed. But we know the rung must have been there, else how could the protein have climbed the ladder? Mung
MT:
Simply put, only part of DNA is gene. Only exons in gene code for protein. In humans genes are about 5% of DNA and exons form 2% of the gene,
That requires editing and splicing. Both processes require knowledge of what to edit and what to splice. Your position cannot account for either of those processes. Nice own goal... Virgil Cain
Zachriel:
The upright stance of humans required many coordinated changes in the hip, back and neck.
This is true and you are unable to connect those with changes in the genome.
Or we might consider that about 1% of their nucleotide sequences differ, which is about thirty-five million nucleotides.
The 1% is a gross misrepresentation. So it figures that Zachriel would use it. Virgil Cain
gpuccio: If you were kind enough to explain your thought with real examples Well, we could refer to virtually any of the characteristics that distinguish humans from chimpanzees. The upright stance of humans required many coordinated changes in the hip, back and neck. Or we might consider that about 1% of their nucleotide sequences differ, which is about thirty-five million nucleotides. Or you could observe the substantial difference in brain size and structure. As for molecules, you might consider any number of so-called human accelerated regions, any one of which is beyond evolutionary expectations without intermediates*, but when in combination represent an unbridgeable "jump". Based on this, evolutionary biologists posit intermediate species between humans and chimpanzees, with each branch evolving over time from common ancestors. According to your statement above, there should be extant examples of those intermediates. However, we know 1) extant intermediates between humans and chimpanzees don't exist. 2) fossils of extinct intermediates do exist. 3) This applies any number of taxa. This contradicts your position that intermediates are expected to survive in most cases. Extinction is rampant in the history of life. What evolutionary theory expects is that the pattern of leaves will describe the growth of the tree. * E.g. HAR1. See Pollard, An RNA gene expressed during cortical development evolved rapidly in humans, Nature 2006. Zachriel
Me_Think: "is it prudent to search for intermediaries based on amino acid sequence in protein?" We look for intermediaries of protein functional information in the sequences of protein coding genes. Prudent or not, it is certainly reasonable. Of course, new protein genes can come from non coding regions, and they do, but obviously NS cannot apply to those cases, so they can be explained only by design (or mere luck, against all reasonable probability laws!). gpuccio
gpuccio @ 565 Simply put, only part of DNA is gene. Only exons in gene code for protein. In humans genes are about 5% of DNA and exons form 2% of the gene, so is it prudent to search for intermediaries based on amino acid sequence in protein? Me_Think
Hi Troll!
A prig (/?pr??/), sometimes spelled prigg, is a person who shows an inordinately zealous approach to matters of form and propriety—especially where the prig has the ability to show superior knowledge to those who do not know the protocol in question. They see little need to consider the feelings or intentions of others, relying instead on established order and rigid rules to resolve all questions. The prig approaches social interactions with a strong sense of self-righteousness. Daniel King
Dionisio:
Daniel King @547 & @548 Any problem responding 532?
Hi Dionisio. There are references in that post to several other posts and I honestly don't understand what you're asking. My time on this planet is limited. Kindly get to the point before the hearse comes: What is your question? Daniel King
Zachriel: If you were kind enough to explain your thought with real examples, maybe I could understand what you are thinking. At present, the true nature of your "argument" is the only conundrum I can see. gpuccio
gpuccio: I supposed that humans and chimps were very similar at the molecular level, as far as we understand, especially at the level of protein coding genes. They are different enough that it represents a jump far beyond what can be expected of an evolutionary process. There are no extant intermediates. What a conundrum! Zachriel
Daniel King @547 & @548 Any problem responding 532? :) Dionisio
Zachriel, why are you pretending that evolution of proteins doesn't involve gene duplication? Mung
Zachriel, why are you pretending that evolution only takes place in a single lineage? Mung
Zachriel: I am not sure I understand. I supposed that humans and chimps were very similar at the molecular level, as far as we understand, especially at the level of protein coding genes. If you want to look at molecular intermediates, we must first decide what are the differences for which we are looking at intermediates. If proteins are almost identical between chimps and humans, what are we looking for? Of course, I do believe that there are great differences between chimps and humans, as everybody with a little sense should understand. But the point is, they are probably mainly regulatory and epigenetic, and we still don't understand well their molecular nature. If we don't understand where the difference is, how can we look for intermediates of that difference, be they extant or extinct? gpuccio
Zachriel:
However, when we look at the fossil record, we find all sorts of extinct intermediates.
That is an opinion and not science. Virgil Cain
Forest. Trees. mike1962
gpuccio: Molecular intermediates? Or are you changing games again? We're looking for extant intermediates between humans and chimpanzees, molecular or otherwise. There are none. So then we might suppose there was a jump between chimpanzees and humans. However, when we look at the fossil record, we find all sorts of extinct intermediates. Your claim that such intermediates should be extant is contradicted. Zachriel
Zachriel: "Which is why we have a reasonably complete set of extant intermediates between humans and chimpanzees." Molecular intermediates? Or are you changing games again? gpuccio
Zachriel:
Which is why we have a reasonably complete set of extant intermediates between humans and chimpanzees.
Nonsense.
This was a common creationist belief, by the way, that because God’s Creation was perfect, extinction couldn’t occur
And yet Creationists accept the Flood which wiped out many populations and led to mass extinctions. Obviously Zachriel is just spewing nonsense, again. Virgil Cain
gpuccio: Why? If A2 has expanded “imperfectly” into A3, then there are survivors of A2, too. Under some rock. Which is why we have a reasonably complete set of extant intermediates between humans and chimpanzees. Zachriel
Zachriel: "However, if we have A0 replaced by A1 which diverges into A1x and A1y, then A1x replaced by A2 replaced by A3, while A1y finds a home under a rock somewhere, then when we look under the rock, we will find an intermediate between A1 and A2, but not between A2 and A3." Why? If A2 has expanded "imperfectly" into A3, then there are survivors of A2, too. Under some rock. "And if we drop the rock on A1y, then we have no extant intermediates at all." You have to drop really a lot of rocks, to get what we observe today. "Sure it can, but not every divergence will leave vestiges." I have never said that every divergence will leave vestiges, but simply that many of them will. And remember, a jump of 600 bits, which is what we were discussing here, requires a lot of steps on its supposed ladder, and a lot of expansions, and will leave many vestiges, even if not all. "This was a common creationist belief, by the way, that because God’s Creation was perfect, extinction couldn’t occur, and every form that ever existed must exist somewhere on Earth." This seems really foolish to me. Why do you quote that? Have I ever made that kind of arguments with you? Remember, I am not a creationist. Even if I believe in creation, I am not a creationist. I don't think that scientific reasoning must rely on any kind of religious faith. gpuccio
gpuccio: A ladder is always required, even if there are branches. That's a funny looking ladder. gpuccio: Each branch has to be a ladder, if there has to be a probabilistic gain. Simple branching does not help: it’s only the positive expansion that helps. A particular branch may or may not lead to the adaptation you are considering. However, without side-branches, you don't expect the intermediates to survive. That was the point, if you remember. If we have A0 replaced by A1 replaced by A2 replaced by A3, then we don't expect to find intermediates in extant organisms as A3 is the only extant member. However, if we have A0 replaced by A1 which diverges into A1x and A1y, then A1x replaced by A2 replaced by A3, while A1y finds a home under a rock somewhere, then when we look under the rock, we will find an intermediate between A1 and A2, but not between A2 and A3. And if we drop the rock on A1y, then we have no extant intermediates at all. gpuccio: However, there are still 2^46.68 bacteria with the A0 trait. That sub-population can certainly follow a different evolutionary path, and survive, and carry the A0 trait into the current proteome. Sure it can, but not every divergence will leave vestiges. Even with random mutation and random extinction, there's just not that much room in the present to represent the entirety of evolutionary history. We provided a simple example @537. This was a common creationist belief, by the way, that because God's Creation was perfect, extinction couldn't occur, and every form that ever existed must exist somewhere on Earth. This is the basis of King Kong and other such adventure stories. However, it turns out that the vast majority of organisms that ever existed have gone extinct. For example, there are no extant intermediates between humans and other apes. Zachriel
Zachriel: A ladder is always required, even if there are branches. Each branch has to be a ladder, if there has to be a probabilistic gain. Simple branching does not help: it's only the positive expansion that helps. And a ladder does not mean that the steps are perfect. Please, go back to my post #541. Let's discuss again the case of a starting population of 2^50 bacteria, A0. So, let's say that the new trait, A1, after arising by random mutations in one bacterial clone, expands rapidly because of the reproductive advantage it confers. But, as I have tried to explain, and for the many reasons I have mentioned, it is unrealistic to expect that after the expansion, and before the following step takes place, A1 is present in the whole population. So, let's say that it expands to 90% of the original population. That means that the new A1 population is of about 2^49.85 bacteria, a significant probabilistic gain. However, there are still 2^46.68 bacteria with the A0 trait. That sub-population can certainly follow a different evolutionary path, and survive, and carry the A0 trait into the current proteome. That is true of each step where there is expansion, because the expansion is not perfect. Positive selection is a rare event, and rarely a completely powerful event. If even genes of diseases can survive purifying selection, imagine how normal, functional genes can survive the positive expansion of a new trait. gpuccio
gpuccio: “A ladder of positively selected steps” is the only hypothetical scenario which can minimally “help” your theory in generating functional information of some complexity. If there is a ladder, we don't expect to find intermediates. A3 replaced A2, which replaced A1, which replaced A0. A0 is extinct in the ladder model. That's not the only model, though. Rather, there is a branching process, with the survival of the various branches depending on various factors, including varying environmental niches. However, when there is rapid adaptation, the various branches may be short and leave no descendants. That returns us to A0, A1, and A2 being extinct, leaving only A3. Zachriel
Is this how you practice medicine: by making unsupported assertions (with exclamation points)? Hi Troll! Mung
gpuccio:
And computer programming (by human beings) has everything to do with Intelligent Design.
Everything? How so? Have you really thought this through? Daniel King
Daniel King: “Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo?” gpuccio: Again: absolutely not!
How not? Is this how you practice medicine: by making unsupported assertions (with exclamation points)? Daniel King
All the rest is irrelevant to the problem of probabilistic barriers.
gpuccio This is exactly right but I find the few people really understand the magnitude of the probabilistic barriers that Yockey introduced in his 1977 paper.http://dx.doi.org/10.1016/0022-5193(77)90044-3 bill cole
Zachriel: “A ladder of positively selected steps” is the only hypothetical scenario which can minimally "help" your theory in generating functional information of some complexity. All the rest is irrelevant to the problem of probabilistic barriers. That's why I "introduced" that scenario. gpuccio
Zachriel conflates Darwin's simplistic representation for what we should expect. Talk about desperation... Virgil Cain
gpuccio: Just to be clear, in order for all intermediates to be permanently erased, you, need that A1 completely erases A0, and so on. That was the scenario you just introduced, "a ladder of positively selected steps". But consider the case of multiple divergence. This is what you will expect (compare a10 to f10 to m10): http://darwin-online.org.uk/converted/published/1872_Origin_F391/1872_Origin_F391_figdiagram.jpg Even with random extinction, there will be significant gaps. Zachriel
Zachriel:
It’s a consilience of the evidence that lends confidence to scientific claims.
ID has a consilience whereas your position doesn't even have a methodology to test its claims.
Or that they adapted through natural selection.
Or more likely they adapted through built-in responses to environmental cues. Virgil Cain
Zachriel: I suppose that you should understand that your comments do not address what I have said in my post #538. Just to be clear, in order for all intermediates to be permanently erased, you, need that A1 completely erases A0, and so on. Now, let's say that A0 is a population of, say, 2^50 bacteria, dispersed in various parts of the planet. So, one of these bacteria undergoes some random variation which gives it a true, important reproductive advantage. In order to be the next step of the ladder, that single clone has to expand by positive NS. IOWs, what was in the beginning one modified organism must expand to, say most of the original population. Now, that is already unlikely, because those 2^50 bacteria are not at all in the same lab, or place. So, there is a space problem. And some of them, in parts of the population, may expand against the new trait by mere drift, as you well know. And some of them could have developed some other advantage, so that they can compete with A1 while retaining the old trait. And so on. The point is, some of the original population will survive. And it has good chances to undergo some other kind of evolution, following other paths. And retaining the old trait, A0. So, we will find traces of A0 in the current proteome, together with A1. Why? Because it was once a widespread trait, a functional widespread trait, and traces of it will very likely survive. That is true of A1, A2, and so on. gpuccio
gpuccio: Those intermediates that your theory needs are proteins which must expand to great part of a population. That, and only that, gives a probabilistic advantage. Otherwise, probabilities still multiply and are incompatible with any reasonable “ladder”. Let's assume the simplistic "ladder" of selection you suggest. Strain A0 is replaced by A1, which is replaced by A2, which is replaced by A3. There is no extant representative of A0 because it has been replaced by a selectively superior version. Zachriel
gpuccio: I think that you still do not consider the necessity of positive selection based on true reproductive advantages. Let's consider the null-case first, with no selection. Even then, there are gaps, no residue of the ancestral strain “SHCA”. The longer the process continues, the more likely such strains will not be represented in the extant population. That's because there is much less room in the present, than in the history of presents over millions of years. Zachriel
Zachriel: I think that you still do not consider the necessity of positive selection based on true reproductive advantages. Those intermediates that your theory needs are proteins which must expand to great part of a population. That, and only that, gives a probabilistic advantage. Otherwise, probabilities still multiply and are incompatible with any reasonable "ladder". So, we have functional intermediates which expand to great part of a population. But not all. Certainly, parts of the population remain not involved in the expansion, because of those which I have called "stochastic factors": for example, space separations, or simply non selective drift, or still the influence of other variations in other genes. IOWs, many organisms will follow different lines of evolution, and will not be erased by the expansion of the "next intermediate". Therefore, molecular traces of the "previous intermediate" are expected to survive: maybe not always, but in most cases. Sequences are revealing markers, and the traces of informational paths are very difficult to erase, much more difficult than you seem to think (probably, just because your way of thinking supports your theory). gpuccio
Zachriel: Mammals all look pretty much alike — unless you happen to be one. Dionisio: No, that’s very inaccurate. My orange tabby cat was much nicer and prettier than the rest of the cats in the neighborhood. My golden retriever was much friendlier and smarter than the rest of the dogs in town. And that’s not only my opinion – my wife and my kids agree with me on this. Do you and your family happen to be a non-mammals, then? gpuccio: Exactly. And the simple reason for that is that they are designed ... Or that they adapted through natural selection. gpuccio: Why do you shift to the fossil record as soon as it is more comfortable for you? Because you can't justify ignoring an entire line of evidence that undermines your position. It's a consilience of the evidence that lends confidence to scientific claims. Zachriel: Even with random extinction, we expect large gaps at the leaves. With natural selection, the gaps will typically be even larger.” gpuccio: Your opinion. No. It's easy to test. Let's consider a population of sequences. In each generation, each sequence clones with a chance of random mutation. The number of species is limited by random extinction of lineages. R~~~E~ V~~~E~ SHCA~~ SHCAK~ ~HX~~~ ~HXM~~ ~KX~~~ TKX~~~ ~MXV~~ ~HXV~~ After just seven generations, we still have enough information to reconstruct the nested hierarchy, but there are obvious gaps (e.g. "SHCA"). With more generations, the gaps will become even more pronounced. http://www.zachriel.com/nested/Images/Genesis-Nested.gif As for natural selection, a simple example is a population of beetles, some living on the rock, some living under the rock. (See Wallace 1858.) Over generations, they will adapt to their separate environments, both to improve their local efficiency, and to reduce competition. Natural selection pushes them apart. Beetles, in particular, speciate rapidly to increase the rate of divergence. Zachriel
To all: I have just posted a new OP, which is, in some wayc a follow up to this one. I hope you will be patient enough to give it a look. We could also continue the discussion on the new thread, avoiding the burden of a 500+ posts sequence. :) gpuccio
Daniel King @531
"Does Intelligent Design of biological entities involve creation ex nihilo?”
As far as I'm aware of, the (intelligent) designing activity originates in the mind, hence the resulting (intelligent) design comes out of the mind, not out of nothing. Consciousness and mind are something. We can (at least partially) detect their effect, even though we can't characterize them precisely. I think someone said that 'nothing' is what rocks dream about, but I don't recall the exact phrase. In any case, always verify and double check whatever I write here (or anywhere else). Dionisio
Zachriel: "Adaptation is usually limited in space AND time, so rapid transitions will be unlikely to leave detailed fossils." Exactly. And the simple reason for that is that they are designed, and that they don't pass through the positive expansion of lots of intermediates. "All we have are the leaves of the tree, which are separated by the divergence of the branches." Exactly. See previous point. "We don’t expect “most of them” to be preserved in the fossil record, but the fossil record is characterized by divergence, not linear progression." I was speaking of molecules. Why do you shift to the fossil record as soon as it is more comfortable for you? I have never made arguments about fossils, and you know it. "That is incorrect. Even with random extinction, we expect large gaps at the leaves. With natural selection, the gaps will typically be even larger." Your opinion. I absolutely disagree. gpuccio
Daniel King: "Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo?" Again: absolutely not! And computer programming (by human beings) has everything to do with Intelligent Design. About the who, what, when, and how, look for a start at my post #381 here. gpuccio
Daniel King @531 My reading comprehension is quite poor. But now I see that I'm not alone on this struggle. :) It's written that we (humans) all have reading comprehension difficulties. However, apparently the seriousness of the problem varies among people. :) Don't get discouraged. There's hope. BTW, would you mind answering the questions posted @512, @513 and @523? There are many similar examples in the biology literature, but those three should suffice for now. Thank you in advance for taking a look at those posts. Also, communicating ideas clearly doesn't seem like an easy task for us humans. Please, note that @510 you referred to 'people' in general. Generalizing may render sentences inaccurate. Sometimes even on the borderline with senseless hogwash. You may want to review your comment @510 and consider rewriting it? Have a good day! Dionisio
Daniel King: “When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?” gpuccio: Absolutely not. Is Windows Vista a creation ex nihilo?
There is a difference between "Design," which refers to the belief system of the Intelligent Design community, and "design," which refers to the actions of human designers of things like Windows Vista. What does computer programming (by human beings) have to do with Intelligent Design (by who, what, when, and how)? Please address my question: Does Intelligent Design of biological entities involve creation ex nihilo? Daniel King
Zachriel @529 "Mammals all look pretty much alike" No, that's very inaccurate. My orange tabby cat was much nicer and prettier than the rest of the cats in the neighborhood. My golden retriever was much friendlier and smarter than the rest of the dogs in town. And that's not only my opinion - my wife and my kids agree with me on this. Actually, my pets were much nicer and friendlier than many people in this world, including myself. :) Dionisio
drc466: Stasis is the rule for fossils – bats, crocodiles, rodents, canines, horses, etc. – fossils clearly either ARE or ARE NOT nearly identical to modern species. No. That's what is known as a shade of gray comparison. Ancient rodents do resemble modern rodents, but are not the same, and someone familiar with rodents can tell them apart, including other rodents. On the same line, humans are just modified deuterostomes, tubes with appendages to shove food into one end. Microevolution. drc466: Some of the parts might be slightly larger or smaller, and you think there might be one or two new or missing pieces, but it is otherwise identical. This still depends on the claim that rodents haven't evolved. Mammals all look pretty much alike — unless you happen to be one. http://phenomena.nationalgeographic.com/2015/02/04/giant-fossil-rodent-had-an-awesome-bite/ Zachriel
wd400: Do you realise that trees are estimated by shared differences in genetic sequences? IF all they were looking at was the shared differences in mice and humans that would not tell us much. Mung
Mice do look like humans. video evidence Mung
I'm afraid you are just very confused. The oldest mouse fossil is about 17 million years old. The last common ancestor of mice and men may have looked more mouse-like than human-like, but I don't know why you think that matters when we are talking about myoglobin? Mouse muscles need oxygen too. (And that common ancestor is also an ancestor of rabbits, tree shrews, monkeys...) I'm afraid it's very hard to extract anything of meaning from this post. Why do you think anything had to evolve "in-synch"? Do you realise that trees are estimated by shared differences in genetic sequences? It's not about counting how many differences there are, but discovering the pattern in which differences are distributed. wd400
wd/Zach, Thanks for the replies. Based on those, I am going to discard the "mice genetic code was immutable" option, and discuss the "mice and humans are genetically equidistant from their LCA" option. To be clear, I don't have any issues with these two statements of evolutionary thinking that you've posted:
Mouse and human myoglobins have both changed (the mouse probably at a somewhat higher rate).(wd400) Rodents have evolved substantially over the 70 million years of their existence or so. Hemoglobin has also evolved over that period.(Zachriel)
Based on these assertions, if you told me that the last common ancestor of mice/humans was 100myo, and looked nothing like mice or humans, and had myoglobin that was 80% similar to mice and humans, I'd accept that as logical, but unsupported by evidence (no such genetic or fossil evidence exists), and therefore un-helpful to the "this supports common descent" argument. The problem is that prehistoric mice exist* combined with this assertion on wd's part:
Those changes are both material and “visible”. Why would you claim otherwise?
My response to this statement is to simply point up to Zachriel's comment above - "Rodents have evolved substantially over ... 70 million years..." Stasis is the rule for fossils - bats, crocodiles, rodents, canines, horses, etc. - fossils clearly either ARE or ARE NOT nearly identical to modern species. So a mouse fossil from 70mya is nearly identical to a modern mouse* - some of the pieces/parts might be larger/smaller, but they're essentially all there. And as an evidence for common descent, this is illogical! Allow me an analogy. Imagine you are in a car lot, and the salesmen pulls out a brand new Honda Accord and a brand new..Ford Model T. Both are "descendents" of a 100-year old Class known as "automobiles". In examining the brand new Model T, it appears 99% identical to a 1910 model of the same car - same body, same engine, same mechanical design, same tires, etc. Some of the parts might be slightly larger or smaller, and you think there might be one or two new or missing pieces, but it is otherwise identical. Now, your car salesmen evolutionist tells you "The [Honda Accord] and the [Model T] have both changed (the [Model T] probably at a somewhat higher rate)." Or maybe he says "[The Model T family] have evolved substantially over the [100] years of their existence or so. [Engines have] also evolved over that period." And yet the body still has the same shape, and the engine in the Model T is still a 20hp 177 cu. in. 4cyl engine. Now if a car salesman told you that, you'd look at him like he's an idiot. Yet this is exactly what evolutionists who claim "synonomous mutations...support the phylogeny" are saying. Or, to use gpuccio's numbers: modern mice and humans "share 129 AAs out of 154, and 141 positives". To assert that this is due to common ancestry, you have to claim that our last common ancestor had some # of shared AA's smack dab in between 129 and 154 (or equidistant from), yet looked nearly identical to a mouse and nothing like a human. And that all of Zachriel's "synonomous" mutations ALSO had some proportion of AAs equidistant from modern mice and human proteins, that they somehow managed to mutate in synchronization from genus to genus over 100my, and yet this last common ancestor with near perfect intermediate genetic code looked almost exactly like a mouse** and nothing like a human! This. Is. Not. Logical. This leaves us with the Alicia option: Myoglobin is an example of convergent evolution and has nothing to do with common descent. Unfortunately, this path eliminates Homology in general as ever being evidence for common descent. The most sensible explanation for the similarity in myoglobin (and other homologies) is thus the Creationist/ID position that similarity is a function of function and form, not common descent. *example of a 30myo mouse that has "changed...probably at a somewhat higher rate" and those "changes are both material and 'visible'": Link **appearance of "oldest mammal fossil": Link drc466
Virgil Cain @522 "...common design" Is that what CD stands for? :) Dionisio
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the paper referenced in the comment posted @31 in the below linked thread are saying when they use that same term (in past tense) twice in their abstract? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-538316 Dionisio
wd400:
You guys seem to be forgetting modern lineages are related to each other
Via a common design. Virgil Cain
Zachriel:
Even with random extinction, we expect large gaps at the leaves. With natural selection, the gaps will typically be even larger.
Science via bald proclamation! How typical. Also Zachriel is lying about nested hierarchies. Virgil Cain
When people say “Design,” they’re saying “Creation ex nihilo“. Hi Troll! Mung
gpuccio: For positive selection to have some role in the RV + NS algorithm, it must expand the original organism where a step variation happens to a significant part of the original population, otherwise there is no effect on the probabilistic barriers. IOWs, those intermediates must have been abundantly represented, at some time. Adaptation is usually limited in space AND time, so rapid transitions will be unlikely to leave detailed fossils. In any case, most molecular evolution doesn't leave fossils. All we have are the leaves of the tree, which are separated by the divergence of the branches. gpuccio: Unless positive selection of one step is perfect, abundant traces will remain of the previous step. Not at the leaves. Generally, all you have is the nested hierarchy. gpuccio: IOWs, in a ladder of positively selected steps, it is absolutely reasonable to expect a lot of remnants of all the steps, or at least of most of them. We don't expect "most of them" to be preserved in the fossil record, but the fossil record is characterized by divergence, not linear progression. gpuccio: Even if each time the reproductive advantage brought by one step variation were so great that it really could strongly compete with the previous one, still even purely stochastic factors would always favor some survival of the previous molecular forms. That is incorrect. Even with random extinction, we expect large gaps at the leaves. With natural selection, the gaps will typically be even larger. drc466: Mice (or rodents virtually identical) existed 100mya. Rodents have evolved substantially over the 70 million years of their existence or so. Hemoglobin has also evolved over that period. drc466: 3) Homologies in genetic code reflect relative similarities in function, not ancestry. The closer the form and function, the closer the genetic code and proteins. Sure, but that doesn't explain why synonymous mutations also support the phylogeny. drc466: 6) Taking points 2 and 5 in tandem, the “homologous” genetic code is NOT true homology – it is comparing millions of years of accumulated genetic mutation in one mammal to millions of years of accumulated genetic mutation in another. It's not just the differences, but the similarities that define phylogeny. And it's not just a linear relationship, but the nesting of different character traits. Zachriel
gpuccio @516
Is Windows Vista a creation ex nihilo?
No, absolutely not! As everybody knows, it was the result of many random mutations + natural selection acting on Windows XP. BTW, the evolution of the Windows OS taxon didn't stop at Windows Vista. After a long and winding road with many random mutations + natural selection operating on Windows Vista we got Windows 7, which eventually evolved into Windows 8, which recently evolved into Windows 10. Was Windows 9 an intermediate step that disappeared for some unknown reasons? As you can see, you cannot claim a big jump from Windows 8 to 10, because there was an intermediate Windows 9, even though we don't have any way to verify it, but we still can assume it. After all, how else could it go from 8 to 10? It's widely accepted that 8+1=9, not =10! Ya'll have to start from learning basic arithmetic rules, before you get involved in any serious discussion on evolution. Besides, there's nothing to discuss about evolution. That's a settled matter. Widely accepted. :) This shows that ALL your interlocutors' arguments were correct after all. Can you finally accept this? Please? :) Dionisio
wd400: "Mouse and human myoglobins have both changed (the mouse probably at a somewhat higher rate)." OK, but not too much: they still share 129 AAs out of 154, and 141 positives. Are you saying, like Alicia, that it's the result of convergent evolution? Have you performed a Ka/Ks analysis? gpuccio
Daniel King: "When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?" Absolutely not. Is Windows Vista a creation ex nihilo? gpuccio
wd400: "You know molecules have lineages too, right?" Yes. That's what I am discussing, I suppose. "In finite populations it’s inevitable that all modern versions of a gene share a (pretty recent) common ancestor." Maybe. And so? "Cumulative change to sequences is just inevitable." Not too much, if sequences are conserved by negative/purifying selection. That's the whole point. Functional constraints limit the change. "But you don’t seem to be able to grasp these points, so I guess I’m wasting my time." Maybe. Maybe I am wasting mine, too. We all waste a lot of time in our lives. gpuccio
Daniel King:
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
That is sometimes true (or correct), but not always. GaryGaulin
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the paper referenced in the comment posted @1562 in the below link are saying when using the word 'designing'? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597764 Dionisio
Daniel King @510
When people say “Design,” they’re saying “Creation ex nihilo“. Is that correct?
Is that what the authors of the papers referenced in the comments posted @1553, @1583 in the below links are saying when they used that same term? https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-597094 https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-598657 Dionisio
Popular Posts (Last 30 Days) A world-famous chemist tells the truth: there’s no… (15,317) Durston and Craig on an infinite temporal past . . . (2,799) Homologies, differences and information jumps (2,383) Larry Moran needs to do some more reading (1,663) A Little Timeline on the Second Law Argument (1,412)
:) Dionisio
When people say "Design," they're saying "Creation ex nihilo". Is that correct? Daniel King
Throw 100 tennis ball out of plane at 10000 ft. How many of them will be at intermediate altitudes an hour later? An analogy worthy of Elizabeth Liddle herself. Where do we look for the ones with intermediate tennis ball fitness? Mung
Throw 100 tennis ball out of plane at 10000 ft. How many of them will be at intermediate altitudes an hour later? wd400
wd400: Intermediate means between, the fitness of a variant is the expected number of offspring for a carrier of that variant. It’s not too hard to connect those is it? I thought we were talking about proteins, not protein carriers. ...a protein is of intermediate fitness between to others... Do you mean a protein that is intermediate between two other proteins? Protein A evolved into protein B which evolved into protein C but we should not expect to see protein B or protein A because they were intermediate and thus had intermediate fitness? How does that follow, even using DarwinLogicTM? Mung
You are confused.
1) Mice myoglobin, and the genetic code underlying it, hasn’t changed in 100my. It (along with all other homologs of common similarity to humans) is immutable in mice, while changing/mutating at some constant rate in the long line of ancestral life forms leading up to humanity. 2) Mice myoglobin, and the genetic code underlying it, has changed in 100my at the same rate as it has in the line leading up to humanity (again, along with all other homologs), but has done so without any material/visible change in the mouse life form! 3) Homologies in genetic code reflect relative similarities in function, not ancestry. The closer the form and function, the closer the genetic code and proteins.
Mouse and human myoglobins have both changed (the mouse probably at a somewhat higher rate). Those changes are both material and "visible". Why would you claim otherwise? wd400
Zach and wd's assertions are excellent examples of why evolutionary theory makes no sense to me. Let me see if I can make the issue clear: 1) We do not have "Ancient" genetic material - only modern genetic material (modern meaning thousands of years old max). 2) We have empirical evidence that all genetic material in higher order animals (e.g. mammals) undergoes a continuous process of mutation - there is no such thing as perfectly immutable genetic code. 3) As evidence for #2, we use the mutability of genetic code for a variety of purposes - detecting diseases, genetic bottlenecks in ancestry, mitochondrial Eve, y-chromosome Adam, nearness of relationships, geographical distributions, etc. None of these processes are viable if you do NOT assume continuous genetic mutation. 4) Evolutionists assert the genetic homology between MODERN genetic code is evidence for common descent. 5) Yet evolutionists ALSO assert that our last common ancestor (LCA) was millions of years in the past. 6) Taking points 2 and 5 in tandem, the "homologous" genetic code is NOT true homology - it is comparing millions of years of accumulated genetic mutation in one mammal to millions of years of accumulated genetic mutation in another. As an example, let's consider gpuccio's myoglobin. The relative similarity (and % thereof) between mouse myoglobin and human myoglobin is presented as evidence that mice and humans share a common ancestor, where mice and humans are equidistant from that common ancestor. And here's where the theory that "homology indicates CD" smashes into a brick wall of logic: Mice (or rodents virtually identical) existed 100mya. This leaves us 1 of 3 possibilities: 1) Mice myoglobin, and the genetic code underlying it, hasn't changed in 100my. It (along with all other homologs of common similarity to humans) is immutable in mice, while changing/mutating at some constant rate in the long line of ancestral life forms leading up to humanity. 2) Mice myoglobin, and the genetic code underlying it, has changed in 100my at the same rate as it has in the line leading up to humanity (again, along with all other homologs), but has done so without any material/visible change in the mouse life form! 3) Homologies in genetic code reflect relative similarities in function, not ancestry. The closer the form and function, the closer the genetic code and proteins. Evolutionist protestations to the contrary, it is simply inconceivable to me that anyone, evolutionist or otherwise could believe either proposition 1 or 2, that either a) some animals have undergone NO significant genetic mutation over periods of millions of years, or b) animals HAVE undergone significant genetic mutation at rates similar to the mutations that lead to the opposite end of the animal spectrum, yet show no recognizable form/function change in the fossil record. If you believe a, you deny the reality of #2 at the top of this post. If you believe b, you have no empirical evidence that such a ludicrous proposition is possible (e.g. that modern mice and modern humans are genetically equidistant from ancestral mice ten's of millions of years old). Now anticipating the response the change does occur, but that it is different between mice and mice-men lineage, or that is "highly conserved" in myoglobin and the other homologs - if this is so, you are simply cherry-picking data. If change rates are random and inconsistent across the genetic code, there is no way to tell how far myoglobin in mice/men is from their LCA, and so the % similarity is meaningless. Not to mention the whole issue of having to assume that myoglobin et. homologs mutated "in-sync"* all the way from pre-historic rodent to man! Does it make sense that, oh, say 60% (whatever the # is) of mice's genetic code managed to stay in-sync %-wise (i.e. 60% is 80% similar) over 100mya while undergoing non-constant rates of change? Or does it make sense that 60% of mice genetic code is 80% similar to human genetic code because that is relative to the similarity in form and function (eyes, lungs, pentadactyl limbs, organs, etc.)? If anyone can explain the logic hole in the above objection, I'm all ears. I just find "homology" to be completely illogical in terms of evidence for common descent over long periods of time. *wd400's "intermediate proteins" can form their own boy band - InSync! drc466
Intermediate means between, the fitness of a variant is the expected number of offspring for a carrier of that variant. It's not too hard to connect those is it? wd400
But you don’t seem to be able to grasp these points, so I guess I’m wasting my time. I think that started about the time you brought up intermediate fitness of proteins as an excuse for why they leave behind no trace of their existence. What does that even mean, intermediate fitness of a protein? Mung
We have robust mechanisms that explain missing data. Mung
It should say positive selection means intermediates don't last as long (i.e. changes pile up more quickly). My mistake. The rest of your post is just utterly wrong headed. You know molecules have lineages too, right? In finitie populations it's inevitable that all modern versions of a gene share a (pretty recent) common ancestor. Cumulative change to sequences is just inevitable. But you don't seem to be able to grasp these points, so I guess I'm wasting my time. wd400
wd400: "but selection means those intermediates last longer" We are talking about positive selection here, not negative/purifying selection. For positive selection to have some role in the RV + NS algorithm, it must expand the original organism where a step variation happens to a significant part of the original population, otherwise there is no effect on the probabilistic barriers. IOWs, those intermediates must have been abundantly represented, at some time. Unless positive selection of one step is perfect, abundant traces will remain of the previous step. Perfect positive selection is almost impossible. IOWs, in a ladder of positively selected steps, it is absolutely reasonable to expect a lot of remnants of all the steps, or at least of most of them. Remember, we are not talking of diseases here, but of functional genes, so functional that at some moment they are positively expanded because of their reproductive advantage. The model of a ladder of functional steps where each one completely erases any memory of the previous one is simple folly. Even if each time the reproductive advantage brought by one step variation were so great that it really could strongly compete with the previous one, still even purely stochastic factors would always favor some survival of the previous molecular forms. gpuccio
gpuccio, What proportion of diesase alleles in human populations do you think have existed since the human-chimp common ancestor? wd400
You guys seem to be forgetting modern lineages are related to each other (and perhaps they populations are finite if I read you right!). Perhaps it would to draw (or at least imagine) populations evolving (i.e. accumulating changes) down a tree with relatively long inter-node lengths. It should be obvious that most intermediate forms aren't represented in modern populations. That would be true without selection, but selection means those intermediates last longer. wd400
gpuccio: Completely different from what? Design is an observed “class of causation”, if so you like to call it. Not in the relevant history of biological organisms. It's like saying you need design to explain the origin of the Moon's orbit. Even if we don't know all the details of the origin of the Moon's orbit, we have robust mechanisms that explain the formation of planetary systems, and design would be introducing a completely different class of causation. You are "assuming some non-observed pattern in missing data, just to support the hypotheses you like most." Zachriel
wd400 "If a protein is of intermediate fitness between to others why should it exist in a modern population?" Oh, dear. How is "now" different from the past? EugeneS
wd400 "If a protein is of intermediate fitness between to others why should it exist in a modern population?" Oh, dear. Your reasoning is 'why should it exist now?". How is "now" different from the past? At some point, according to evolutionary logic, it must have happened. So who says it should not be happening now? Evolution is happening now. Again, according to evolution, it should have gaps, so it should NOT be happening now. Can you see the problem? How can you, guys, assert mutually exclusive things all the time and get away with it? EugeneS
Zachriel: "Which is exactly what does. It envisions a completely different class of causation when we already know of robust mechanisms capable of explaining the data." Completely different from what? Design is an observed "class of causation", if so you like to call it. Certainly, it is an observed fact. No need to "envision" it. Robust mechanisms? !!! No comment. gpuccio
wd400: "Is this not exactly what you are doing?" An easy question, an easy answer: no. I am reasoning about existing data. Nothing in my arguments depends on the imaginary form of missing data. gpuccio
wd400: "If a protein is of intermediate fitness between to others why should it exist in a modern population?" Why do we have genetic diseases in human population today? Certainly, neo darwinian mechanisms will erase all of them, as soon as humans become "a modern population". Only neo darwinian dogmatism can conceive that the mechanism of positive selection can erase all traces of thousands or millions or billions of intermediates "of intermediate fitness" which were functional enough to be, each of them, positively expanded at some time. gpuccio
But we cannot certainly assume some non observed pattern in missing data, just to support the hypotheses we like most.
Is this not exactly what you are doing? wd400
Gupuccio, I'm really not sure I can be any clearer. If a few minutes pondering this statement...
The discussion here is about the chances that the neo darwinian mechanism (RV + NS) may generate hundreds of bits of functional information without leaving any trace of the supposed functional intermediates on which positive selection should act
..doesn't make this mistake obvious I'm not sure what will. If a protein is of intermediate fitness between to others why should it exist in a modern population? wd400
gpuccio: But we cannot certainly assume some non observed pattern in missing data, just to support the hypotheses we like most. Which is exactly what does. It envisions a completely different class of causation when we already know of robust mechanisms capable of explaining the data. Zachriel
wd400: "The point it that the gaps between functional proteins or morphology or whatever largely correspond to those that we would expect to arise under gradual evolution given the way lineages are related to each other." I hope you understand that the discussion here is not about common descent or relation between lineages, which I have not only assumed, but used in my reasonings. The discussion here is about the chances that the neo darwinian mechanism (RV + NS) may generate hundreds of bits of functional information without leaving any trace of the supposed functional intermediates on which positive selection should act. Just to clarify. That's why the concept of information adds a lot to the discussion. gpuccio
wd400: "It seems fairly obvious to me that ignoring the pattern of missing data is a terrible mistake in any analysis." Not sure what you mean. If data are missing, I suppose we don't know their pattern. My point is that we can assume, with the necessary caution, a pattern similar to what we observe in available data (unless we have reasons to suspect systematic missingness, or any other specific bias). But we cannot certainly assume some non observed pattern in missing data, just to support the hypotheses we like most. Do you disagree with that? gpuccio
Dionisio: Thank you! I am certainly a minority guy, but I do not necessarily require absolute solitude. :) gpuccio
gpuccio @476 You may count on my support, and I'm sure other folks here support you too. Dionisio
Well, the key word, I guess, is ‘largely’
...
However, any researcher involved in actual scientific projects would agree that no scientific theory predicts anything perfectly.
...
No matter what happens, it wins.
wd400
wd400,
The point it that the gaps between functional proteins or morphology or whatever largely correspond to those that we would expect to arise under gradual evolution given the way lineages are related to each other.
Well, the key word, I guess, is 'largely' ;) Don't read me wrong. I am not against evolution as a phenomenon. But empirical evidence suggests that evolution is secondary to design. Design goes first. Evolution is a background noise incapable of creating genuine functional novelty. Evolution selects from among already existing functions, it does not have the power to select for a future function, for which it needs foresight and the capability of making decisions, i.e. to be intelligent. Functions must first be present, and only then can evolution automatically select. EugeneS
Eugene, I'm really not sure you've read this thread. No one has claimed "there must be intermediates, except in cases where there must not be". The point it that the gaps between functional proteins or morphology or whatever largely correspond to those that we would expect to arise under gradual evolution given the way lineages are related to each other. wd400
There must be intermediates, except in cases where there must not be. The most interesting thing about discussions like this one is that when people say data is missing, the usual response is that even the absence of data proves the mighty theory of evolution. No matter what happens, it wins. However, any researcher involved in actual scientific projects would agree that no scientific theory predicts anything perfectly. Except the theory of evolution... It predicts anything with an absolute certainty. Dialectically, that a theory is not perfect in its predictions proves it is a working scientific theory. If it is perfect, it is not science. The art of making no mistakes is in formulating the most general statements. Stuff happens... EugeneS
Which has nothing to do with my point. And then went on with other elusive statements.
Well, obviously I disagree those statements are unrelated. It seems fairly obvious to me that ignoring the pattern of missing data is a terrible mistake in any analysis. The pattern of missing data in this case is a direct prediction of common descent and divergent evolution (and indeed natural selection). I'm sorry that I can't provide a more useful discussion here. I haven't read the whole thread, but the OP is just a much worse version of the sorts of analysis moleculer/genomic evolutionists use every day. The addition of "information" (where the values relate only to the particular data-set under consideration) adds very little. wd400
You all just need to learn some basic biology. We know evolution can make information-rich proteins be whatever means necessary because we can show that these proteins exist in some taxa and that they are missing in some taxa. You should find an information-rich protein that exists in all taxa. No missing intermediates. Mung
Alicia:
If the discovery institute could find anything even remotely close to a “reasonable object for a strong design inference,” they would be doing exactly that…trumpeting it from the hills.
They have found such and they have trumpeted it. OTOH people like you just deny it and handwave it away.
Unfortunately, getting us to the answer, at any rate, does not involved a design inference. Unless that designer is nature.
Unfortunately for you there isn't any way to test the claim that nature designed biology. You can't even test your claim that nature produced the genetic code. If you had such a test you could possible win millions of dollars. That the money is still uncollected is proof tat you have nothing but your standard bloviations. Virgil Cain
wd400: My point was. "One thing, certainly, you cannot do: you cannot imagine that the missing data would be completely different from what you are observing, and that you would find in them confirmation of some model which, instead, does not fit in any way the available data." You commented: "For the record — this is precisely what data analysts should be wary of with missing data. Ignoring “Systematic missingness” or “Missing not at random data” is bound to ruin inferences." Which has nothing to do with my point. And then went on with other elusive statements. Usually, you are more reliable in a discussion. gpuccio
Alicia: Wonderful! After Zachriel's argument that I am not supported by the vast majority of biologists, now comes your argument that I am not supported by the Discovery Institute. My minority becomes smaller and smaller... Wonderful. gpuccio
Zachriel at #463: A good summary of neo darwinian catechism. Totally unconvincing, but you do your best, as always. gpuccio
Please Querius, get real. If the discovery institute could find anything even remotely close to a "reasonable object for a strong design inference," they would be doing exactly that...trumpeting it from the hills. But they don't have anything of the sort and pucci's science certainly isn't anything close either. And the "design inference vs. assume it's evolutionary junk" doesn't even really exist for most researchers. Researchers in genetics, for instance, study their largely lab-specific subset of processes/elements and many of them naturally search for function. Whether they focus on coding regions, non-coding regions, transposons, whatever it is; they are looking for function. So don't you worry your little head about "getting us to the answer faster," the people who know what they are doing will take care of it. Unfortunately, getting us to the answer, at any rate, does not involved a design inference. Unless that designer is nature. Alicia Cartelli
Alicia, science is not supposed to be an adversarial courtroom with a winning side "trumpeting it from the hills." The design inference should get us to the answer faster than the "assume-it's-evolutionary-junk" inference . . . EVEN IF IT WASN'T DESIGNED! Good questions, Bill. Let's see whether we get any substantive answers. Daniel, do this experiment. Substitute other things into your assertion to see whether the logic still makes sense. Wait, I'll even do it for you.
Until _______ has created ______ by design, the ID argument is fatuous:
a. a human, life (argument that only humans can design things) b. a modern human, Inca wall (argument that Inca walls are natural formations) c. God, life (If God exists, God has already done this) d. an alien, linear accelerator (argument that aliens can't design things) e. Daniel King, pogo stick (argument that unless Daniel King designs a pogo stick, the ID inference fails). The logic really doesn't work, does it. -Q Querius
Daniel King:
Until someone has created life by design, the ID argument is fatuous:
We know it upsets you because the way to the design inference eliminates your position as a total failure to explain what we observe. And all we know is that life begets life. Virgil Cain
Until someone has created life by design, the ID argument is fatuous: "Somewhere, somehow, sometimes, life was designed...but not lately." Daniel King
Alicia
Well I’ll tell you why: It’s because it is not in any way a “reasonable object for a strong design inference.” You can take any known protein sequence and find “information jumps” similar to what we see here if you go back far enough (because of massive amounts of extinction!)
Do you have evidence of extension that occurred between the protein DNA sequences that gpuccio has cited? How many amino acid changes do you think the mechanisms of modern evolutionary theory can handle given populations and time? When a proteins DNA sequence starts to mutate have you thought through all the steps needed to get a new functioning protein including transcription splicing sequences and proteins that control the timing and degradation? You are trying to mutate randomly through a sequence which is the largest mathematical spaces in the universe. Not sure extension is the answer here but I am interested in your argument. I am not supporting the design inference I just am very skeptical that we understand the mechanism of change at this point. bill cole
Querius: “One would think that strong supporting evidence would follow” For days now I’ve been trying to explain to pucci why his “science” is so ridiculously wrong. I’ve given up. But here’s a thought: If this is such a great example of the “design inference,” why hasn’t the discovery institute (which has “actual” biologists) already come up with it and/or why aren’t they trumpeting it from the hills? I mean, it doesn't even require funding. Protein sequences and BLAST are all public domain, right? Well I’ll tell you why: It’s because it is not in any way a “reasonable object for a strong design inference.” You can take any known protein sequence and find “information jumps” similar to what we see here if you go back far enough (because of massive amounts of extinction!) Like I said, any biologist worth their salt would take one look at this and laugh. Alicia Cartelli
wd400:
Gaps are just a prediction of evolution with descent and extinction.
Not really. For one those extinctions have to be well timed, meaning not just any extinction event will do. And second, as Linne demonstrated with his taxonomy, gaps are expected in a Common Design scenario. Virgil Cain
Zachriel:
Fossils show that complex functional structures can evolve.
No, they do not do that. Fossils show that complex functional structures also existed in the past.
And we have some examples of molecular evolution in human timescales, such as nylonase, or Cit+, or pesticide resistance.
ID is not anti-evolution and you are an equivocator.
Turns out that even random sequences can occasionally fold into functional proteins, so there’s no mystery that novel folds may have formed at different times in the past.
A) Those random sequences were all designed B) Most proteins require chaperones or they do not fold into the shape the cell requires. Virgil Cain
EugeneS, No.To be honest, I don't even know what you mean. wd400
Querius, Actually, you may be right about software generated responses. Why didnt it occur to me? ? Wd400 A valid theory cannot predict A AND NOT(A), right? Evolution, in contrast, predicts absence of data and presence of data at the same time. However, which one is entirely up to a debater. Dont you think so? EugeneS
Gpuccio, The patterns you see here don't actually require systematic missingness, I only commented because it's funny to see someone keen on their high-horse, claim experience then make such a thoroughly wrong statement. Gaps are just a prediction of evolution with descent and extinction. As it happens, there is also a reason to think gaps among living organisms will be even more common than gradual/continous change alone predicts. Natural selection removes intermediates, after all. wd400
gpuccio: One thing, certainly, you cannot do: you cannot imagine that the missing data would be completely different from what you are observing In this case, we can predict the missing data fits the phylogenetic tree, supported by the every newly discovered fossil, while congruence implies that the existence of morphological intermediates means there are molecular intermediates. gpuccio: Naturally selectable steps to complex functional sequences simply do not exist. Fossils show that complex functional structures can evolve. It turns out that complexity can originate stepwise, with each step otherwise unremarkable. Molecular evidence supports the same pattern of divergence and specialization. When we do find rare molecular fossils, they also support this pattern of divergence. And we have some examples of molecular evolution in human timescales, such as nylonase, or Cit+, or pesticide resistance. Notably, YOU point to the evolution of structures that are very ancient, where the gaps are mostly obscured, but then YOU insist there must be some different class of cause than what is necessary to explain all the rest of the data. gpuccio: Again, we have protein superfamilies as evidence of that: “the largest grouping (clade) of proteins for which common ancestry can be inferred”. Turns out that even random sequences can occasionally fold into functional proteins, so there's no mystery that novel folds may have formed at different times in the past. Furthermore, extinction is a rampant characteristic of life, so gaps are the predicted pattern, with larger gaps the further back in time you go. Zachriel
Querius: When Alicia Cartelli (whoever she/he/it is) goes back to derogatory nonsense, I suppose it means that the discussion is good. When she becomes transitorily "reasonable", and even capable of offering arguments, even if bad ones, I tend to feel somewhat worried: what is happening? Luckily, reality soon reestablishes its grip, Alicia becomes Alicia again, and I can relax. :) gpuccio
General observation:
It is so painfully obvious, to someone with a good background in biology, that you have no idea what you are talking about.
One would think that strong supporting evidence would follow, but instead, one is simply left with a stand-alone derogatory assertion that apparently is thought to constitute irrefutable proof in of itself somehow. There are several people spamming UD with such frequency, that it makes me wonder whether their vacuous posts aren't simply generated by a software utility. It would be fairly easy to write. It's fairly tempting. I already have some names picked out . . . -Q Querius
wd400: Why do you think that extinction would generate “Systematic missingness” or “Missing not at random data”? In particular, why should the process erase exactly those data which could support the neo darwinian mechanism of generation of information? Just to know. gpuccio
wd400:
And, of course,presence of large functional gaps between clades is a prediction of gradual evolution, and really an inevitable consequence of divergence and extinction.
Total unsubstantiated nonsense. Virgil Cain
Earth to Daniel King- Unlike your position at least ID has a methodology. Virgil Cain
One thing, certainly, you cannot do: you cannot imagine that the missing data would be completely different from what you are observing, and that you would find in them confirmation of some model which, instead, does not fit in any way the available data.
Exactly why the ID model is vacuous. When you have observed the creation of new body plans by an immaterial designer, let us know. Daniel King
One thing, certainly, you cannot do: you cannot imagine that the missing data would be completely different from what you are observing,
For the record -- this is precisely what data analysts should be wary of with missing data. Ignoring "Systematic missingness" or "Missing not at random data" is bound to ruin inferences. And, of course,presence of large functional gaps between clades is a prediction of gradual evolution, and really an inevitable consequence of divergence and extinction. wd400
Alicia: I don't feel sorry for you, if I must be sincere. Enjoy your good background in biology, while it still exists. Have a nice day. :) gpuccio
Pucci, It is so painfully obvious, to someone with a good background in biology, that you have no idea what you are talking about. I actually feel sorry for you. Enjoy your gaps while they still exist! Have a nice day Alicia Cartelli
Zachriel and Alicia: I would like to make a point about your discussions about extinction and missing data and so on. I have good experience of data analysis in my field, and believe me, in biological sciences, and especially in medicine, you have to deal with missing data quite often, I would say always. So, what do you do when some data are missing, and you still have to analyze the data which are available? Well, you try to cope, and you try to go on with your analysis while acknowledging that some data are missing, and trying to reasonably adjust your analysis for that fact. One thing, certainly, you cannot do: you cannot imagine that the missing data would be completely different from what you are observing, and that you would find in them confirmation of some model which, instead, does not fit in any way the available data. So, you cannot use supposed extinction to think that your theory could explain the evolution of complex functional sequences by thousands of functional, naturally selectable intermediates with growing function, which have never been observed. Another big error, as I have tried to show, is to pass off optimized functional proteins in different species, which have differences due to neutral variation or possible different local functional constraints, as naturally selectable functional intermediates of a functional sequence. They are not. Again, read my post #403, especially the commments about how proteins with the same functionality diverge in time because of neutral variation. Naturally selectable steps to complex functional sequences simply do not exist. Again, we have protein superfamilies as evidence of that: "the largest grouping (clade) of proteins for which common ancestry can be inferred". IOWs, we have at least 2000 grouping of sequences for which common ancestry cannot be inferred. And remember, one thing is common ancestry, all another thing is a naturally selectable path of transitions, even in groupings where common ancestry can be reasonably inferred, each of them increasingly functional, each of them naturally selectable, each of them a sequence step to the final protein. gpuccio
Alicia at #450: You should stop accusing Eric (or me) of "not having read the paper". We have read the abstract, and we have not read the whole paper because it is paywalled. As I told you, you are free to report in as much detail as you deem necessary the arguments that, in your opinion, support your discourse. And again, our argument is not about microevolutionary changes between similar molecules. Those can happen, and they are the only forms of molecular transitions which are documented, even if rarely. The ID argument is about complex functional information. It is about sequences which have a lot of it, hundreds of bits of it, so that the transition cannot happen in reality. It is about complex transitions which cannot be deconstructed into simpler, naturally selectable steps, as your theory badly requires, because those intermediary steps simply do not exist. If you don't understand this, you have understood nothing of ID theory. gpuccio
Alicia: It's not what we were discussing, because it's about "small changes in their protein interaction system ". The first part of Prickle 1 shows steps of 100 - 200 bits. I would not call them "small changes". Moreover, you could maybe profit from reading my post #403, to Zachriel. You say: "I say that 100 million years isn’t so rapid" I say that, for 600 bits of information, 100 million years is the blink of an eye! Remember, we are discussing exponential values. You say: "and that we don’t see any sequence intermediates because we have no sequence data from the organisms that branched off between tunicates and sharks." Again, see my post #403. One thing is that some species, even many of them may do extinct. Another thing is that important steps, functional and many times expanded in natural history, completely disappear without leaving any trace of their existence. The proteome is a very good sample of what happened in natural history. Not complete, but big enough to be representative. I am not ignoring your arguments, As you can see, I discuss them in detail. But I find them biased and irrelevant. It's not the same thing. gpuccio
EA: “Play around with binding sites all you want; it doesn’t help explain the origin of significant amounts of biological information.” The paper demonstrates some of the possible final steps towards the evolution of a protein that exists today. The last few steps in the path. Just because you decided to start using the word “significant” and demanding that we show how evolution traveled the entire path, doesn’t mean you can claim that I “literature bluffed.” I never claimed that the paper demonstrates how a protein evolved from scratch. I said the paper shows how a protein can evolve from intermediates, which is what pucci asked for in an earlier post. “loss of binding site specificity” does not mean loss of information. And actually the same paper demonstrates exactly that. The evolutionary intermediates bound the wild-type partner with less affinity, but they also bound other proteins with significant affinity. (Not that you would know this since you didn’t read the paper) So I would argue that in this case, and probably many others in the course of evolution, that “loss of binding spite specificity” can result in an increase in information. The protein may not be binding as tightly to a single specific protein, but it is now binding tightly to a few other proteins. This is binding promiscuity and is evolution exploring sequence space for binding sites that promote interactions with other proteins. Anyways, even mungy accepts the fact that 99% of species to have ever liver are extinct. He managed to get out of the third grade, why can’t you? Alicia Cartelli
Puccci: “it’s not what we were discussing, except in your imagination.” Then concisely explain to me what we are discussing. “This discussion is and always has been about ‘the origin of significant amounts of biological information’.” Ok, and I’m saying it usually occurs in small steps, which is what we see in most proteins when we look at the sequence data. (look at the first part of prickle 1 in your graph) You say that the second part of prickle came about rapidly with apparently no intermediates. I say that 100 million years isn’t so rapid and that we don’t see any sequence intermediates because we have no sequence data from the organisms that branched off between tunicates and sharks. You ignore this. Alicia Cartelli
Virgil Cain, It's funny watching Zachriel's contortions. In one comment he claims life to be an empirically verifiable example of symbolic control arising naturalistically. In another he says that it is posited that live evolved from a relatively simple replicator. Zachriel apparently thinks that "to demonstrate" and "to posit" are synonyms. EugeneS
Zachriel is bloviating as we cannot study the designers and builders of Stonehenge. Also saying "Evolution only explains diversification and adaptation of existing life" is an equivocation as ID is not anti-evolution. The only way that blind watchmaker evolution can explain the existing diversity of life is if it started with a greater diversity, including the existence of complex metazoans.
Sure, but ignore other evidence. See @440.
Your bloviations aren't evidence, Zahriel. Virgil Cain
EugeneS: So we have positive evidence: – human and animal communication; – human and animal decision making capability (not necessarily conscious); – artificial intelligence and (more broadly artificial information processing systems) – information translation in the cell. That's wonderful. Now that still implies there is a link of causation from the artifact to the art to the artisan. That works quite well with henges, beehives, and computers. However, the same research concerning the posited designer of life appears to be sterile, undermining the claim. EugeneS: What Zachriel also conveniently does not mention, is that evolution is a consequence of information translation Evolution only explains diversification and adaptation of existing life. It's posited that life evolved from a relatively simple replicator. gpuccioAs you can easily see, I use CD and nested hierarchies in my arguments for ID. Sure, but ignore other evidence. See @440. Zachriel
GP, I enjoy reading what you OPs. Sure about patience. After all, Zachriel is more polite than Dr Moran ;) EugeneS
EugeneS: Patience is rewarding, if it allows to deepen a good discussion. And I am very happy of the discussion here. Thanks to your good contributions, too! :) gpuccio
Zachriel: I have never doubted common descent and nested hierarchies. My reasonings are against the explanation of biological information by the neo darwinian theory. As you can easily see, I use CD and nested hierarchies in my arguments for ID. You say: "Perhaps the majority of experts in the field are wrong, but they can’t be discounted without addressing their arguments." Of course. That's why we are here. gpuccio
GP and all, Thanks a lot for your patience. I have lost mine apparently ;) Actually, Zachriel missed out animal communication as another piece of evidence of code having intelligent origin. That is conspicuous by its absence from Zachriel's account, to use an idiom. What he also missed out is the absence of evidence to the contrary. All this is very telling. So we have positive evidence: - human and animal communication; - human and animal decision making capability (not necessarily conscious); - artificial intelligence and (more broadly artificial information processing systems) - information translation in the cell. Evidence to the contrary: - None. What Zachriel also conveniently does not mention, is that evolution is a consequence of information translation, not the other way around. Without the latter, evolution cannot even start. But he is absolutely right in one thing. Ignoring an entire corpus of evidence is hardly persuasive. EugeneS
Zachriel:
1. Morphological traits largely support the same nested hierarchy as molecular traits.
Great as nested hierarchies are only formed by an intelligent design. Virgil Cain
gpuccio: you have made a good enough argument for design Good. So we stated the argument correctly. And understanding the argument, our objections are to the point. gpuccio: Molecular events are what we are really discussing. You go back to fossils, but, as I have told you many times, fossils are of no help, is we don’t know the molecular events which explain morphological changes. Pointing to human ignorance is hardly a persuasive argument, especially as that gap has also been substantially narrowed. 1. Morphological traits largely support the same nested hierarchy as molecular traits. 2. Morphological intermediates are supported by fossil finds of extinct organisms. 3. It's therefore reasonable to conclude that the molecular traits of extinct organisms would also fit this pattern. 4. Extinction is rampant in history, meaning the vast majority of organisms don't have extant relatives, so gaps (or jumps) are the expected pattern. 5. Even then, it turns out that we can sometimes determine the molecular traits of extinct organisms, which again, support the nested hierarchy. Ignoring an entire corpus of evidence is hardly persuasive. gpuccio: And please, excuse me if I find the “explanations” of the “vast majority of biologists” completely unsatisfying: I am really a proud, obstinate, solitary fool. And I like it that way. Perhaps the majority of experts in the field are wrong, but they can't be discounted without addressing their arguments. Zachriel
Mung: A triumvirate is made strong by differences and complementarities. gpuccio
Unlike gpuccio, I look for gaps, or jumps, or discontinuities, call them as you like, in the only place where they really mean something: the mental level. ;) Mung
Please, don’t try to jeopardize our newly formed triumvirate! I wouldn't want all those triumvirate lessons to go to waste! Mung
Zachriel: I think that in #432 you have made a good enough argument for design. My compliments! It is true, life and human artifacts (designed objects) are the only existing examples of a number of formal properties, especially complex functional information and symbolic systems. OK, that is a strong base upon which we infer design. Please, note that it is not only a generic resemblance ("organisms look like complicated machines"). It is a specific occurrence of formal configurations, strictly connected to the processes which cause the result. You say that "the vast majority of biologists point to natural processes to explain how complex adaptations have evolved". OK, that's really news! :) You say: "all you have done is push the question back to another gap, molecular evolution which leaves few fossils outside of extant organisms". But the point is: I have pushed absolutely nothing, least of all a gap. Molecular events are what we are really discussing. You go back to fossils, but, as I have told you many times, fossils are of no help, is we don't know the molecular events which explain morphological changes. Why? It's obvious, but I will say it again, for the nth time: It's at the molecular level that variation happens. It's at the molecular level that information is stored and changed. Where do you think we can find explanations for biological information, if not at the molecular level? So, if gaps exist at the molecular level, I am not "pushing" them from anywhere else. I am only interested in the molecular level, always have been, always will be. Because I am interested in understanding, not in void debating. So, I look for gaps, or jumps, or discontinuities, call them as you like, in the only place where they really mean something: the molecular level. And please, excuse me if I find the "explanations" of the "vast majority of biologists" completely unsatisfying: I am really a proud, obstinate, solitary fool. And I like it that way. gpuccio
mike1962: And if, instead of "consensus", we just called it "appeal to conformistic thought"? OK, I have always stated that I am a minority guy, and maybe it's my weakness that I tend to avoid majorities, especially when important thought and cognitive choices are concerned. But I am happy this way, so please bear with me! :) gpuccio
… Finally, I would remind you to notice where the claim of consensus is invoked. Consensus is invoked only in situations where the science is not solid enough. Nobody says the consensus of scientists agrees that E = mc². Nobody says the consensus is that the sun is 93 million miles away. It would never occur to anyone to speak that way. --Michael Crichton mike1962
Zachriel:
Instead, the vast majority of biologists point to natural processes to explain how complex adaptations have evolved.
LoL! They may point but they never demonstrate such a thing. That means theirs isn't a scientific explanation.
However, that ignores the evidence from biology that complicated machines are evolutionary adaptations
That ignores the fact that there isn't any such evidence. But then again you seem to love your ignorance and want to keep it. Virgil Cain
gpuccio: don’t you think that “life” was a little like begging the question? Isn't it begging the question to exclude life, as had been the case in previous iterations of the question? In any case, let's stipulate that life and artificial intelligence are the only known cases of symbolic processes (for certain definitions of symbolism). So? You then hypothesize they have a common cause, an intelligent agent. That means there is a link of causation from the artifact to the art to the artisan. The obvious entailments trace these links of causation. That works quite well for computer and henges, but not life. Instead, the vast majority of biologists point to natural processes to explain how complex adaptations have evolved. This is no different than saying organisms look like complicated machines (for certain definitions of complicated). Human artifacts and organisms are the only known examples of complicated machines, so we hypothesize they are both the result of an intelligent agent. However, that ignores the evidence from biology that complicated machines are evolutionary adaptations. While the complicated machine gap has been filled, all you have done is push the question back to another gap, molecular evolution which leaves few fossils outside of extant organisms. Zachriel
Zachriel:
We provided what was an honest and what we believe to be an informed answer to your question.
And that is the problem as you answer was neither honest nor informed.
However, just for the record, ignorance is curable,
It could be curable but you have shown no interest in being cured of your ignorance. Virgil Cain
Zachriel: OK, don't you think that "life" was a little like begging the question? Honest maybe, informed certainly, but what about a mix of smart and desperate? :) gpuccio
EugeneS: Either you are not being honest or you are ignorant. EugeneS: You may say whatever you want now. Thanks! We provided what was an honest and what we believe to be an informed answer to your question. However, just for the record, ignorance is curable, so if you feel we are merely ignorant, then that is a valid reason to continue the discussion. Zachriel
Zachriel: Please, don't try to jeopardize our newly formed triumvirate! :) gpuccio
Dionisio: OK, done, my precious peer reviewer! :) You really have no faith in the power of random mutations to convey new and interesting meanings, have you? gpuccio
EugeneS @422 Perhaps your interlocutor meant the concept of "life" that is explained very clearly & accurately in a recent paper referenced @1565 in this link: https://uncommondesc.wpengine.com/intelligent-design/mystery-at-the-heart-of-life/#comment-598212 :) BTW, according to Wikipedia, "Get a life" is an idiom and catch phrase that has gained international usage. It is intended as a taunt, to indicate that the person being so addressed is devoting an inordinate amount of time to trivial or hopeless matters. :) Dionisio
Zachriel #423, "It was an honest and informed answer to your question." You may say whatever you want now. You are either ignorant or being dishonest. End of discussion. EugeneS
Zachriel:
So what has been determined with regard to who, what, when, where, why, and how?
You should focus on your position as it has nothing. At least ID has a methodology for determining design. I remind you, can you kindly provide a single empirically verifiable example where a symbolically controlled system would arise as a result of exclusively the motion of particles of matter.
Life.
Again, what evidence do you have to support the conjectures? :razz: Zachriel, always spewing unsupported crap. Virgil Cain
EugeneS: Either you are not being honest or you are ignorant. It was an honest and informed answer to your question. Zachriel
Zachriel, "Life". Either you are not being honest or you are ignorant of the fact that abiogenesis is a hypothesis. I asked for an empirically verifiable example. End of discussion. EugeneS
gpuccio, @381:
"There is no necessity which can link a specific sequence of nucleotides to a specific functional sequence of AAs through an arbitrary symbolic code. That should be obvious even to you."
Doesn't it seem mysterious that certain things that appear so obvious to some folks, are not seen by others, regardless of educational background or academic credentials? :) BTW, off topic, in your very insightful commentary posted @381 I see this sentence:
"a) At present, the only scientific conclusion we can offer from data in the necessity of some conscious intelligent purposeful being or beings to explain biological design."
I agree, but just wanted to ask if the bold word 'in' is just the product of a 'random mutation' of the word 'is'? Caro Dottore, it's kind of embarrassing for me to point to such a minor, irrelevant detail in the middle of the highly interesting discussion your OP + follow-up comments have provoked in this tread, but given that your comment @381 could be referenced more than once, shouldn't it go through some kind of editorial peer-review before it is published in a high-impact journal, assuming that the neo-Darwinian establishment doesn't censor it? :) Dionisio
Mung: You may be surprised to hear I agree with you. gpuccio: And I agree with you and with Zachriel. So what has been determined with regard to who, what, when, where, why, and how? What direct evidence do we have? EugeneS: I remind you, can you kindly provide a single empirically verifiable example where a symbolically controlled system would arise as a result of exclusively the motion of particles of matter. Life. Zachriel
Zachriel, If you have forgotten, I remind you, can you kindly provide a single empirically verifiable example where a symbolically controlled system would arise as a result of exclusively the motion of particles of matter. After you have presented a single case of that sort, we can engage in a further conversation. EugeneS
Me_Think: A couple of comments to your comments: 1) The intervention of the designer is not certainly at the level of the aminoacid. Rather, it is probably some form of "control" of variation (usually random errors) at the level of DNA replication. Nucleotides, IOWs. So, the random errors in replication can assume a functional meaning for the conscious choices of the designer. This is only one possible scenario, of course. 2) I understand your objection from a classical quantum point of view, but what I am suggesting here is some special form of connection between consciousness and quantum events. A direct connection, such as the one which takes place in our brains. IOWs, an interface. In that sense, the scenario would be very different from a classical quantum scenario where the properties of the quantum wave function are measured by some physical measurement system, determining a random collapse of the wave function itself. The hypothesis here is that conscious events and quantum fields in the brain cells (in the model of humans), or conscious events and biological matter (in the case of biological design) are linked at a definite interface. IOWs, the hypothesis is that consciousness, whatever it is, interacts with matter (or, more generally, objective events) through specific interfaces, one of which is in the human brain and body. Of course, we cannot yet understand how consciousness and quantum wave functions directly interact, because we still understand very little of consciousness and of how it works. We only know that subjective states are a different thing from objective events, and that the two worlds in some way interact. Quantum level remains the best candidate for that interaction, and, as I have said, that is not only my personal idea. gpuccio
GP @ 381 Thanks for your thoughts on Designer. However, note that of all the methods that a Designer could choose to control the biological processes, Quantum mechanics is the worst one. For something as simple as moving an amino acid to a certain place, the designer would need to know the initial positions of the particles in the acid. If he does find the positions, he wouldn't know the momentum (uncertainty Principle),so the position of the particles can't be predicted over time. He can not direct the amino acid to a location precisely. Worse, if He commands the quantum properties to assume certain state (say top spin), all the other entangled particles will assume the opposite spin, essentially creating no change in the system. Then there is the measurement effect (stupidly called observer effect) of Quantum system which would collapse the wave function each time designer tries to measure the state of the particles. QM would have been great if Designer had hidden variables which would allow him to read the properties of particles without disturbing their state, but we know there aren't any(Bell's Inequality). Me_Think
Troll. Mung
You may be surprised to hear I agree with you. If all ID can say is “it’s designed” full stop, then ID hasn’t much chance of success as a science.
It never did. It never will. Daniel King
Intelligent Design is the study of patterns in nature that are best explained as the result of intelligence. -- William A. Dembski
and
“Once specified complexity tells us that something is designed, there is nothing to stop us from inquiring into its production. A design inference therefore does not avoid the problem of how a designing intelligence might have produced an object. It simply makes it a separate question.” Wm. Dembski- pg 112 of No Free Lunch
We have to first determine design exists before we ask any other questions about it.
Intelligent design begins with a seemingly innocuous question: Can objects, even if nothing is known about how they arose, exhibit features that reliably signal the action of an intelligent cause? Wm. Dembski
Yes, they can. Virgil Cain
Mung: "You may be surprised to hear I agree with you. If all ID can say is “it’s designed” full stop, then ID hasn’t much chance of success as a science." And I agree with you and with Zachriel. We are apparently a good trio! :) gpuccio
Mung: Superfamilies are a level of classification in SCOP and in other classifications of proteins. In SCOP, they are more specific than folds, and more general than families. In SCOPe 2.05 there are 203026 Domains, which are grouped into 1208 folds, 1984 superfamilies and 4756 families. Of course, the number can only grow. A superfamily is more or less a group of sequences which have in common a general 3d structure, general function, and sequence homology. According to Wikipedia, "A protein superfamily is the largest grouping (clade) of proteins for which common ancestry can be inferred". IOWs, superfamilies are isolated islands, at all levels, of sequence and structure and function. Families are rather separated too, but can have some sequence and structure and function similarity. These groupings are more severe than mere sequence dissimilarity. Indeed, using ASTRAL (a tool in the SCOP site), and setting the search for groups that have less than 10% similarity, we get about 6700 groupings. That means that in families and superfamilies are grouped sequences that have apparently no sequence similarity, but still some structural similarity. That's why we can consider superfamilies as groupings which are really different one from the other. IOWs groups for which "common ancestry cannot be inferred". My example in the OP, Prickle 1, is essentially made of two parts, in the human/vertebrate form. The part which I have called "red" includes 4 domains. The first one, of about 110 AAs, is located in the N terminal part of the protein ("on the left of the sequence"). It is called PET_Prickle, and is part of the PET superfamily. Then there are three LIM domains, each of about 60 AAs, which are Zinc binding domains, and are part of the LIM superfamily. The rest of the molecule, the "blue" part in the vertebrate form of the protein, is the sequence which is apparently restricted to vertebrates. In it no known domain is recognized, therefore we know practically nothing of its 3d structure and function. In my argument here, I have (very reasonably, I believe) assumed functionality because of its high conservation in vertebrates. It is very likely, IMO, that it is implied in specific regulatory functions, restricted to vertebrate development. gpuccio
Zachriel: Wonderful. Now let’s research it some more. The obvious entailments are the who, what, when, where, why, and how. You may be surprised to hear I agree with you. If all ID can say is "it's designed" full stop, then ID hasn't much chance of success as a science. Mung
Zachriel:
The obvious entailments are the who, what, when, where, why, and how.
That is correct. very good. Here's a cookie.
Evolutionary theory is constantly being tested.
Except no one knows how! For example no one knows how to test the claim that ATP synthase arose via stochastic processes. Zachriel is being deceitful, again. Virgil Cain
Mung: From the data available, we can already deduce it was intelligence at work. Isn’t that amazing?! Wonderful. Now let's research it some more. The obvious entailments are the who, what, when, where, why, and how. Mung: you are happy to wait indefinitely for empirical justification. Not at all. Evolutionary theory is constantly being tested. Zachriel
Hi gpuccio, Are the proteins in a superfamily thought to descend from a common ancestral protein or is there some other basis for classifying them as members of a superfamily? Is your example from the OP a member of a superfamily? Thanks Mung
Zachriel, From the data available, we can already deduce it was intelligence at work. Isn't that amazing?! If you and others in your camp were really interested in the promulgation of science, you would have regarded this inference alone as a major breakthrough, which it is. You are being selectively hyper-critical. I would have said nothing if that hyper-criticism had been fair. But it's not. In the case of totally unwarranted naturalistic fantasy (which isn't even nebulous, it is complete bluff), you are happy to wait indefinitely for empirical justification. At the same time, in the case of the inference to design, you don't want to wait and demand everything at once. That is not the way things happen in science. But it's already good that at least you can see in it a speculative hypothesis. Fine by me. EugeneS
Zachriel:
Mere similarity doesn’t directly support whether an organism is an intermediate, but how it fits the nested hierarchy.
Nested hierarchies can only arise by intelligent design. Common descent expects numerous transitional forms which would ruin a nested hierarchy. Zachriel is either deceitful or willfully ignorant Virgil Cain
gpuccio: It seems that we have a different concept of “intermediate”. Mere similarity doesn't directly support whether an organism is an intermediate, but how it fits the nested hierarchy. Zachriel
Earth to Zachriel: Again, what evidence do you have to support the conjectures? Follow your own words and stop being such a dick. Virgil Cain
Zachriel: It seems that we have a different concept of "intermediate". To be of help in neo darwinian explanations, an intermediate is not only some morphological or molecular feature which is chronological intermediate between two others. IOWs, if we blast human myoglobin against different species with different chronological separations from humans, we get growing similarities with the human sequence: Danio rerio (bony fish): Bitscore 117 bits expect 1e-32 Identities 63/145(43%) Similarities 88/145(60%) Then a bird, Acanthisitta chloris: Bitscore 248 bits expect 2e-82 Identities 118/154(77%) Similarities 135/154(87%) Mouse (mammal): Bitscore 264 bits expect 1e-89 Identities 129/154(84%) Similarities 141/154(91%) OK? Now, that does not mean that, for example, the sequence in birds is an intermediate to the human sequence in the sense that is needed for a darwinian explanation. It just means that it is a chronological intermediate. I will try to be more clear. What your theory need is the presence of functional sequence intermediates which are naturally selectable, and gradually build the final functional sequence. In the case of myoglobin, the differences are best explained as neutral variation, as any evolutionist will say. And may be some local optimization in individual species. But the point is: myoglobin is already there in fishes, functional and optimized. Then it changes as much as it can change in time, because of neutral variation, while keeping its structure and function. This concept is not mine: it is what is usually called "the big bang theory of protein evolution". A neo darwinian path is something completely different. It is something like the following: A. a sequence alredy functional, with its structure and function in species a. A1, A2, A3, B1, B2, B3, B4, B5, .... B Where B is a different sequence, with a different structure and function, which in some way evolves gradually form A (or from some non coding sequence, there is really no difference), and where each intermediate has some growing function, maybe in the beginning unrelated to B, then growing levels of the B function, until the B sequence, optimized, is reached. Now, as you can see, B2, just to say one, is a £step" to B. It has the same function, but at lower levels, However, the function is greater than in B1, and that simple fact must be enough to expand B2 to a relevant part of the original population, otherwise there is no probabilistic gain. So, B2 must have a definite reproductive advantage on B1, and B3 must have a definite reproductive advantage on B2, and so on. IOWs, each intermediate must expand, to be of some help. Now, what we see in the proteome, surprisingly, is only B. Then, once B appears, it may change, retaining its structure and function, like myoglobin, because of neutral variation. Or it may change less, because its functional contraints are greater, like the alpha and beta chains of ATP synthase, which have remained remarkably stable in billions of years. You will say that we can't see B1, B2, B3 and so on because they "have been eaten". IOWs, each of them has been eliminated by the expansion on the following step. But that is simply not credible. That would mean to assume absolutely perfect expansion at each step, which is something absolutely unrealistic. The simple fact is that, if B! is expanded, and then B2 expands on B1, relevant traces of B1 will remain in the proteome. And that is true of each functional, expanding step. For each new proteins which is supposed to evolve by positive NS. Even if extinction can erase part of that testimony, a lot of it must be detectable, for the theory to be credible. Instead, what we observe in the proteome is a series of chronological intermediates which are not sequence intermediate which can explain the birth of a functional protein, but simply neutral variations, or local adaptations, of an already existing, perfectly functional sequence. Or, like in my example in the OP, new functional sequences which just appear, and then meet some limited variation, probably because of neutral variation again, or of slightly different regulatory functions. So, I maintain that we have no evidence at the molecular level of the mechanism supposed to drive functional evolution of proteins: RV + positive NS. We have no evidence in the proteome, and no evidence in the lab. And remember, we have thousands of sequence unrelated, structure unrelated protein superfamilies, arising at different evolutionary times. And, certainly, a lot of similar functional sequences which are not even categorized as "domains", as I have tried to show with my example. All of them are waiting to be explained. They are a living challenge to human dullness, and to the dogmatism of neo darwinian thought. gpuccio
Zachriel: In the sense of being a correspondence, yes. Another Zachrielism. Yes, Zachriel, if there were no correspondence between the two alphabets there would be no code. Don't you have anything better to do with our time? Mung
gpuccio: Phylogenetic trees of proteins are evidence of common descent at the molecular level, as I have always debated. And when sequencing a new organism, there is a general congruence between the morphological and molecular trees, so if an organism is intermediate morphologically, it is probably intermediate molecularly. gpuccio: The simple fact that some dicontinuities can be reasonably expected does not mean, in any way, that the actual, dramatic pattern of discontinuities that we observe is what should be expected. As most organisms that have ever existed have gone extinct, and as we have evidence of fossil intermediates, and evidence of congruence between the morphological and molecular trees, it's clear that if we could sequence the fossils, they would fit the standard tree. Indeed, some fossil proteins have been sequenced, and they support the phylogenetic tree. Consequently, the fossil intermediate between reptiles and mammals implies a molecular intermediate. gpuccio: The claim is that a conscious, intelligent, purposeful being is necessary to generate complex functional information. That's the claim. The entailments are the who, what, when, where, why, and how. gpuccio: That claim is not scientifically sterile, and has a lot of entailments, first of all that we will never demonstrate that complex functional information can be generated without the intervention of a conscious designer. As we have evidence that life evolved, then such a demonstration is refuted. gpuccio: Moreover, that claim is a strong motivation to inquire about how conscious designers can generate complex functional information, and natural systems cannot. That's a lovely thought, but, thus far, scientifically sterile. gpuccio: For example, for the “blue sequence” of my example, I have delineated a reasonable window time of about 100 million years for the design process. That comes from common descent, not design. But we do have a window of time, at least. So, the origin of tetrapods is sometime in the Devonian, and the origin of modern humans in the last hundred thousand years or so. gpuccio: how does our consciousness interact with our body and brain, and generate and control those signals in the nerves that activate the muscles and translate into the physical design? IOWs. how are the conscious representations outputted to the brain and body, in the beginning, through a conscious, cognitive, purposeful act of will? There doesn't seem to be any process in human design that doesn't harness energy to move stuff around at least at some point during the process. Pure thought doesn't seem to manufacture anything. gpuccio: I could simply ask you what evidence do you have to support your conjecture that consciousness is generated by the activity of physical structures (if it is your conjecture) Hypotheses non fingo, but we're concerned with manufacture. Design, in the sense of actually making stuff, entails manufacture. gpuccio: So, I could simply say that the evidence is that no configuration of software has ever generated consciousness, or ever will (entailment) "Humans will never fly" is not a properly constructed scientific hypothesis. gpuccio: a) New genes arise rather suddenly in natural history. Some undoubtedly do. So? Gee whiz, even random sequences can sometimes form active enzymes. Zachriel
Zachriel: I suppose we are at a point where we understand quite well each other's position, at least about the points discussed here. So, I will just give a few more suggestions about my personal view of things, answering some of your comments. I think we agree that the neo darwinian algorithm is not a laws, but a process which, as you correctly say, is based on the "interaction of physical laws and contingency". The point, obviously, remains of establishing if it can have any explanatory power for biological complex functional information. We have clearly different ideas about that, and we have probably clarified well enough why. Phylogenetic trees of proteins are evidence of common descent at the molecular level, as I have always debated. You have no need to emphasize that to me, of all people. They are not, certainly, evidence of the validity of the proposed mechanism of generation of information. "The question then is whether the gap is due to an actual discontinuity, or an observational artifact." I think we agree on that. And again, we have different ideas. The simple fact that some dicontinuities can be reasonably expected does not mean, in any way, that the actual, dramatic pattern of discontinuities that we observe is what should be expected. It is not, absolutely. The claim is that a conscious, intelligent, purposeful being is necessary to generate complex functional information. That claim is not scientifically sterile, and has a lot of entailments, first of all that we will never demonstrate that complex functional information can be generated without the intervention of a conscious designer. Moreover, that claim is a strong motivation to inquire about how conscious designers can generate complex functional information, and natural systems cannot. IOWs, it is a strong scientific motivation to inquire about the nature of consciousness and of its abilities, a very important matter which is at present underemphasized because of the and influence of bad scientific theories like neo darwinism and strong AI, true science stoppers in all senses. "That’s very nice, but you forgot to answer the question “how” or “when”. No. For example, for the "blue sequence" of my example, I have delineated a reasonable window time of about 100 million years for the design process. That's an example of how the procedure can be used to answer the question "when". About the how, I have discussed it in the following paragraphs (see also later in this post). "Through signals in the nerves that activate muscles." Obviously, that's the final path. But you are too intelligent not to understand what my question was. I will formulate it better for you, anyway: OK, we design through our physical body, but the interesting question is: how does our consciousness interact with our body and brain, and generate and control those signals in the nerves that activate the muscles and translate into the physical design? IOWs. how are the conscious representations outputted to the brain and body, in the beginning, through a conscious, cognitive, purposeful act of will? "That’s also very nice. What evidence do you have to support your conjecture?" The theory of a quantum interaction between consciousness/mind and the brain is not mine, there is a vast literature about it. I could simply ask you what evidence do you have to support your conjecture that consciousness is generated by the activity of physical structures (if it is your conjecture), but I am sure that you understand well that the problem of explaining consciousness or simply trying to understand its relationship with matter is too vast to be trivialized in a question like: "What evidence do you have to support your conjecture?" We are speaking of one of the basic problems in human thought of all times. We have discussed it many times, and we will discuss it again, certainly. Here, like in the problem of functional information, the evidence is in what we observe, both objectively and subjectively, and in the nature of those facts and of the possible intellectual explanations which can be given. So, I could simply say that the evidence is that no configuration of software has ever generated consciousness, or ever will (entailment), and you will answer that you can still hope or desire that sometime like that will happen, or that the cases where stones have become conscious and have written poems have gone extinct (just joking!). This is essentially a clash of conceptions about science and epistemology. You keep yours, and I will keep mine. Finally, you could at least admit that my proposals about the "how", for example guided mutation, or intelligent selection, or guided transposon activity, do have entailments, and that future data can certainly help clarify or falsify those scenarios. I will just give you an example. Let's assume that, in 30 years, a lot of new data have been gathered about genomes, proteomes, fossils, and whatever you can imagine or not imagine. Let's say that the overwhelming thread in those data is that: a) New genes arise rather suddenly in natural history. b) They are preceded by more gradual modifications at the level of non coding DNA, due mainly to high transposon activity. c) Those non coding "precursors" have never been transcribed or translated into proteins before the appearance of the new gene. d) The appearance of the new gene in a specific species is obtained by the sudden acquisition of one or two mutations which transform the non coding sequence into an ORF. e) The new gene was already optimized in its original form, and the following modification are well explained by neutral variations which do not change the function, or by specific adaptations which optimize the original function for new contexts. OK, this is only an imaginary scenario, but you certainly know that some observations already exist which are compatible with it. Moreover, it is a possible scenario, which can certainly be tested by acquiring new data, absolutely in the range of what molecular biology can find. Now, my question is: if that scenario were true and strongly supported by facts, 30 years from now, what would it imply for the theory of RV + NS as an explanation of the formation of genes? Would it make the design explanation much stronger? Are these entailments, or not? gpuccio
gpuccio: Natural selection is not a law, rather a process which includes some components of necessity. So is snowflake formation, yet this complex process is due to the interaction of physical laws and contingency. gpuccio: And you really have no evidence that such a process can link a specific sequence of nucleotides to a specific functional sequence of AAs through an arbitrary symbolic code. Any example of molecular evolution under selection would do. gpuccio: In all scientific reasonings, corroboration can only come from observed facts and good reasoning. The two are linked. Scientific confirmation comes from empirical observations of entailments. gpuccio: At the molecular level, I would say that’s more or less the case. Then explain why proteins form phylogenetic trees. gpuccio: To observe objective discontinuities of information which need to be explained is sound scientific reasoning. Discontinuity = gap. The question then is whether the gap is due to an actual discontinuity, or an observational artifact. As we know extinction is rampant in biological history, discontinuities are expected. gpuccio: look at my post #381. gpuccio: That’s why the neo darwinist hypothesis is not based on laws, but on hypothetical processes incorporating a random component (RV) and a component which in part operates by necessity (NS). But again, even that hypothesis is not a law. Both those processes, and their interaction, are observable and due to physical interactions (laws). gpuccio: a) At present, the only scientific conclusion we can offer from data in the necessity of some conscious intelligent purposeful being or beings to explain biological design. So there are no entailments. The claim is scientifically sterile, which undermines the claim. gpuccio: b) A much more treatable problem, as far as science is implied, is the problem of implementation. How is the functional information inputted into biological objects? While this is certainly a vast question, some aspects can be answered by facts. For example, we can ask when the information input happened. The facts currently available (genome sequences, proteome sequences, fossils, and so on) can certainly help. That's very nice, but you forgot to answer the question "how" or "when". gpuccio: We are designers, and we can observe ourselves as we design. OK, we design through our physical body, but the interesting question is: how does our consciousness interact with our body and brain? Through signals in the nerves that activate muscles. gpuccio: A quantum interface is the best way ot model design: it allows to change reality without violating apparently the laws of probability in quantum systems, but realizing a specific order through them. That's also very nice. What evidence do you have to support your conjecture? gpuccio: Guided mutation could be a way. IOWs, mutations which are usually random could be occasionally guided, so that a specific result is obtained. Intelligent selection, exactly as in our protein engineering, is another possibility. Finally, I have defended many times here a possible role of the transposon system, a role which is already documented in many cases of origins of new genes. For many reasons, transposons could be perfect tools of biological design. Again, what evidence do you have to support the conjectures? Zachriel
Zachriel: "Now to corroborate the hypothesis you need to deduce specific empirical observations concerning the who,what, when, where, why, and how." For a start, look at my post #381. gpuccio
Zachriel: "The original post made such an argument." This is a gross verbal trick. To observe objective discontinuities of information which need to be explained is sound scientific reasoning. An argument of the gaps is a completely different thing. You cannot argue that any observed discontinuity should be interpreted merely as a gap in scientific knowledge. That is foolish, and a serious cognitive bias. Discontinuities mean a lot, if they are true discontinuities. If you cannot even try to distinguish between what is reasonably observed or observable and what you merely hope or desire could be observed to support your theory, then you cannot do serious science. gpuccio
Zachriel: Natural selection is not a law, rather a process which includes some components of necessity. And you really have no evidence that such a process can link a specific sequence of nucleotides to a specific functional sequence of AAs through an arbitrary symbolic code. "That’s like saying a snowflake isn’t a law. No, a snowflake is not a law, but it is due to the complex interplay of physical laws." Which is exactly what I said. A process, not a law. "And what is the corroboration, the independent lines of evidence that support the proposed design history of the genetic code?" In all scientific reasonings, corroboration can only come from observed facts and good reasoning. ID is no exception. Neither is neo darwinism. "You’re right! No intermediates have been discovered since Darwin." At the molecular level, I would say that's more or less the case. gpuccio
gpuccio: Design is all about “configurable switches”, to use an expression dear to Abel. And configurable switch is not a concept of physics or chemistry. It is a logical concept. PATTEE, H.H. (1974b) Discrete and Continuous Processes in Computers and Brains. In M. Conrad, W. G?ttinger & M. DalCin (eds.) The Physics and Mathematics of the Nervous System, New York: Springer, pp.128-148. Life depends on semiotic controls. - H.H. Pattee Only Symbol-Matter systems evolve. - H.H. Pattee Mung
Zachriel:
Can you point to some entailments of the existence of a nebulous “intelligent being”?
The design is such an entailment.
That means work was done.
The code is evidence for work Virgil Cain
EugeneS: Who : an intelligent being. Can you point to some entailments of the existence of a nebulous "intelligent being"? EugeneS: How: by instantiating symbolic control into physicality, by organizing the designed system and appropriately implementing the design. That means work was done. That implies time, space, materials, etc. Where is the evidence? Zachriel
Zachriel, Ok. Who : an intelligent being. How: by instantiating symbolic control into physicality, by organizing the designed system and appropriately implementing the design. Cf. human technology. EugeneS
Zachriel:
Again, none of the species that lived in the Permian are alive today, yet the Permian had a complex ecosystem including mollusks, ginkgos, roachids, ferns, and cynodonts.
And your position cannot account for any of them. Nice own goal Virgil Cain
The only known cause for codes is via intelligent agencies. Add to that the fact that no one even knows how to test the claim that mother nature can produce a code and we get to the design inference for the genetic code. Science 101 Virgil Cain
Eric Anderson: So it is perfectly reasonable to ask again, what is the basis for this claim that the vast majority of the species that have ever lived have gone extinct? Again, none of the species that lived in the Permian are alive today, yet the Permian had a complex ecosystem including mollusks, ginkgos, roachids, ferns, and cynodonts. Each age of the Earth is characterized by a succession of different species most of which only lasted a few million years. Zachriel
EugeneS: The ID argument is not that of the gaps. It is based on the observation that all symbolically controlled systems we know of (except from living systems, which are the case in point) are of intelligent origin. That might do for a speculative hypothesis. Now to corroborate the hypothesis you need to deduce specific empirical observations concerning the who,what, when, where, why, and how. EugeneS: Where are the gaps you are talking about? The original post made such an argument. Zachriel
Alicia:
EA, now you want a demonstration of “the origin of significant amounts of biological information,” well you can continue moving the goalposts all you want, I don’t care.
This is the issue on the table. If you don't care about it, then that helps explain why you are pointing to a paper that doesn't address the issue. Furthermore, no-one is even demanding a live demonstration. Just something that is relevant and has a reasonable, non-laughable, chance of getting us there. The paper you cited absolutely does not get us anywhere down that path. Play around with binding sites all you want; it doesn't help explain the origin of significant amounts of biological information. You tried a literature bluff. We called you out on it. You can either be intellectually honest and admit it, or at least move on. Look, let me help you out here. You don't need loss of binding site specificity (loss of information, ironically) to help your theory. Your theory is so vague and general and simplistic that it doesn't need another vague, general and simplistic example to help it. Just say what your theory really is and be done with it: mutations occurred, accidents happened, things changed, and here we are! The Great Evolutionary Explanation Stuff Happens. And the reason we don't see it happening today? Well, it takes too long. And the reason we don't see it in the fossil record? Well, the fossil record stinks and isn't a very good data set.
Again, you haven’t read the paper, you probably shouldn’t try to speak with such authority about what the paper says.
My assessment is based on the abstract, as well as your description of what the paper says. Are you now claiming that you didn't describe the paper accurately and that the paper says something other than what the abstract lists? If not, then drop the sanctimonious nonsense.
There’s a little over a million species known today, about 8 million predicted to exist currently, and the fossil record has about 200,000 species in it.
Great. So by the actual empirical, observed fossil record we can say that at least 2.5% of the species that ever lived have gone extinct. 200,000 of them. Where are the other 799,800,000 species in the fossil record? The Darwinian explanation: "Aw, the fossil record stinks. You can't take it seriously." Perhaps. Hypothetically, it might be true that 99% of all species that have ever lived have gone extinct. But it is definitely not a fact. Definitely not a fact that is beyond dispute. Not even close. Not even in the ballpark. So it is perfectly reasonable to ask again, what is the basis for this claim that the vast majority of the species that have ever lived have gone extinct? Simply because I dared raise the question, dared question a doctrine of Darwinian orthodoxy, you keep making snide remarks about me not having been through the third grade. Unfortunately, you seem to be stuck there. I get it. Sometimes it is intellectually uncomfortable to realize that something you thought all these years was indisputable fact from the third grade turns out to be based, not on empirical evidence, but on assumptions, hypotheses, suppositions, conjecture. Eric Anderson
Zachriel:
One hypothesis is that the genetic code evolved from simpler relationships, such as a doublet code, and that from even simpler relationships.
It is an untestable hypothesis. Virgil Cain
Zachriel, You do not know what a testable scientific claim is then. The ID argument is not that of the gaps. It is based on the observation that all symbolically controlled systems we know of (except from living systems, which are the case in point) are of intelligent origin. Animal or human communication is based on code. Some complex human artifacts are based on code. At the same time, there are no observations of code based systems arising as a result of exclusively the laws of nature. All this leads to the inference about the intelligent origin of the biological systems themselves. Where are the gaps you are talking about? It is a purely scientific inference. Inference to design is the only correct inference one can get in this case given the data. I am still waiting to hear from you about actual empirical evidence in favor of naturalistic origins of code-based systems. Don't bother wasting the bandwidth on account of scientifically sterile naturalistic OOL hypotheses. EugeneS
Me_Think @374:
The nucleotide sequence is not just a sequence. It is pairing of 3D structure of chemicals.
What chemical or physical law determines the sequence of nucleotides in DNA that you refer to? Be very specific. Do not rely on vague generalizations and simplistic claims about chemicals reacting with each other or physical interactions. What determines the sequence of nucleotides in DNA? Eric Anderson
gpuccio: There is no necessity which can link a specific sequence of nucleotides to a specific functional sequence of AAs through an arbitrary symbolic code. Natural selection. gpuccio: But again, even that hypothesis is not a law. That's like saying a snowflake isn't a law. No, a snowflake is not a law, but it is due to the complex interplay of physical laws. gpuccio: I believe that all science is simply a hypothesis in need of corroboration. And what is the corroboration, the independent lines of evidence that support the proposed design history of the genetic code? gpuccio: I must have missed all those gaps being filled. You're right! No intermediates have been discovered since Darwin. Zachriel
Zachriel: "Well, it might constitute a hypothesis in need of corroboration." It's fine with me. I believe that all science is simply a hypothesis in need of corroboration. :) "In any case, when a gap is filled, ID just points to another gap." I must have missed all those gaps being filled. :) And I am rather loyal to my gaps. ATP synthase remains one of my favorite issues, after many years. gpuccio
Me_Think: "How would you know the origin has nothing to do with chemical or physical laws?" Because laws cannot generate functional sequences any more than they can generate poems. Laws work by necessity. There is no necessity which can link a specific sequence of nucleotides to a specific functional sequence of AAs through an arbitrary symbolic code. That should be obvious even to you. That's why the neo darwinist hypothesis is not based on laws, but on hypothetical processes incorporating a random component (RV) and a component which in part operates by necessity (NS). But again, even that hypothesis is not a law. "You are a doctor." Yes. "How do you even believe some designer front loaded information about the sequence using some unknown mechanism?" Because it's the best scientific explanation for what we observe in biological beings. "(I mean I get the CSI and UPB calculations for ‘detecting design’, but how could someone load the sequence at all ?)" OK. Design detection is one thing. That is what we usually discuss here. The reasons why biological objects suppor t a design inference. Obviously, if we assume design for biological objects, at least two important questions remain: a) Who is the designer or designers? b) How was the functional information implemented? I have debated both aspects here many times. This is what I think: a) At present, the only scientific conclusion we can offer from data is the necessity of some conscious intelligent purposeful being or beings to explain biological design. Why? Because design is by definition the work of conscious, intelligent, purposeful beings. I am afraid that at present scientific inference is limited about the identity of the designer, so everyone can try to give his answers on the plane of philosophy, or religion, or whatever. There is the problem: is the designer of physical being? (beware, I am not saying "natural"). My idea is that the answer is no, but obviously there is at least one possible scenario compatible with designers having a physical body, in particular biological design by aliens. It's not my scenario, but it is a possibility. Another possibility is the existence of conscious beings who do not need a physical body (as we understand it) to exist and act. b) A much more treatable problem, as far as science is implied, is the problem of implementation. How is the functional information inputted into biological objects? While this is certainly a vast question, some aspects can be answered by facts. For example, we can ask when the information input happened. The facts currently available (genome sequences, proteome sequences, fossils, and so on) can certainly help. Other facts will be accumulated in the near future. My reasoning in the OP is a tentative example of how we can identify information inputs, and in some way restrict them to some chronological window. Observation of facts and good scientific reasoning should be able, in time, to answer another fundamental question about implementation: is it gradual, or rather sudden? Another important point is: if the designer has no physical body as we understand it, how can he (she, they) interact with matter, in particular biological matter? This seems a question beyond the boundaries of science, but it is not necessarily so. I have suggested many times that we have an observable model from which we can start: ourselves. We are designers, and we can observe ourselves as we design. OK, we design through our physical body, but the interesting question is: how does our consciousness interact with our body and brain? IOWs with matter? I am not giving here any specific definition of consciousness: only the empirical fact that we can observe consciousness in ourselves, and that design starts in consciousness, under the form of conscious representations and purposes. I have suggested many times that the best way to explain the interactions between our consciousness and our brain and body is through some quantum interface in the brain, as suggested by other eminent thinkers, like Eccles, Beck, Penrose and others. A quantum interface is the best way ot model design: it allows to change reality without violating apparently the laws of probability in quantum systems, but realizing a specific order through them. Design is all about "configurable switches", to use an expression dear to Abel. Quantum events are probably the "configurable switches" which our consciousness can operate upon in our brain. So, if that kind of interface can happen in our brains, it can potentially happen in biological matter. Some consciousness can interact with biological matter in the same way that our consciousness interacts with our synapses. How? That is interesting. Guided mutation could be a way. IOWs, mutations which are usually random could be occasionally guided, so that a specific result is obtained. Intelligent selection, exactly as in our protein engineering, is another possibility. Finally, I have defended many times here a possible role of the transposon system, a role which is already documented in many cases of origins of new genes. For many reasons, transposons could be perfect tools of biological design. gpuccio
EugeneS: Genetic and other codes in an organism are codes in the true sense. In the sense of being a correspondence, yes. One hypothesis is that the genetic code evolved from simpler relationships, such as a doublet code, and that from even simpler relationships. The origin of the genetic code is very ancient, so it will be difficult to untangle. Simply saying "design" is not a testable scientific claim. Zachriel
gpuccio: The argument to design is rather that we have no known example of symbolic systems that are not designed. Well, it might constitute a hypothesis in need of corroboration. gpuccio: The genetic code, obviously, or any other symbolic system in biology, is the issue we are debating. Thought you were arguing about gaps in protein descent. gpuccio: I am not sure what it is. That it evolved from simpler relationships. The proposed hypotheses are speculative, but keep in mind that biologists consider that evolution is otherwise strongly supported, and these hypotheses have empirical implications which can be independently verified. In any case, when a gap is filled, ID just points to another gap. The more ancient the transition, the more obscure will be its history. Zachriel
Lots of new interesting posts since I was here last. MeThink and Zachriel, Code denialism will take you nowhere. It's been debunked. Genetic and other codes in an organism are codes in the true sense. It is a commonplace now. In contrast, chemical laws do not constitute code because they exclude arbitrariness. Law is necessity without any options. Biological form is options themselves. In this sense, biology is like an art. A sculpture while being subject to the laws of nature cannot be explained using only the laws of nature. The same mass of gypsum can be arranged into a different sculpture without violating the laws of nature. EugeneS
GP @ 376
However, as I am in a good mood at this point of time, I will just remind you that ID theory has nothing to so with supernatural, and that it is about explaining what we observe and understanding it by facts, and by good scientific reasoning.
But its origin as a sequence with a functional meaning has nothing to do with chemical or physical laws. If you cannot understand that, you really have a problem
How would you know the origin has nothing to do with chemical or physical laws? You are a doctor. How do you even believe some designer front loaded information about the sequence using some unknown mechanism? (I mean I get the CSI and UPB calculations for 'detecting design', but how could someone load the sequence at all ?)
??? Inebriated again?
:-) Nope. 2-amino-8-(2-thienyl)purine and pyridine-2-one is unnatural base pair developed by Ichiro Hirao’s group in Japan.About the DNA base pair ATCG - TATC , you know C-T can't pair. So if you find any of those, you know it is designed. Me_Think
Me_Think: As you are back with arguments, here are a few answers for you: 1)
I am sure you know that elements other than H and He could not have formed under normal conditions on Earth. If we hadn’t discovered the fusion process in stars, you would think all elements other than H and He would have to be put together by Intelligent being by some kind of instruction. It would be even more puzzling to figure out how elements with protons above 26 (Fe) would form if we hadn’t figured out about supernova. That process too would have been considered supernatural.
The "argument" that humans consider supernatural what they still don't understand and that science gradually explains what was considered supernatural is so trivial and foolish, as related to ID theory, that it would not even deserve a comment. However, as I am in a good mood at this point of time, I will just remind you that ID theory has nothing to so with supernatural, and that it is about explaining what we observe and understanding it by facts, and by good scientific reasoning. Which is much more than what can be said of neo darwinism. 2)
The nucleotide sequence is not just a sequence. It is pairing of 3D structure of chemicals. You are seeing a refinement of billion years of bio-chemical and biomechanical process. What you are seeing is – as Zac elegantly puts it – a correspondence.
Utter nonsense! The nucleotide sequence is a sequence which stores information. It has nothing to do with chemical laws. It is duplicated by chemical laws in DNA duplication. It is translated by the translation system. But its origin as a sequence with a functional meaning has nothing to do with chemical or physical laws. If you cannot understand that, you really have a problem. Let's go to the correspondence, the mapping of codons to AAs, IOWs the genetic code. That, too, has nothing to do with chemical or physical laws. As discussed many times, the mapping of the genetic code is accomplished by the 20 aminoacyl t-RNA synthetases (aaRS), 20 big and complex functional proteins which recognize, indipendently, the tRNA with the correct codon and the correct aminoacid which has to be linked to it. The mapping takes place because there is a translation system with its specific proteins and structures (including, obviously, also the ribosome). Therefore, it derives from a configuration of the system, and not from natural laws of any kind. IOWs, it is a perfect example of symbolic system. 3)
You can claim intelligence if there is anomaly in the natural bonding or, say, if you find an unnatural base pair of 2-amino-8-(2-thienyl)purine and pyridine-2-one or if you find a DNA sequence with base pair
??? Inebriated again? 4)
A lot of things in Nature do look intelligently designed but are not.
Sure. That's why we need a design detection theory, with quantitative and qualitative procedures to detect true design, like those based on functional complexity or symbolic properties. 5)
As you probably know, even the trajectory of a ball which is thrown can be construed as being directed by intelligence, because the path followed by the ball minimises the Action (The total of Kinectic energy-Potential energy at every point of the path or the Lagrangian) . Would you say ball calculated the Integral of Lagrangian over dt [Integral]L [Differential]t and decided to follow the path of Least Action according to Principle of least action ?
Of course, the trajectory of a ball follows a definite law. That laws of nature could be designed is all another issue. Whatever they are, laws are laws, they work always in the same way and can be used to explain observed facts according to necessity principles. Complex functional information and symbolic systems cannot be explained by laws. Even the suggested "explanations" of neo darwinism are not laws, but rather hypothetical processes (which, however, cannot even begin to explain what they try to explain). So, your example of the trajectory of a ball is completely out of order. Again, ID theory is not about the supernatural or about what we still don't know, but rather about what cannot be explained in certain ways, because we do know that it cannot be explained in those ways. It is about fetaures which are empirically linked to conscious design, and only to conscious design. Are you really so unfamiliar with what ID says? gpuccio
mike1962: Thank you! Yes, the discussion has been interesting. I am very happy of that. gpuccio
Eric Anderson @ 356
“Of course natural laws exist and they operate throughout their range of influence. But natural laws do not explain the existence of information-rich symbolic systems like what we see in a living organism. There lots of materials available for study, but if you are sincerely interested in this topic, you might take some time to think through the difference between, say, a stretch of DNA containing a nucleotide sequence for a protein, and a salt crystal.”
The nucleotide sequence is not just a sequence. It is pairing of 3D structure of chemicals. You are seeing a refinement of billion years of bio-chemical and biomechanical process. What you are seeing is - as Zac elegantly puts it - a correspondence. You can claim intelligence if there is anomaly in the natural bonding or, say, if you find an unnatural base pair of 2-amino-8-(2-thienyl)purine and pyridine-2-one or if you find a DNA sequence with base pair ATCG TATC A lot of things in Nature do look intelligently designed but are not. As you probably know, even the trajectory of a ball which is thrown can be construed as being directed by intelligence, because the path followed by the ball minimises the Action (The total of Kinectic energy-Potential energy at every point of the path or the Lagrangian) . Would you say ball calculated the Integral of Lagrangian over dt [Integral]L [Differential]t and decided to follow the path of Least Action according to Principle of least action ? Me_Think
GP @ 353
“Just the forces wouldn’t create those. Every atom has to be ‘instructed’ to align in certain ways, and have specific number of protons and electrons and energy levels to form elements.” Instructed by whom or by what? Please, clarify.
I am sure you know that elements other than H and He could not have formed under normal conditions on Earth. If we hadn't discovered the fusion process in stars, you would think all elements other than H and He would have to be put together by Intelligent being by some kind of instruction. It would be even more puzzling to figure out how elements with protons above 26 (Fe) would form if we hadn't figured out about supernova. That process too would have been considered supernatural. Me_Think
gpuccio, Again, thank you for your time and patience. This has turned out to be a very interesting thread. mike1962
Me_Think: "From my inebriated condition at that point of time " That's a good scientific explanation, for once! :) "Ha, OK." Ha, OK. gpuccio
GP @ 351
Where did you get those strange statements?
From my inebriated condition at that point of time :-) GP @ 353
I really don’t understand what you say.
Ha, OK. Me_Think
1. we have sequenced only a small fraction of the organisms alive today True, but so what. Organisms alive today are not ancestors of organisms alive today. 2. all the organisms alive today are only a small fraction of the organisms to have ever lived. True, but so what. Sequence homology isn't limited to scenarios that span different taxa. If there was an instance of gene duplication and then divergence this would all take place within the same lineage. Mung
...but they do show how small changes in their protein interaction system can model the evolutionary steps toward the wild-type system we see today. map. territory. By the way, no one is denying the existence of promiscuous proteins. I hope that's not too far beyond basic biology for you. Mung
Alicia: "It’s not massive changes in protein structure and function (which would be virtually impossible to demonstrate in a single study), but they do show how small changes in their protein interaction system can model the evolutionary steps toward the wild-type system we see today." IOWs, it's not what we were discussing, except in your imagination. I will answer some of your comments to EA, too, just for the sake of discussion. "EA, now you want a demonstration of “the origin of significant amounts of biological information,” well you can continue moving the goalposts all you want, I don’t care." Moving the goalposts? Are you kidding? This discussion is and always has been about “the origin of significant amounts of biological information”. Can you read my OP? Can you understand what "information jump" means? "The fact is, the paper demonstrates possible evolutionary paths to the wild-type protein. This is exactly what pucci is looking for in the sequence databases (and claims never existed because he can’t find them). Unfortunately he has overlooked the fact that 1. we have sequenced only a small fraction of the organisms alive today, and 2. all the organisms alive today are only a small fraction of the organisms to have ever lived." Repeating the same wrong argument does not make it true. Your argument remains unsupported by facts. Wishful thinking. A bad and trivial fairy tale. "Again, you haven’t read the paper, you probably shouldn’t try to speak with such authority about what the paper says." As for me, I will go on speaking "with authority", the authority of my reason and conviction, about what the abstract says. You can report details of the paper and discuss them, if you like. gpuccio
Virgil Cain: "As everyone knows evolutionism cannot explain the existence of ATP synthase." Absolutely true. ATP synthase is and will remain one of the best examples of falsification of neo darwinism. But it is equally true that ATP does not "create" energy, as Me_Think seems to think (post #348). ATP is a high energy molecule which can be reused when energy is necessary. The high energy in its third phosphate comes from the energy in a proton gradient, which in turn is established from other energy sources, like the digestion of food which comes in the ultimate sense from photosynthesis or chemosynthesis. The conversion of energy from the proton gradient to the phosphate in ATP is accomplished by our excellent friend, ATP synthase. Therefore, ATP does not "create" energy, in any sense. Me_Think, where are you? gpuccio
Pucci, "Not only you did not offer intermediates which build a sequence path to a new complex functional structure.." That's exactly what the Aarke paper does. It's not massive changes in protein structure and function (which would be virtually impossible to demonstrate in a single study), but they do show how small changes in their protein interaction system can model the evolutionary steps toward the wild-type system we see today. EA, now you want a demonstration of "the origin of significant amounts of biological information," well you can continue moving the goalposts all you want, I don't care. The fact is, the paper demonstrates possible evolutionary paths to the wild-type protein. This is exactly what pucci is looking for in the sequence databases (and claims never existed because he can't find them). Unfortunately he has overlooked the fact that 1. we have sequenced only a small fraction of the organisms alive today, and 2. all the organisms alive today are only a small fraction of the organisms to have ever lived. Again, you haven't read the paper, you probably shouldn't try to speak with such authority about what the paper says. You can be skeptical all you want, but the fact is that you have no idea what you are talking about, so neither your opinion or how skeptical you are matters to anyone actually in the biological sciences. There's a little over a million species known today, about 8 million predicted to exist currently, and the fossil record has about 200,000 species in it. You really didn't make it through the third grade, did you? Alicia Cartelli
Zachriel: "There is a correspondence between codons and amino acids, if that is what you mean." Yes. And: "The concept apparently concerns the arbitrariness of the relationships." Yes, again. I know you understand things. A systematic correspondence which is arbitrary, in the sense that it is not linked to natural laws, is symbolic. "However, evolution provides an alternative hypothesis for the origin of the genetic code, so just calling it a symbol doesn’t constitute an argument to design." Yes, again. The argument to design is rather that we have no known example of symbolic systems that are not designed. The genetic code, obviously, or any other symbolic system in biology, is the issue we are debating. And ehm... yes, in a sense, "evolution provides an alternative hypothesis for the origin of the genetic code". Maybe. I am not sure what it is. I cannot even criticize it, because I have never seen a distantly reasonable scenario clearly explained. Maybe I am missing something. "In any case, that doesn’t directly impact the example you provided." Yes, again. My argument is based on the quantitative evaluation of functional complexity, which is an indicator of design because in all known cases it is found only in designed things. Empirical argument. UB's argument is rather based on the qualitative assessment of symbolic systems, with all their necessary properties, which are an indicator of design because in all known cases they are found only in designed things. Empirical argument. Convergent evolution of valid arguments? However, you are right: my argument in the OP is not based on symbolic systems, but the issue came into the discussion at some point, so I expressed my thoughts about it too. So, that's why you remain one of my favorite interlocutors: you understand things. gpuccio
Zachriel:
There is a correspondence between codons and amino acids, if that is what you mean.
There is a representation-> mRNA codons represent amino acids. It is a code is the same sense as Morse code.
However, evolution provides an alternative hypothesis for the origin of the genetic code,
Wrong- evolutionism requires an alternative hypothesis for the origin of the genetic code. It has yet to provide one that can be scientifically tested and validated. Virgil Cain
gpuccio: Protein coding genes are symbols: they represent the protein according to a code. There is a correspondence between codons and amino acids, if that is what you mean. gpuccio: For a definition of symbolic relationships, you could well refer to UB’s website. Don't see where he defines symbols. Don't mean to quibble over semantics. The concept apparently concerns the arbitrariness of the relationships. However, evolution provides an alternative hypothesis for the origin of the genetic code, so just calling it a symbol doesn't constitute an argument to design. In any case, that doesn't directly impact the example you provided. Eric Anderson: The “possible” small steps you allege to have happened are nothing more than a hypothetical, Darwinian gloss on the evidence. Actually, biologists have documented many such transitions, so it is reasonable to suppose that other transitions work by similar means. You don't have to drop a feather on the far side of the Moon to be pretty sure it will fall much like a feather on the near side of the Moon. https://www.youtube.com/watch?v=5C5_dOEyAfk Eric Anderson: (1) How many species are estimated to currently live on Earth? and (2) How many species have been identified in the fossil record? Again, none of the species that lived in the Jurassic are alive today, yet the Jurassic had a complex ecosystem including fish, ichthyosaurs, insects, mammals, ferns, and conifers. Each age of the Earth is characterized by a succession of different species most of which only lasted a few million years. Zachriel
Alicia: You keep claiming evidence where none exists. You keep harping on about the paper, but it is a red herring. By your own admission, "they test the nearby sequence space of a protein and how it altered binding to certain proteins. For the last time, what they found was that possible intermediates very closely related to the wild-type protein were capable of binding other proteins while also conserving wild-type function." We already know that evolution can result in loss of information, such as a loss of binding specificity. Interesting work. Interesting result. Makes a nice paper, no doubt. But it certainly does not demonstrate anything about the origin of significant amounts of biological information -- the very question at issue. -----
This is demonstrating some of the possible small steps that each intermediate took through the course of evolution, which is what you asked for in comment #58.
It is demonstrating nothing of the sort. It is demonstrating that with a loss of binding site specificity, there is a potential to "bind other proteins while also conserving wild-type functions," as you put it. It in no way provides an answer to the question at hand. The "possible" small steps you allege to have happened are nothing more than a hypothetical, Darwinian gloss on the evidence. Look, we can all make up stories about "possible" steps that could have occurred. Nothing but wishful thinking. This is a literature bluff in the clearest sense.
Did you not finish the third grade?
Sure. Did you? I'm just skeptical, I guess. I don't have the blind faith to accept all the Darwinist propaganda without some actual evidence. But, hey, don't let me shake your faith. Maybe you need to move beyond whatever propaganda you think you received in third grade that I (thankfully) missed. Hint: If you want to start thinking about this issue seriously, ask yourself the following questions: (1) How many species are estimated to currently live on Earth? and (2) How many species have been identified in the fossil record? This won't get us to an answer, but it will raise some questions and should start some wheels turning if you are willing to approach the question with intellectual honesty. Eric Anderson
Alicia: Eric and I could not read the whole paper, because it is paywalled, but we could read the abstract. Indeed, I have posted the whole abstract here. And it is informational enough to undertsand that it is not pertinent to the discussion here (well, not informationla enough for you, probably). In my comment #58 I gave an outline of how perfectly selectable intermediates could lower the probabilistic barriers. Not only you did not offer intermediates which build a sequence path to a new complex functional structure, but you seem to ignore the aspect of positive selection which requires a real reproductive advantage, so that the new tract will be expanded as much as possible in the original population, and fixed. You have provided absolutely no evidence of such a process. If you want to know my ideas about natural selection, you could give a look to my OP here: https://uncommondesc.wpengine.com/intelligent-design/natural-selection-vs-artificial-selection/ It could give you some inspiration for new irrelevant ramblings. :) gpuccio
MT:
As everyone knows non-living things don’t have ATP to create energy, ...
As everyone knows evolutionism cannot explain the existence of ATP synthase. Virgil Cain
EA, I’m really confused. How can you tell me the paper I cited: 1 - doesn’t “address the issues gpuccio has raised” 2 - doesn’t “give any empirical support to the idea that a protein could evolve through intermediates” When you’ve already admitted to not even being able to read the paper? I couldn’t pick a better quote than this one to demonstrate your total lack of the required knowledge for this conversation though: “We’re still waiting for you to provide evidence for the claim that almost all species that have ever lived have gone extinct” Did you not finish the third grade? Alicia Cartelli
“the paper” refers to the Aakre paper, which you have commented on, but apparently have no idea or understanding of what the paper says (you and EA). This is despite me explaining what the main finding of the paper is and exactly how it translates to our conversation. The david baker lab is a well-known biochem lab involved in protein folding and protein design. I know they have substituted huge amounts of amino acids in certain proteins and functionality was maintained. I’m pretty sure it was around 95% of the protein, using only a subset of the amino acids (alanine, glycine, an acidic and basic, and a hydrophobic amino acid). “the sudden appearance of 600 bits of functional information.” Sure, if you call 100 million years “sudden.” “This has nothing to do with small variations at the level of an active site” The intermediates that you claim don’t exist evolved through small changes to binding sites as evolution tested the nearby sequence space of the protein. This is exactly what the researchers did in the Aakre paper, they test the nearby sequence space of a protein and how it altered binding to certain proteins. For the last time, what they found was that possible intermediates very closely related to the wild-type protein were capable of binding other proteins while also conserving wild-type function. This is demonstrating some of the possible small steps that each intermediate took through the course of evolution, which is what you asked for in comment #58. I have no problem with being quantitative, but when conclusions are based on only half the story, that’s where things go off the rails. Let me sum up what the problem is: Pucci – “in the 100 million years between tunicates and chondricthyes, there is no evidence of protein intermediates demonstrating the evolution of the prickle 1 protein based on sequence data.” Alicia – “that’s because there is no sequence data representing the lineages that branched off within those 100 million years of chordate evolution. There is no sequence to search within.” Pucci – “who cares” Alicia Cartelli
Me_Think @348:
Yes, the relation is defined by natural laws.
In other words, it is not a symbolic system, by definition. Action purely by natural law is anathema to the formation of an information-rich symbolic system. What you are referring to is precisely the opposite of what is needed to explain such a system. ----- Of course natural laws exist and they operate throughout their range of influence. But natural laws do not explain the existence of information-rich symbolic systems like what we see in a living organism. There lots of materials available for study, but if you are sincerely interested in this topic, you might take some time to think through the difference between, say, a stretch of DNA containing a nucleotide sequence for a protein, and a salt crystal. Understanding and appreciating that difference is the first step to understanding this issue and its broader ramifications. Eric Anderson
By the way, Alicia. We're still waiting for you to provide: (a) evidence for the claim that almost all species that have ever lived have gone extinct; and (b) acknowledgement that your multiple statements like this: "So during the same time that some of the chordates were evolving a bony spine, a protein now known to be involved in spinal development also evolved?" are circular. The entire question at issue is the provenance of that biological change. You don't get to avoid the question by cute statements that assume the very thing in question. The latter issue is less related to the evidence and more a matter of logic 101. Eric Anderson
Alicia: The paper you cited not address the issues gpuccio has raised. Nor does it give any empirical support to the idea that a protein could evolve through intermediates into a significantly different protein function. You have a couple of options at this point: A. Be Intellectually Honest. Two possible approaches here: (1) Admit that you didn't quite understand what gpuccio was driving at and that, upon further reflection, the paper you cited doesn't address his issue. You are welcome to add that you nevertheless believe it provides one possible theoretical avenue to larger changes in a protein over time. (2) Admit that you didn't really look at the paper carefully (after your 5 seconds of search), that it doesn't address what gpuccio was driving at, and withdraw your claim that you have provided a literature reference on point. You are welcome to add that you believe there must be a paper on point, but that it will take more time to find something directly addressing his issue. B. Dig in your heels and continue to assert that the paper addresses the key point in issue, even though it clearly does not. Eric Anderson
Me_Think: I really don't understand what you say. "Just the forces wouldn’t create those. Every atom has to be ‘instructed’ to align in certain ways, and have specific number of protons and electrons and energy levels to form elements." Instructed by whom or by what? Please, clarify. gpuccio
gpuccio @350 That's not quote mining. I showed you the relevant parts !
Is it clear now?
No. What do you mean by non-living nature? If you want a system which is non-living and creates symbolic representations, every element, every molecule is an example. Just the forces wouldn't create those. Every atom has to be 'instructed' to align in certain ways, and have specific number of protons and electrons and energy levels to form elements. Me_Think
Me_Think: Where did you get those strange statements? 1) "ATP to create energy" ??? ATP does not create energy. What a strange idea! 2) Energy or bio-chemical forces certainly do not create "arbitrary symbols". If that were true, you could easily generate symbolic systems in the lab, without the help of intelligence: both energy and biochemical forces are certainly present in the lab, so arbitrary symbols should be very easy to be generated. Without the help of intelligence, obviously. gpuccio
Me_Think: Where did you learn to quote-mine? The question was: “Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence.” IOWs, so that even you can understand: Please provide a single empirical case where, in nonliving nature, the four basic types of physical interaction can generate some system which includes some form of symbolic representation and control, without recourse to intelligence. IOWs, some system which originates from the working of natural laws, but where you can see a symbolic connection between parts of the system, so that some parts of the system can control other parts of the system not because of natural laws, but because of the special configuration of the system. IOWs, some system like the genetic code, generated by the working of natural laws. Is it clear now? gpuccio
Mung: You have stated the simple, incontrovertible truth. Very "ad hoc", and extremely wishful! :) gpuccio
gpuccio @ 341
The reason why atoms are not symbols of elements, or elements of molecule, is that the relationship between those categories is defined by natural laws, and not by an arbitrary code of association.
Yes,the relation is defined by natural laws.The question was
...nonliving nature just by means of the four basic types of physical interaction
I presume four Physical interaction means four Natural forces: gravitational, electromagnetic, strong nuclear and weak nuclear. As everyone knows non-living things don't have ATP to create energy, so obviously without those or bio-chemical forces, arbitrary symbols (in the sense of gene sequence) can't be created. Me_Think
Alicia is too nice to be keiths. Mung
My explanation is that the sequence evolved through intermediate forms which have since gone extinct along with the species they were in. And left behind no evidence they ever existed. That's not an explanation, that is ad hoc exercise in wishful thinking. Mung
Just as a clarification for all: Alicia is obviously partial and confused. The information jump of which we have been discussing is, indeed, an information jump. The particular example given in the OP is the sudden appearance of 600 bits of functional information. This has nothing to do with small variations at the level of an active site, which is what apparently Alicia would like to use as an "argument". 600 bits of information means that a lot of AAs are conserved. In the example of the "blue" part of Prickle 1, 350 AAs are conserved between sharks and humans. 350 AAs, not one or two. That's why I have called it an "information jump". Alicia simply tries to ignore the issue, and that is completely consistent with her unfair style of discussion that we all well know. OK, neo darwinists do not like being quantitative, as far as functional information is concerned. But Alicia is bringing the "non quantitative" approach to new heights. gpuccio
Alicia: What paper? If you quote a paper, it is normal courtesy to give a reference to it. I suppose it's not the Aakre paper, about which I have already commented. That's indeed pure literature bluff from you. "David baker lab" is not a reference to a paper, as far as I can say. So, please give the correct reference. gpuccio
EA, see above. Possible intermediates and hypothetical avenues are exactly what we are talking about. And unless you have a time machine, that is the best we can do right now. The paper most certainly does provide examples of protein function through evolutionary intermediates. Obviously not all the intermediates from A to Z, but it does show possible Xs and Ys on the way to Z. If you understood a bit of experimental biology, or just biology in general, you would know how ridiculous it is to ask scientists to explain the evolution of a protein “from A to Z.” “situations like your vague reference to a protein involved in spine development.” Did you not read the original post? Everything we have talked about has stemmed from the supposed absence of intermediates for a protein that plays an important role in spine development. I figured I could be vague when many of the details have already been mentioned. I love that you are confident enough to admit “I unfortunately was unable to see the paper,” while also accusing me of a “literature bluff” with the same paper, all in a single post. The amount of idiocy I see here at UD amazes me sometimes. Alicia Cartelli
“Except maybe facts and good scientific reasoning?” Are we talking about the same thing here? Because your original post has very little in the way of facts and even less “good scientific reasoning.” Your statement was completely ambiguous, you even had a sentence at the end of the paragraph about abolishing function. “you cannot easily build new complex information (a transition from one superfamily to another one, for example) with small changes.” Obviously. A superfamily is so high up within protein structure hierarchy, being able to transition from one to the other with small changes would be completely contradictory. Take a look at the david baker lab. They did the work showing that certain proteins could tolerate substitutions at 95% of positions. Again, that’s 95%. The paper demonstrates the evolution of a wild-type protein through intermediates which not only retain their original binding ability, but also bind to other proteins. They show possible intermediates in the evolution of this protein and that these intermediates are abundant in sequence space. Again, it demonstrates evolutionary protein intermediates. I’m pretty sure the vast majority of this discussion has been about the supposed absence of evolutionary intermediates for the Prickle protein, no? This is what you said in comment #58: “what is needed is the demostration (real demonstration) of intermediates at sequence level which are naturally selectable.” That is exactly what this paper provides. Alicia Cartelli
Zachriel: Protein coding genes are symbols: they represent the protein according to a code. For a definition of symbolic relationships, you could well refer to UB's website. The reason why atoms are not symbols of elements, or elements of molecule, is that the relationship between those categories is defined by natural laws, and not by an arbitrary code of association. That is not true of codons and AAs: the genetic code is a symbolic code. gpuccio
Me_Think: "Sorry I don’t get it. I believe I have answered his question" Well, I don't know if it's painful, but clear certainly it is not. Atoms ->Elements ???? What do you mean? That atoms represent symbolically elements? I understand that it is probably painful for you to write more than a couple of words, but please, have compassion of our limited minds! gpuccio
EugeneS: I said nothing about extinction in this thread apparently. You did say something about fossils showing gradual evolution. While the fossil record is necessarily incomplete, there are some excellent examples of gradual evolution, such as in Peruvian sloths, or even the skulls of hominids. Of course, the overall fossil record shows generally incremental change. Zachriel: The sun evaporates water and moves it uphill; the water then has a higher potential energy. EugeneS: Potential energy of the whole system must be consideted. Energy from the Sun enters a plant's chloroplast and flows downhill from there. When the sun stops shining, the system stops. Energy from the sun moves water in a continuous cycle. When the sun stops shining, the system stops. EugeneS: Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence. The claim at issue concerned potential energy. Are genes symbols? an object that expresses or represents a particular idea or quality? gpuccio: A very good request! The question presumed a queer definition of symbol, and excluded the very thing under discussion. Zachriel
Eric Anderson @ 334
Wow. Just wow. It is painful just to watch that assertion advanced. Go back and read up on the issues.
Sorry I don't get it. I belive I have answered his question Me_Think
UB: It's always a pleasure to hear from you. I must say that I am really happy of the discussion in this thread. In the beginning, I was truly afraid that the OP was too technical to be of interest to many. But it seems that it has gained some attention, after all! :) gpuccio
Alicia: You are always of help, by your simple existence! :) "Everything we know about historical biology and molecular biology supports my explanation." I must have missed something. "Nothing supports your explanation." Except maybe facts and good scientific reasoning? "First you disagree with “small variations in sequence can drastically change function,” and then you say “As we well know, even one AA change is often enough to make a protein non functional.” Make up your mind." You are really trying to equivocate. Of course, "change function" in my statement meant "change one function to another function". The meaning would be clear even to a child, or at least to a honest child. I disagree that "small variations in sequence can drastically change function", but I say that it is very easy to destroy function, even with slight changes. Was my statement ambiguous? Not at all. Just read again, with a little intelligence and honesty, what I wrote. I paste it here for your convenience: "(1)small variations in sequence can drastically change function" Not as a rule. Small variation at the active site can change the substrate affinity, but the general 3d structure and folding are usually much more difficult to change with little sequence modifications. Of course, they can often be easily disrupted. As we well know, even one AA change is often enough to make a protein non functional (see mendelian diseases). The idea is simple: you can destroy information with small changes, but you cannot easily build new complex information (a transition from one superfamily to another one, for example) with small changes. Small changes at the active site, however, can modify substrate affinity, as clearly stated in my answer, while the general 3d structure and folding of the molecule is retained. "In fact, labs have replaced 95% of the amino acids in some proteins and function is still present." Maybe in some proteins, not certainly in the general case. However, please give references even for those cases which you apparently quote. Excuse me, but I have no reason to believe what you say blindly. Regarding the Aakre paper you quote, I cannot read it entirely, but form the abstract it is quite obvious that it is in no way pertinent to the discussion here. I paste here the abstract:
Interacting proteins typically coevolve, and the identification of coevolving amino acids can pinpoint residues required for interaction specificity. This approach often assumes that an interface-disrupting mutation in one protein drives selection of a compensatory mutation in its partner during evolution. However, this model requires a non-functional intermediate state prior to the compensatory change. Alternatively, a mutation in one protein could first broaden its specificity, allowing changes in its partner, followed by a specificity-restricting mutation. Using bacterial toxin-antitoxin systems, we demonstrate the plausibility of this second, promiscuity-based model. By screening large libraries of interface mutants, we show that toxins and antitoxins with high specificity are frequently connected in sequence space to more promiscuous variants that can serve as intermediates during a reprogramming of interaction specificity. We propose that the abundance of promiscuous variants promotes the expansion and diversification of toxin-antitoxin systems and other paralogous protein families during evolution.
It is pretty obvious that the paper is about manipulations of a specific interaction. At best, it can be an example of the concept that I have clearly expressed just from the beginning: Small variation at the active site can change the substrate affinity. Maybe you should dedicate more than five minutes (and some intelligence and honesty) to your searches. "These homologs are derivations of the intermediates along the evolutionary path to humans." I absolutely disagree. For example, take the first bitscore you quoted: 130 bits of homology in Danio rerio. That is derived from an alignment of the blue sequence of the human Prickle 1 protein with: prickle-like protein 2 isoform X1 The same protein has a bitscore of 388 bits with the blue sequence from human Prickle 2 protein. Have you read what I wrote to you in my posts #127, #138 and #144? As I have explained, those bitscores of about 100 - 150 bits are clearly cross alignments between Prickle 1 and Prickle 2 proteins. Far from being evidence of previous intermediates, they are two different homologous proteins, with differentiated functions, which both appear in cartilaginous fishes, both with high homology to the corresponding two proteins in humans. As I have said, some intermediate levels of homology in different species can be easily explained as functional, or even non functional, isoforms of the protein, for example from alternative splicing, or simply indels. There is absolutely no support to your ad hoc idea that they represent old intermediates, because all those variant sequences are definitely younger than the sequence which we find in sharks, and which has been conserved up to humans. IOWs, there is no trace of them before, and you cannot assume for your convenience that they are testimony of past intermediates which have all gone extinct. Diversification of function in different species and contexts, and partial or total loss of function are much simpler and good explanations. Well, I doubt that I can be of any help to you, but I am glad just the same. gpuccio
Is "Alicia" actually "keiths"? "She" argues in the same slanted myopic "logic" as "keiths" Just curious mike1962
Me_Think @330: Wow. Just wow. It is painful just to watch that assertion advanced. Go back and read up on the issues. Eric Anderson
Alicia: You are talking about possible intermediates and potential hypothetical avenues. Furthermore, it appears to be a general proposal that a reduction in binding specificity (evolution, as essentially it always does, breaking things again) might permit the evolutionary process to continue without a breaking point, because it allows a complementary molecule to undergo change while still preserving some binding affinity. I unfortunately was unable to see the paper, but that much seems to be the case from the abstract. This does not demonstrate actual intermediates between an ancient protein and a modern one. It does not demonstrate contemporary change. It most certainly does not present evidence of the increase in information content necessary to get from A to Z -- either in the kinds of situations gpuccio is talking about, or in situations like your vague reference to a protein involved in spine development. There is precisely no evidence that a natural process -- whether by a reduction in binding site specificity or otherwise -- can produce the kind of information needed. You have not provided an example of protein evolution via intermediates in any meaningful sense of what this whole thread is about. Literature bluff. Eric Anderson
Both, EA. A quick search to find it, I skimmed the figures and subtitles, and read the discussion. Pucci asked for an example of protein evolution via intermediates in the literature, and I provided one. The paper looks at how wild-type proteins can be mutated at just a single site (or more) to produce the possible “promiscuously binding” intermediates involved in the evolution of that protein. They found that these promiscuous mutants were abundant and easy to find in sequence space when starting with the wild-type protein. Did you take a look at the paper? Alicia Cartelli
GP, I am looking forward to sitting down and reading the OP thoroughly, and the comments as well. I can't do it just now, but soon. I always learn from you. Upright BiPed
EugeneS @ 324
Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence.
Atoms ->Elements Me_Think
Alicia @327:
Here’s an example of protein evolution through intermediates which took me all of five seconds to find: Aakre et al. Evolving New Protein-Protein Interaction Specificity through Promiscuous Intermediates
Did you even read this, or just do a search for a couple of key words? What do you think Aakre demonstrates that is relevant to something like the Prickle example gpuccio highlighted in the OP? You wouldn't be engaging in a literature bluff, now would you . . . Eric Anderson
Alicia Cartelli:
You don’t have an explanation other than “the designer did it.”
That is a start and at least it is correct. You don't have any explanation at all. How can we test the claim that chordates evolved from invertebrates? And how can we test the claim that some chordates evolved into vertebrates? Talk about basing one's conclusion on the absence of data... Virgil Cain
"You mean your imagination?" No, I mean the time period when chordates developed a spine. That would seem like the most likely time for a protein involved in spine-development to have evolved, no? For the last time: We see this huge jump in bits and we have a huge gap in sequence data. You don’t have an explanation other than “the designer did it.” My explanation is that the sequence evolved through intermediate forms which have since gone extinct along with the species they were in. Everything we know about historical biology and molecular biology supports my explanation. Nothing supports your explanation. First you disagree with “small variations in sequence can drastically change function,” and then you say “As we well know, even one AA change is often enough to make a protein non functional.” Make up your mind. “Most” is certainly an exaggeration.’ No, it is not. In fact, labs have replaced 95% of the amino acids in some proteins and function is still present. “wild-type levels are what we observe in nature” …you don’t say. “It’s what we have to explain.” Yes, and in explaining the function of these proteins by sequence comparisons, you can’t ignore the extant organisms carrying snapshots of the evolution of this protein, which have unfortunately also gone through evolutionary changes from their lineage branching to today. This makes things more complicated, but you can’t just ignore them. Especially when there are no extant organisms from the lineages branching off during the time this protein evolved. Here’s an example of protein evolution through intermediates which took me all of five seconds to find: Aakre et al. Evolving New Protein-Protein Interaction Specificity through Promiscuous Intermediates Your post #279, point 4: “Equally pitiful is the attempt by the notorious Alicia to use homologues present in the proteome in species after the first appearance of the sequence, and with lower homology values, as possible ‘intermediaries’.” These homologs are derivations of the intermediates along the evolutionary path to humans. Also from your post #279: “no subset of those 600 bits of functional information is detectable in any species which antedates the cartilaginous fishes – bony fishes split.” That would be because the species with a spine that also predated the cartilaginous/bony fish split are all extinct. It’s kinda hard to look for sequence homology when you have no sequence to search. But that doesn't stop pucci! You are basing your conclusions on the absence of data instead of analyzing everything that is available (and instead of actually understanding what you are talking about). Always glad to be of help! Alicia Cartelli
Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence. I'd start by looking for the absence of any sorting mechanism. Just think if nucleotides were always in the same order. Mung
EugeneS: "Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence." A very good request! I suppose Zachriel will elegantly ignore the issue... :) gpuccio
Zachriel. I said nothing about extinction in this thread apparently. Definitions see Abel. Potential energy of the whole system must be consideted. Please provide a single empirical case of formation of symbolic representation and control in nonliving nature just by means of the four basic types of physical interaction without recourse to intelligence. EugeneS
Alicia Cartelli: Learn some basic biology, then get back to me. Ah. I finally see the problem. You are stuck at basic biology and the concepts we are discussing are above your head. We should dumb things down for you? Mung
However, restricted it is anyway: there is apparently no trace in other cnidaria, and obviously in all other metazoa.
Maybe. Some genes are restricted to lineages... so what? wd400
Your hypothesis is untestable. Once existed but disappeared and left no trace is untestable. Mung
Zachriel:
Scientists look to all available evidence.
Not when it comes to evolutionism. They can't even figure out how to test its claims. For instance no one knows how to test the claim that ATP synthase arose via natural selection, drift or neutral construction
For instance, studies of embryos indicated that, given common descent, the mammalian middle ear evolved from the reptilian jaw.
That is incorrect as development has nothing to do with evolution.
Extinction is a key observation, and a core component of evolutionary theory.
Except no one can actually reference this alleged evolutionary theory so we can all see what it really says. Bottom line is Zachriel is spewing nonsense, as usual. Virgil Cain
Me Think @ 311- You are sadly mistaken as A) ID does not require the Bible, B) ID is not anti-evolution and C) does not require God. Three strikes on your ignorance. Nice job Virgil Cain
Mung: Should I search for the missing intermediates or just claim they were there in the past but went extinct and save myself the time and effort? Scientists look to all available evidence. For instance, studies of embryos indicated that, given common descent, the mammalian middle ear evolved from the reptilian jaw. That meant that the jaw of the intermediate species had to continue to work while providing a continuous improvement in hearing. It seems contrary to common sense. Would looking for such an intermediate fossil be like looking for unicorns? EugeneS: The old claim that almost all species that have ever lived have gone extinct . . . Seriously? Let's start with the fact that there are no T. Rexs running around or Metanephrocerus flying about. You do realize that there are no species from the geological past alive today. Even so-called livings fossil are not the same species as lived in previous eras. during the Age of Dinosaurs, yet the Age of Dinosaurs included a complex ecosystem of plants, insects, mammals, reptiles, etc. There have been vast changes in the ecosystems of the Earth over billions of years, and most of that history is still obscure. gpuccio: So, it is really surprising that we can have any evolutionary understanding of natural history at all! Yes, science is amazing that way. gpuccio: 1) Extinction has nothing to do with the facts we observe which are the foundation of evolutionary theory: we can observe homologies, differences, neutral variation, and build evolutionary trees in spite of the generalized extinction, but That is incorrect. Extinction is a key observation, and a core component of evolutionary theory. gpuccio: 2) Extinction can certainly explain the complete absence of any trace of positive NS in the proteome, for example the absence of functional sequence intermediaries. That's is also incorrect. In many cases, we can trace the ancestry of proteins. However, in other cases, we cannot. This may be due to observational limitations, or because the intermediates left no descendants. As for your broader point, even though our data only reveals a tiny sliver of life's history, it is more than sufficient to support the nested hierarchy, and we have evidence of common ancestors in many cases. EugeneS: Quality of service is a utility measure and it is defined formally. Water cycle or convection in general does not minimize quality of service, does it? It's hard to tell because "quality of service" usually refers to consumer services, such as computer networks, not the water cycle. However, rain is certainly of utilitarian value to humans. EugeneS: It reduces to minimum potential energy. The sun evaporates water and moves it uphill; the water then has a higher potential energy. EugeneS: Nature does not minimize QoS Can you provide an explicit definition of how you are using "quality of service"? Zachriel
wd400: OK, maybe it is restricted to medusozoa. We will know when other medusozoa are sequenced. However, restricted it is anyway: there is apparently no trace in other cnidaria, and obviously in all other metazoa. gpuccio
Zachriel, Utility: absolutely. Quality of service is a utility measure and it is defined formally. Water cycle or convection in general does not minimize quality of service, does it? It reduces to minimum potential energy. However, photosynthesis does not. It is an integrated circuit part of a whole number of subsystems producing jointly homeostatic state far from thermodynamic equilibrium. It is symbolically controlled along with other integrated circuitry in living systems. These, in contrast to convection or any other purely physical effect for that matter, do NOT reduce to minimum potential energy. Nature does not minimize QoS, the only thing it can be said to minimize is energy. That, if you wish, can be labelled utility as well. But there is utility and utility, as you can see from the examples. In general, quality of service is different from min energy (trivial default utility) and is not physicalistic. Nature does not choose. But organization fundamentally is based on choice and implements choice. EugeneS
Alicia: Ah, now I recognize you! But you can do better than that. :)
Your hypothesis is untestable.
This from the person who wanted to explain homologies as convergent evolution. Ah, Ah!
You use sequence data to look at the evolution of a protein, but there is no sequence data where the protein is actually most likely to have evolved.
You mean your imagination?
Function can be maintained even with large amounts of changes in amino acid sequence.
Whoever said anything different? That's exactly my point. Many proteins have large tolerance to sequence change. I have given the example of myoglobin exactly to show that point. That's exactly the reason why, when sequence is highly conserved, we can assume strong functional constraints: those proteins have not a large tolerance to sequence change. Can you understand the point?
Yes, sequence conservation implies function,
Thank you for the concession. But please, don't become reasonable again.
(1)small variations in sequence can drastically change function
Not as a rule. Small variation at the active site can change the substrate affinity, but the general 3d structure and folding are usually much more difficult to change with little sequence modifications. Of course, they can often be easily disrupted. As we well know, even one AA change is often enough to make a protein non functional (see mendelian diseases).
(2)large changes in sequence can exist in proteins with the same function
Obviously. Whoever said anything different? See before.
We certainly can explore the functional space of proteins, and we have.
My statement was: As we cannot yet explore in detail the functional space of proteins, conservation remains the best indirect way to assess the functional constraints of a sequence. (emphasis added) Do you disagree with that?
As I have said before, most amino acids in any given protein are replaceable.
"Most" is certainly an exaggeration. Many would be better. And so? See previous points.
Conserving function and conserving wild-type levels of function are two completely different things.
Well, wild-type levels are what we observe in nature. It's what we have to explain. But you can still analyze non wild type levels and show in the lab how there is a reasonable step by step path to existing wild-type levels, with each step increasingly functional. I am sure that you can offer us a lot of examples of that in the literature, with your cast and clear understanding of biology. I am waiting. But I am not holding my breath.
Remind me again, what was your explanation for the lower homologies seen in other vertebrates?
See, for example, my post #279, point 4.
Extinction has killed +99% of species to have ever lived.
So, it is really surprising that we can have any evolutionary understanding of natural history at all! Let me sum up: 1) Extinction has nothing to do with the facts we observe which are the foundation of evolutionary theory: we can observe homologies, differences, neutral variation, and build evolutionary trees in spite of the generalized extinction, but 2) Extinction can certainly explain the complete absence of any trace of positive NS in the proteome, for example the absence of functional sequence intermediaries. OK, what was your first point? Ah:
Your hypothesis is untestable.
Now I recognize you! But you can do better than that. gpuccio
Ah, yes. The old claim that almost all species that have ever lived have gone extinct . . . Anyone have a source for that claim? Eric Anderson
“it does not contradict my points” That would be because nothing can contradict your points. Your hypothesis is untestable. You use sequence data to look at the evolution of a protein, but there is no sequence data where the protein is actually most likely to have evolved. It’s that simple. How many times do I (and others) have to say it? I’m glad you agree that sequence conservation and function are not exactly the same thing. Because they aren’t even close. Function can be maintained even with large amounts of changes in amino acid sequence. Yes, sequence conservation implies function, but (1)small variations in sequence can drastically change function and (2)large changes in sequence can exist in proteins with the same function Obviously it's more complicated than sequence=function. We certainly can explore the functional space of proteins, and we have. As I have said before, most amino acids in any given protein are replaceable. Conserving function and conserving wild-type levels of function are two completely different things. Remind me again, what was your explanation for the lower homologies seen in other vertebrates? 600 bits over 100 million years, of which we have no information on evolution of the protein in question? Argument of the gaps much? “..extinction is so hyperselective that it can erase any trace of the intermediaries that your theory badly needs.” Completely wrong again. Extinction is the opposite of hyperselective. Extinction has killed +99% of species to have ever lived. Learn some basic biology, then get back to me. Alicia Cartelli
Why? Because the protein is absolutely restricted to the species Hydra vulgaris. Absolutely no other hit is found in the whole proteome. Pretty sure Hydra vulgaris is the only Medusozoan with a genome sequence. In most studies the number of so-called orphan genes is correlated with the nearest relative with a genome/transcriptom available. wd400
Virgil @ 302 Rake, Rake, Rake, we must Rake, through the Bible and through the ID literature, we must Rake, to prove Evolution is fake, for God's Sake. Me_Think
GP @ 304
Isn’t all this truly interesting?
All taxonomically restricted genes are interesting.This could be possible explanation :
Massively parallel RNA sequencing (RNA-Seq) has revealed that a large fraction of the genome extending far beyond the set of annotated genes is transcribed and possibly translated. Many genes that are annotated as long non-coding RNAs (lncRNAs) are lineage-specific and display high transcriptional turnover. The high transcriptional activity of the genome provides abundant raw material for the birth of new genes.
I Would certainly not claim Taxonomically Restricted Genes is designed and rest is evolved. Me_Think
Virgil Cain @ 278
So natural forces can fuse an amino acid in the Atlantic ocean with one in the Pacific?
Across 6,447 miles? You could certainly conceive such a scenario :-) , but certainly not with the forces I have mentioned. GP @ 280
I must remind you that biological information in proteins is established at the level of the nucleotide sequences that symbolically code for the AA sequence. All the rest is about biochemical laws, and has little to do with sequence information. Variations in the gene are supposed to be due mainly to random errors in replication. Or to design.
Of course I agree. My comment was in response to posts above 277 which discusses forces and algorithm. EugeneS @ 281
Drop the single quotes around the word “algorithm” and defend your thesis. Talk precisely and produce a single example of {algorithm, processor} complex formation by means of natural forces alone
Here you go: Let's say in a biological system, there is Typtophan on top layer and Serine and Histidine on a lower layer which is at some distance from the top layer.If side chain has to be formed, the lower layer has to meet the upper layer.Assume the vertical void between the layers act as a capillary.If the capillary void near Serine has a radius less than Histidine capillary void, Serine will raise higher up to Typtohan as h= 2T/Rho*rg Although both Serine and Typtophan had equal chance of combining with Typtophan, Serine had the advantage of resting in a narrower capillary, which ensured it succeeded in combining. Diffusion of salts in Serine capillary void would change the result as due to higher density, Serine might not be able to reach Typophan. Similarly, although phi and psi values for an amino acid in a protein ranges from -180 to +180, some values of phi and psi are forbidden due to Steric Clash. This restriction controls protein structure. It can be seen that bio-mechanical forces form an algorithm which determines which amino acids fuse together. Me_Think
VC Hehe, right on, bro mike1962
gpuccio: Isn’t all this truly interesting? Fascinating! Should I search for the missing intermediates or just claim they were there in the past but went extinct and save myself the time and effort? Mung
Zachriel: In fact, we have substantial evidence of intermediate species from fossils. So? If only we were talking about fossils. Mung
gpuccio
Isn’t all this truly interesting?
"Interesting" is an understatement. :) Dionisio
I suggest that all those interested in this discussion look at the following new OP: https://uncommondesc.wpengine.com/evolution/genes-that-come-from-nowhere-so-it-seems/ The issues debated there are certainly relevant to the discussion here. The linked Ann Gauger piece is a good introduction to the issue, but I would definitely recommend the following paper, linked by Gauger: https://www.researchgate.net/publication/26776433_More_than_just_orphans_Are_taxonomically-restricted_genes_important_in_evolution It is really interesting. Just to check, I have blasted one of the proteins quoted in the paper, spinalin, which is "a structural component of spines inside the capsule" of nematocytes. A functional protein, certainly, whose function and location are known. Well, spinalin is a 254 AAs long protein. Its maximum potential bit score, as Alicia would say, is 541 bits (the bit score of the protein with itself). The interesting thing is that identity is the only homology that we can get when we blast it. Why? Because the protein is absolutely restricted to the species Hydra vulgaris. Absolutely no other hit is found in the whole proteome. So, how did this protein "evolve"? Zachriel will say that all the intermediaries have gone extinct. OK, is that true of all the 10 - 20% orphan (taxonomically restricted) genes that are apparently present in each existing species? By the way, it could be interesting to mention here that I have briefly analyzed the sequences which are associated to the domain part of Prickle 1 in Drosophila melanogaster: IOWs I have blasted the "blue" sequences in the Drosophila Prickle 1 (which, in Drosphila, has two different forms). Well, the interesting facts are: 1) Those "blue" sequences are completely different from the "blue" sequence in the vertebrate Prickle 1 (which was already obvious in my OP). 2) Those "blue" sequences are essentially restricted to flies, exactly as our original blue sequence is restricted to vertebrates. Isn't all this truly interesting? gpuccio
Rough draft for the entire song "Magical Mystery Change" (to the tune of Magical Mystery Tour): Hold on hold on for the Mystery Change Hold on hold for on the Mystery Change Hold on That’s a blind mutation hold on for the Mystery Change Hold on A DNA mutation Hold on for the Mystery Change The Magical Mystery Change is coming to change you this way, change you today All in all in for the mystery change All in all in for the mystery change All in They are everywhere you need All in for the mystery change All in They will happen guaranteed All in for the mystery change The magical mystery change is hoping to make you this way Hoping to get started today Hold on hold for the Mystery Change Hold on hold for the Mystery Change Hold on That’s a blind mutation hold on for the Mystery Change Hold on A DNA mutation Hold on for the Mystery Change The Magical Mystery Change is coming to change you this way, change you today The magical mystery change you will die or make it this way You will die or make it today, be here to stay Virgil Cain
OK, OK, I got it: Hold on hold for the Mystery Change Hold on hold for the Mystery Change Hold on That's a blind mutation hold on for the Mystery Change Hold on A DNA mutation All in for the Mystery Change The Magical Mystery Change is coming to change you this way, change you today Virgil Cain
Mike1962, For the song we would have to change it to "magical mystery change" "The Magical Mystery Change is coming to change you this way, change you today" :cool: Virgil Cain
Virgil Cain: magical mystery mutations We'd love to take you away. Love it. mike1962
Zachriel:
In fact, we have substantial evidence of intermediate species from fossils.
The result of phenotypic plasticity, no doubt. Virgil Cain
Zachriel:
It doesn’t have to be “hyperselective”...
It just happened to be hyperselective, duh. You know just like those magical mystery mutations just happened Evolutionism's grandeur is nothing to be schlepped away :cool: Virgil Cain
Mung: The absence of intermediate sequences is all the evidence we need to know that that those sequences once did exist but must have existed in some species that must have gone extinct. In fact, we have substantial evidence of intermediate species from fossils. Zachriel
The absence of intermediate sequences is all the evidence we need to know that that those sequences once did exist but must have existed in some species that must have gone extinct. Ain’t evolutionism grand. Mung
gpuccio: What I do doubt is that extinction is so hyperselective that it can erase any trace of the intermediaries that your theory badly needs. It doesn't have to be "hyperselective" when the vast majority of species that have ever existed have gone extinct, including entire lineages, especially during bouts of adaptive radiation. Zachriel
Zachriel: "What’s folly is to ignore the evidence of extinction." Why do you make me say what I have not said? Who has ever "ignored" the evidence of extinction? Of course extinction happens. What I do doubt is that extinction is so hyperselective that it can erase any trace of the intermediaries that your theory badly needs. A very "darwinist friendly" extinction pattern, indeed! gpuccio
Alicia at #289: An almost reasonable post from you! You can always surprise me. :) And, because it is almost reasonable, it does not contradict my points. Of course 600 bits of homology is not the maximum bit score: the shark sequence is not the same as the human. But believe me, 600 bits are a lot of homology, under all points of view. And of course conservation and functional specification are not exactly the same thing, but the fact remains that conservation implies functional specification. As we cannot yet explore in detail the functional space of proteins, conservation remains the best indirect way to assess the functional constraints of a sequence. I have already commented on the possible explanations of the lower homologies in other vertebrate species. The fact remains that 600 bits are conserved between shark and humans. Unless you want to argue that humans are very similar to sharks (which is certainly an interesting point of view), that simple fact remains unquestionable. I must say that I am a little worried of our new "communication level". Please, reassure me and go back to your old dear self! :) gpuccio
Zachriel:
The evidence that entire lineages have gone extinct doesn’t go away just because you don’t know how to quantify it.
Nice non-sequitur. Not only that you can't quantify anything pertaining to evolutionism.
What’s folly is to ignore the evidence of extinction.
And another non-response to what gpuccio posted. Virgil Cain
Alicia Cartelli:
And when we do this (as I’ve shown), we see various species with various numbers of homologs, all with varying amounts of sequence similarity.
You just assume they are homologs because your position requires it. Gene duplication? Really? In order for gene duplication to do anything it has to also have a binding site. It then has to be expressed meaning it has to be on the right part of the coiled DNA and that binding site has to align with it along that coil. Then for changes to happen specific mutations have to occur. Yet Durrett and Schmidt have shown that waiting for two specific mutations may be out of the reach of stochastic processes. Yet your scenario requires many specific mutations to occur. And all of that means you have no clue what you are talking about, as usual. Virgil Cain
gpuccio: I don’t discuss fossils and morphological evolution, because I think that no quantitative argument can easily be made about those issues. The evidence that entire lineages have gone extinct doesn't go away just because you don't know how to quantify it. gpuccio: But to invoke selective and total extinction of all the intermediate forms of a sequence in natural history is folly. What's folly is to ignore the evidence of extinction. EugeneS: Organized systems exhibit symbolic representation and control. That's not the usual definition, but okay. So photosynthesis is not an "organized system". EugeneS: Being organized means being able to achieve a maximum of non-physical utility (business quality, quality of service). That works as long as you can explicitly define utility. The water cycle has utility by some measures. Zachriel
“Neo darwinists don’t like my equaling conservation to functional specification” Because they are not equal. It is well known that many amino acids can be changed in just about any given protein and function is conserved. There is a difference between conserving function and conserving wild-type levels of function. A point that I think is important, which you left out, is the max bit score for the second region (the bit score of a perfect match for the second region of the protein): 1065 bits 0 to 597 and 0 to 597/1065 This doesn’t change your main point, but it does add some perspective to your sequence conservation/functionality conservation claim. 468 bits missing, but we still see function… Protein structure in general is much more conserved than amino acid sequence. The fact is that you are looking for intermediates of a protein which would be most likely present in species that have all since gone extinct. So the best we can do is look at the other branches of the chordates. And when we do this (as I've shown), we see various species with various numbers of homologs, all with varying amounts of sequence similarity. So again we are looking at either conserved function while sequence changes or the results of various evolutionary mechanisms (gene duplication for example) which have been able to explore new sequences and functions over the past 400 million years (or more likely a combination of both). Alicia Cartelli
It's the incredible disappearing DNA sequences! they don't just become junk DNA, they vanish! Not even any fossils left to indicate they ever existed. Ain't evolutionism grand. Mung
thanks again gpuccio. If a nucleotide sequence or amino acid sequence has high similarity across many taxa then it is assumed that the sequence has remained unchanged for many many years under the assumption of common descent. The reason it is so similar must be due to functional reasons. There really is no other acceptable explanation. Even if the sequences are not considered to be homologous their similarity must be due to functional reasons. So this sequence must have some meaning in the context of the organism, and it is then no wonder that we see the sequence as being informational. It is meaningful. Again I don't see how this can be questioned. IOW, I agree with what you say and just say it again in different words. Of coursed, if someone really wanted to, they could claim that the sequences are so similar because they were created yesterday and have had no time to diverge. ;) Mung
Stuff Happens. Zachriel and Alicia might evolve! Mung
Zachriel: As per definitions of order, complexity, organization I am referring to D. Abel, "The First Gene" and "Primordial Prescription". Both are accessible via Amazon. Organized systems exhibit symbolic representation and control. Being organized means being able to achieve a maximum of non-physical utility (business quality, quality of service). Examples of non-physical utility include: - accuracy of hitting a target area by a guided missile; - buoyancy of a vessel; - precision of mechanical processing; - level of biological function; - minimax criteria such as best service achievable at minimum financial costs; - fail-safety maximization; - information loss minimization; - reliability; - longevity; - durability; - accuracy of replication; - quality of noise filtering; etc. Why is quality of service not physical? Simply because QoS is formally defined, even though it is applied to systems composed of physical bodies and subject to physical constraints. As the designer of a system, I determine what level of quality of service is acceptable for me. I provide for the designed system appropriate means to measure and control QoS. Nature does not care about QoS. The motion of a guided missile, for example, regardless of whether it destroys its target or not, is described by the same equations. I, the designer, purposefully choose the appropriate initial conditions and motion control in order to make sure it hits the target. Control necessarily involves memory to record a representation of past states, measurement of the current state and regulation signal to steer the current state towards desired goal states. None of that is achievable by physicalistic means (by means of natural forces alone without first introducing symbolic control into the system), simply because nature is indifferent to the satisfaction of formal functional criteria. No appeal to osmosis, capillary effects, electrostatic attraction, gravitation etc. can achieve a system with memory, symbolic representation and control. EugeneS
Zachriel: As you know, I don't discuss fossils and morphological evolution, because I think that no quantitative argument can easily be made about those issues. But to invoke selective and total extinction of all the intermediate forms of a sequence in natural history is folly. Sequences, as a rule, are conserved and leave detectable traces in the existing proteome. We are speaking of huge numbers of sequences still represented in the existing proteome, which are very good samples of the processes which took place at the molecular level. To argue that thousands, maybe millions, of intermediate sequences which are absolutely necessary for your theory to be credible simply were lost because of hyperselective extinction of all the species which had some testimony of them is taking cognitive bias to new and unprecedented levels of excellence. gpuccio
EugeneS: The reason is because you fail to distinguish between order and organization. Scientists say that storms are a form of self-organization. As you seem to be using the terms in a different manner, please provide your operational definitions. gpuccio: NS requires functional intermediaries at the sequence level. Yes. gpuccio: Those intermediaries must have been functional enough to be expanded by positive selection to a big subset of the initial population, otherwise the probabilistic barriers reamin exactly the same. Each of them must have expanded. Therefore, the complete absence in the proteome of intermediary sequence before the appearance of the functional sequence is an extremely strong falsification of the NS explanation. Um, no. It's called extinction. gpuccio: How can these people really believe that tens of functional intermediaries existed, in different species, expanded by positive selection, each of them, so that they could be steps towards the final functional sequence, and that not one of those sequences has survived in the proteome? They went the same way intermediates between reptiles and mammals did. They went extinct. gpuccio: It seems that big changes of both sequence and structure are necessary, for example, to get a new protein superfamily. What does that imply in terms of your “fragility”? Protein sequence is flexible enough that novel protein folds can be discovered through stochastic processes, processes that predominated in the early history of life. gpuccio: The sequence we have discussed here is 517 AAs long. How many “fragile” changes were necessary to get to it apparently from scratch, after the appearance of chordates, and in time for the appearance of vertebrates? Maybe no one knows. So? Your argument becomes, there's a gap, so design. It's no different in kind than looking at the irreducibly complex structure of the mammalian middle ear and saying it couldn't have evolved. How could it? Besides, where are the intermediaries in extant nature? Zachriel
Zachriel: "Human-devised computer languages are fragile, that is, they typically break when mutated; contrary to protein sequences, wherein small changes to sequences often result in small changes to the structure." It seems that big changes of both sequence and structure are necessary, for example, to get a new protein superfamily. What does that imply in terms of your "fragility"? The sequence we have discussed here is 517 AAs long. How many "fragile" changes were necessary to get to it apparently from scratch, after the appearance of chordates, and in time for the appearance of vertebrates? gpuccio
"Natural forces [...] can combine to create complex ‘algorithm’" What?! Drop the single quotes around the word "algorithm" and defend your thesis. Talk precisely and produce a single example of {algorithm, processor} complex formation by means of natural forces alone. If you do not drop your quote marks, there will be no substance to discuss. EugeneS
Me_Think: You are definitely clever in saying things that apparently have no meaning. Would you care to explain your thoughts, if they deserve to be explained? I must remind you that biological information in proteins is established at the level of the nucleotide sequences that symbolically code for the AA sequence. All the rest is about biochemical laws, and has little to do with sequence information. Variations in the gene are supposed to be due mainly to random errors in replication. Or to design. So, what have your cryptic statements to do with all that? gpuccio
Eric: Thank you for your intervention! OK, I think that we agree on many things. I will try to stress here a few points. 1) Sequence conservation over long periods of time, according to evolutionary theory, is a reliable indicator of functional constraints on the sequence. I fully accept this point. And this is a very important point for ID theory, because this is the best way to measure functionally specified information in protein sequences. The Durston method is based on that concept. In my post, I have used the bit score from the blast of sequences separated by a large time window as a measure of functionally specified information, and as a way to ascertain when that amount of information appears in the proteome according to existing data. 2) Neo darwinists don't like my equaling conservation to functional specification: don't listen to them. It's their own theory which requires that interpretation. There is absolutely no way they can explain 600 bits of conserved sequence in 400+ million years, unless they accept functional constraints. Even Alicia Cartelli has practically abandoned her pitiful attempt at invoking "convergent evolution" to explain sequence homologies, maybe advised by someone who understands things better. The simple truth is: if 600 bits of information survive from sharks to humans, they must be functionally constrained. 3) No natural process can explain the appearance of 600 bits of functional information by random variation. Even neo darwinists, or at least the less foolish among them, admit that simple point. So, the only reasonable hope for them is to invoke NS. Well, NS requires functional intermediaries at the sequence level. Those intermediaries must have been functional enough to be expanded by positive selection to a big subset of the initial population, otherwise the probabilistic barriers reamin exactly the same. Each of them must have expanded. Therefore, the complete absence in the proteome of intermediary sequence before the appearance of the functional sequence is an extremely strong falsification of the NS explanation. together with the complete absence of any other positive support from facts. IOWs, known facts not only do not support the NS explanation (because there is no positive fact in its support), but also do falsify it (for the strong negative fact of the absence of any intermediaries in the proteome). How can these people really believe that tens of functional intermediaries existed, in different species, expanded by positive selection, each of them, so that they could be steps towards the final functional sequence, and that not one of those sequences has survived in the proteome? This is complete denial of any scientific principle. It is a simple denial of the importance of facts. 4) Equally pitiful is the attempt by the notorious Alicia to use homologues present in the proteome in species after the first appearance of the sequence, and with lower homology values, as possible "intermediaries". Obviously, after a functional sequence has already appeared in natural history, there are a lot of possible explanations for a lower homology in some sequences and in some species (for example, different functional requirements in different species, or simply loss of function in some sequences, and so on). The simple point is: those 600 bits have survived from sharks to humans, and it is absolutely impossible to attribute that simple fact to chance. And no subset of those 600 bits of functional information is detectable in any species which antedates the cartilaginous fishes - bony fishes split. I hope this is a clear summary of my argument in this thread. gpuccio
So natural forces can fuse an amino acid in the Atlantic ocean with one in the Pacific? Is that your "argument" Me Think? Virgil Cain
Natural forces (Say, simple forces like capillary pressure,osmosis and torsion angles - apart from inherent chemical properties) can combine to create complex 'algorithm' to fuse specific amino acids lying at different places without need for 'intelligence'. Me_Think
Zachriel, "Both are examples of organization." Even worse. Your argumentation is flawed. The reason is because you fail to distinguish between order and organization. "Gravity is a mechanism".
Google: 1. a system of parts working together in a machine; a piece of machinery. 2. a natural or established process by which something takes place or is brought about.
Gravity is a force, not a mechanism. EugeneS
gpuccio: Interesting post. I apologize for not participating sooner, as I am just now getting back to UD tonight after a week+ out of pocket. I think you raise some valuable points and some issues well worth discussing. You don't address the question of common descent we were discussing previously, which is perfectly fine -- I realize for purposes of this post you are assuming common descent and seeing where that takes us. I'm with you on the quasi-neutral mutation and purifying selection concepts, with the caveat that I'm not sure I would say purifying selection is the "main principle" which limits random variation. It is cellular mechanisms and error-correction processes which are the primary drivers of integrity over time. But I get your point that, assuming a mutation slips past the error-correction machinery, then purifying selection is the primary limiting factor from that point on. This doesn't address the issue of how much variation is allowed to slip past the error-correction machinery in the first place (and we probably don't know at this point), nor whether tolerance levels are different for different parts of the genome (likely), but for purposes of discussion it is probably workable to point to purifying selection in a broad sense as having the central role you mention. I also think that, given your assumptions, you draw some reasonable conclusions. However, I still feel a little unease about something that I'm not sure I can adequately articulate. Perhaps it is this: The question of whether something has a strong functional constraint is logically separated from whether something is designed. The Darwinist, for example, has no trouble with the idea that a particular sequence is highly constrained throughout history. It just means that evolution blindly stumbled upon a particularly important sequence early in the history of life. Nor does the Darwinist have any trouble with the idea that a particular sequence is not highly conserved. It just means that there is a wide range of functional options and evolution is still blindly stumbling around among a range of options. Nor does the Darwinist have any trouble with the idea that a particular sequence shows up only in one particular type of organism, such as vertebrates. It just means that evolution blindly stumbled upon something that was needed for vertebrates. All just part of the blind, bumbling miracle of evolution. Thus we get a comment like the one from Alicia: "So during the same time that some of the chordates were evolving a bony spine, a protein now known to be involved in spinal development also evolved? Wow!" See it all "evolved," meaning, of course, by purely natural and material processes. That part is never questioned by the Darwinist. Thus, at least insofar as one might be seeking to counter the blind-purposeless-natural-process claim of Darwinian evolution, it would appear that any arrangement of sequences, conserved, disparate, across groups, within groups, or otherwise, presents no particular logical problem for Darwinian evolution. After all, evolution has no underlying substantive approach that can be refuted. It is, when boiled down to its pure essence, just a claim that Stuff Happens. And whatever we happen to see must have been what happened. Insofar as you are speaking to someone with an ID viewpoint, I think your observations are both interesting and worth further investigation. But as far as any particular pattern demonstrating design as a more likely candidate for the origin of certain systems than blind, undirected processes, it seems we still need to focus on the basic design inference. And given that some of the more recalcitrant crowd refuse to accept the design inference (at least in biology), it becomes almost impossible to have a rational discussion. No matter what evidence you point to, they will always fall back on the Great Evolutionary Explanation: Stuff Happens. Eric Anderson
EugeneS: Gravity is not a mechanism Merriam-Webster: mechanism, the fundamental processes involved in or responsible for an action, reaction, or other natural phenomenon EugeneS: To draw an analogy between a storm, on one hand, and algorithmic representation and control, on the other, is not even wrong. It wasn't an analogy. Both are examples of organization. Zachriel
Zachriel, Gravity is not a mechanism, Zachriel. To draw an analogy between a storm, on one hand, and algorithmic representation and control, on the other, is not even wrong. I believe you are intelligent enough to see that this is true, and yet you insist on your flawed argumentation. Why?! EugeneS
Zachriel- The master of writing posts that say absolutely nothing of substance. Virgil Cain
Mung: According to you the formation of stars and planets is due to some sorting mechanism. Yes, gravity is a powerful sorting mechanism. Consider the Earth's internal structure. EugeneS: When you say that biological metabolism is an ordered state, you are categorically wrong. Our statement was that metabolism was on the cusp of chaos and order. EugeneS: It is an organized state, not ordered. Yes, metabolism is organized, as are storm systems. Zachriel
Mung, Thanks very much. Of course, everything is designed except God. E.g. God designed inanimate nature in such a way that the result of the natural formation of snow flakes is every time an intricate aesthetically pleasing and unique form. When referring to teleology, I was talking rather in a very narrow sense of choice contingency, which is exclusively a result of intelligence. Choice contingent causation is only present in life forms and in humans or animal artifacts. Inanimate nature is not capable of making choices. This is what I meant by saying it was not teleological. Zachriel, When you say that biological metabolism is an ordered state, you are categorically wrong. It is an organized state, not ordered. "Many examples are considered organization" And wrongly so. Many people say wrong things. Even very intelligent people say grossly wrong things. Organization =/= order. You cannot explain an implemented and executed algorithm in terms of just order and chaos. This is why I keep saying your argumentation is fundamentally flawed. EugeneS
Hi EugeneS, The teleological argument from Aquinas is based on the natural end-directedness (teleology) of inanimate matter. We see that things which lack knowledge, such as natural bodies, act for an end, and this is evident from their acting always, or nearly always, in the same way, so as to obtain the best result. Hence it is plain that they achieve their end, not fortuitously, but designedly. Now whatever lacks knowledge cannot move towards an end, unless it be directed by some being endowed with knowledge and intelligence; as the arrow is directed by the archer. Therefore some intelligent being exists by whom all natural things are directed to their end; and this being we call God (Aquinas, Summa Theologica, Article 3, Question 2). Mung
It's all in your head Zachriel. According to you the formation of stars and planets is due to some sorting mechanism. On that view, what isn't. Mung
EugeneS: In these examples no organization, no code processing, no read/write from memory, no symbolic representations are used. The example provided was sorting. Many examples are considered organization, however, not code processing. EugeneS: These examples and more are natural effects under the categories of {1. chaos; 2. order; 3. phase transitions between 1 and 2.} Yes, they are natural effects. Biological metabolisms are also on the cusp of chaos and order. Zachriel
Zachriel, Also, the centrifugal force will cause ordering of sand particles on a sandy river bank. These examples and more are natural effects under the categories of 1 - 3 in my list above. In these examples no organization, no code processing, no read/write from memory, no symbolic representations are used. EugeneS
Mung, Can you give a bit more detail on teleology in inanimate nature? In my opinion, it is not teleological (at least not in the same sense as artefacts including life are). There is no inherent choice ability and, consequently, no goal-orientation in inanimate nature. There are only energy differentials. If you label minimum potential energy states as goal states, then yes, I agree that in this limited sense inanimate nature is goal-oriented. But by goal-orientation I rather mean the ability of a system to choose/prefer a path through certain physically equivalent states (states with the same values of energy differentials). Physicality does not choose. EugeneS
Mung: They looked unsorted to you. A simple example is the evaporation of water, which takes water in dirt, or salt water in the sea, and converts to a much more pure form. Or you could prospect for gold, or just look at a piece of common quartz. Zachriel
Zachriel: They were unsorted before. They looked unsorted to you. Zachriel: Sorted afterwards by observable mechanisms. They looked sorted to you. It does not follow that there was some sort algorithm being executed outside your head. You were the one doing the sorting. Mung
(1) : a natural phenomenon marked by gradual changes that lead toward a particular result Yes, nature is teleological. Welcome to ID. Mung
EugeneS:
By the way, even the phrases “natural processes”, “stochastic processes” are not correct, strictly speaking. A process is something that has a goal and refers to “processing”. There are no goals as such or processing of anything in inanimate nature.
I both agree and disagree. A process is end-directed, as you say. By definition and by observation. But inanimate nature is end-directed (teleological). :) Mung
EugeneS: In fact, putting aside living systems, you cannot distinguish between a natural effect (something that happens in inanimate nature) and a system that can model this natural effect by using a complex of an algorithm and its processor. Models are not the thing being modeled, if that is what you mean. -- All models are wrong, but some are useful. — George E. P. Box Zachriel
Zachriel, Ok, I am happy to use the word "process" as MW dictionary prescribes but it does not get us anywhere substantially because substantially you have a flaw in your reasoning that I mentioned. In fact, putting aside living systems, you cannot distinguish between a natural effect (something that happens in inanimate nature) and a system that can model this natural effect by using a complex of an algorithm and its processor. EugeneS
Zachriel:
Human-devised computer languages are fragile, that is, they typically break when mutated; contrary to protein sequences, wherein small changes to sequences often result in small changes to the structure.
That is due to the fact a higher intelligence designed the language of proteins. Virgil Cain
EugeneS: A process is something that has a goal and refers to “processing”. Merriam-Webster: process: a (1) : a natural phenomenon marked by gradual changes that lead toward a particular result (2) : a continuing natural or biological activity or function Wikitionary: natural process, A process existing in or produced by nature (rather than by the intent of human beings). For example, volcanic activity and tidal activities. Zachriel
Mung: From the fact that you assert the result is sorted it does not follow that a sort took place. A sort algorithm is not a feature of physics or chemistry. They were unsorted before. Sorted afterwards by observable mechanisms. gpuccio: I pointed to a sorting algorithm as an example of prescriptive complex functional information which can perform a function: the kind of sorting which the algorithm does, which is different from the natural “sortings” that you mentioned. So nature is more elegant. gpuccio: Prescriptive functional information which is complex enough not to be “evolvable” by natural procedures. Human-devised computer languages are fragile, that is, they typically break when mutated; contrary to protein sequences, wherein small changes to sequences often result in small changes to the structure. Zachriel
By the way, even the phrases "natural processes", "stochastic processes" are not correct, strictly speaking. A process is something that has a goal and refers to "processing". There are no goals as such or processing of anything in inanimate nature. EugeneS
"So? It’s clear that human artifacts won’t occur absent humans." Shall I congratulate you on becoming an ID supporter or are you still playing your word games? You sound as if you don't know that it all depends what makes an artifact an artifact and what kind of artifact it is. EugeneS
Zachriel: "You pointed to a sorting algorithm as if sorting was something unique to artificial mechanisms." You don't understand, apparently. I pointed to a sorting algorithm as an example of prescriptive complex functional information which can perform a function: the kind of sorting which the algorithm does, which is different from the natural "sortings" that you mentioned. Prescriptive functional information which is complex enough not to be "evolvable" by natural procedures. It's the complex configuration of bits, finalized to the function, which is the important issue, not the sorting itself. Artificial mechanisms are characterized by that kind of complex and purposeful arrangement of bits. Natural systems have not that property. So, it's not the function itself, but the complexity linked to the function, which is a distinctive property of designed objects. It's strange that, after years of debating ID, you still seem to miss that basic point. gpuccio
Zachriel: The result is sorted, whatever semantic arguments you make. From the fact that you assert the result is sorted it does not follow that a sort took place. A sort algorithm is not a feature of physics or chemistry. Mung
Zachriel:
1) New functions can evolve incrementally...
Evolve how? By natural selection or by design?
The example provided was of a fin evolving into a leg.
There isn't any evidence for that claim nor any way to scientifically test it.
A leg clearly performs a different function than a fin, yet we can show intermediates between the two structures.
The existence of intermediates doesn't mean "naturalselectiondidit".
2) New functions can evolve by recombination.
Great, recombination is a design function. So Zachriel agrees that new functions can evolve by design. We already knew that Virgil Cain
EugeneS: You are not capable of telling a model from reality. Here's gpuccio's argument: "a new, complex function or meaning cannot evolve by gradual steps, simply because the function or the meaning is not present in simpler parts" Our response is that 1) New functions can evolve incrementally because there is often no strict dividing line between a previous function and a new function. The example provided was of a fin evolving into a leg. A leg clearly performs a different function than a fin, yet we can show intermediates between the two structures. 2) New functions can evolve by recombination. As gpuccio used word-evolution as a analogy, we provided the example of the difference between a can and a can-can. An even simpler example is a change in a punctuation mark. https://cybertext.files.wordpress.com/2012/11/baby_seals.jpg Mung: Sorting requires comparison and there is no comparison function in physics or chemistry just as there is no sort function in physics or chemistry. The result is sorted, whatever semantic arguments you make. Zachriel
gpuccio:
We are just using words in different senses. The sorting of a sorting algorithm is different from the natural “sortings” referred to by Zachriel.
:) Perhaps Zachriel does not care for playing word games, but I thought he wrote an entire program for playing with words. Mung
When stars form, or planets, this is not due to sorting of space/matter. That is just an abuse of language. Sorting requires comparison and there is no comparison function in physics or chemistry just as there is no sort function in physics or chemistry. There is no prescription for sequence. The basic idea behind a sort is that of categorization. There is no categorization function in physics and chemistry. sort: to separate and arrange according to kind or class Kind and class or not concepts of physics or chemistry. Mung
Zachriel, You are not capable of telling a model from reality. EugeneS
EugeneS: {non-living} natural processes themselves DO NOT utilize algorithmic control, which includes memory and symbolic representations. So? It's clear that human artifacts won't occur absent humans. EugeneS: Your argumentation is fundamentally flawed. Our argument is @232. Zachriel
Zachriel, I think everybody who has contributed to this thread understands that while natural processes can be modeled algorithmically, natural processes themselves do not utilize algorithmic control, which includes memory, symbolic representations of physical states in memory, and read/write from/to memory to steer systems to goal states. Natural processes at most exhibit the rudimentary function of self-ordering, which is entirely due to the minimal potential energy principle. Organized systems, in contrast, are categorically not explicitly describable in terms of the minimum of potential energy, just like pieces of art, while being physical, are not fully describable in those terms. The exhaustive list of naturally occurring 'mindless' phenomena includes states that exhibit: 1. chaos; 2. order; 3. phase transitions between 1 and 2. Living things exhibit a qualitatively different phenomenon of symbolic representation and control, which is absent from inanimate nature (except where intelligence has instantiated them into physicality). Points 1-3 above are nowhere near to and nothing like symbolic representation and control present only in complex artifacts and in biological life. Therefore the hypothesis that life has an intelligent origin and is consequently itself an artifact, is well empirically warranted. At the same time, an alternative hypothesis that symbolic representations and control have naturalistic 'mindless' origin has no empirical support. Organization =/= order. Your argumentation is fundamentally flawed. EugeneS
gpuccio: The sorting of a sorting algorithm is different from the natural “sortings” referred to by Zachriel. Yes, different sorting mechanisms are, well, different. There are various artificial and natural sorting mechanisms. You pointed to a sorting algorithm as if sorting was something unique to artificial mechanisms. gpuccio: the quicksort algorithm, like any similar algorithm, is based on a complex functional arrangement of bits, which is in no way “natural”: it is the result of intentional intelligent design So is the Mona Lisa. So? Zachriel
Zachriel and Mung: We are just using words in different senses. The sorting of a sorting algorithm is different from the natural "sortings" referred to by Zachriel. We may go on playing with words, or just try to face the true issue: the quicksort algorithm, like any similar algorithm, is based on a complex functional arrangement of bits, which is in no way "natural": it is the result of intentional intelligent design. Water can be purified by evaporation, Zachriel, but are you really arguing that it is the same thing? gpuccio
sort: the arrangement of data in a prescribed sequence Physics and chemistry know nothing of sorting. Mung
Mung: Which sort algorithm do they use? If you mean process, then minerals can be sorted by running water, while water can be purified by evaporation. Zachriel
gpuccio: And do you mean that the code of the quicksort algorithm can evolve from natural processes who have a similar function? No more than many other human constructs won't evolve absent humans. However, nature is full of sorting mechanisms. Zachriel
Zachriel: So do natural processes. Which sort algorithm do they use? Mung
Zachriel: Being subject to criticism is probably the natural condition of everything that exists in the world of phenomena. And do you mean that the code of the quicksort algorithm can evolve from natural processes who have a similar function? Just to understand. gpuccio
gpuccio: And so? It simply means that your argument based on the meaningfulness of a string of letters is subject to criticism. gpuccio: OK, it's probably less beautiful than the Shakespeare sonnet, but it is functional: it sorts inputs. So do natural processes. Zachriel
Mung: Zachriel has always ideas. That's why I like him! I am not joking, he is the only interlocutor from the other side who has discussed with us seriously in this thread, and if I make counter-arguments, he usually responds. OK, usually. And I know his arguments in general, because they are arguments and they do not change abruptly, which is much more than can be said for other personages. OK, Alicia is quite consistent too, at least in her basic ideas, like the concept that we are all idiots. :) gpuccio
I think it's possible to evolve a quick sort algorithm from a slow sort algorithm. :) Not sure what we could evolve to get a slow sort algorithm. Maybe Zachriel has an idea? Mung
EugeneS: Thank you for your ideas. As Zachriel does not seem to like my incursions into language (probably his private realm), I will try to express the same concept with prescriptive information. Here is a C++ version of a common sorting algorithm, quicksort: void quickSort(int arr[], int left, int right) { int i = left, j = right; int tmp; int pivot = arr[(left + right) / 2]; /* partition */ while (i <= j) { while (arr[i] pivot) j--; if (i <= j) { tmp = arr[i]; arr[i] = arr[j]; arr[j] = tmp; i++; j--; } }; /* recursion */ if (left < j) quickSort(arr, left, j); if (i < right) quickSort(arr, i, right); } OK, it's probably less beautiful than the Shakespeare sonnet, but it is functional: it sorts inputs. It is complex functional prescriptive information. Here again, the concept is: you need the whole thing to have the function. While simpler parts may have a sense, they certainly do not sort inputs. The idea is the same: in descriptive information you convey meaning to another conscious observer. In prescriptive information, you generate some object which can do something. A conscious observer, here, is not necessary for the function to work. However, a conscious observer is still necessary to recognize that there is a function acting. In this kind of things, everything starts in consciousness, and everything ends in consciousness. gpuccio
Zachriel: "YOU introduced word evolution. YOU introduced human notions of meaning as a measure of function." And so? Is that a sin? Meaning and function are two aspects of a similar reality: meaning is descriptive information, function is prescriptive information. Complexity applies to both, in the same way. Assigning a purposeful landscape to your examples to generate what you are looking for is design. Concepts are simple, after all. YOU try to make them complex! :) gpuccio
gpuccio: My example was trying to convey the idea that a new, complex function or meaning cannot evolve by gradual steps, simply because the function or the meaning is not present in simpler parts. Missed that. It has to be a new function, rather than a function that becomes more complex over time. Of course, there may not be a strict dividing line between function A and function B, if A evolves into B by gradual change. A fin evolving into a leg may have intermediates, even though a leg has a new function. Furthermore, a new functional structure can be had by concatenation or recombination of other structures — as is certainly the case with word evolution. It's the difference between a can and a can-can. gpuccio: As far as you have to “assign levels of fitness”, you are designing. YOU introduced word evolution. YOU introduced human notions of meaning as a measure of function. Zachriel
GP, "But we can never originate a new, original, complex function" Absolutely! Natural selection is a secondary (non-telic) phenomenon, it cannot create a new function because it merely only selects from among existing functions. It has zero potential to select for a future function. Only a mind in practice has a property to steer events to a goal state. Non-living nature is non-telic while life is. An incredible gap unbridgeable for naturalism! You are absolutely right regarding the necessity to assign in order to create new functions! Zachriel is wrong as usual because he is implicitly closing the epistemic cut by assigning values to variables and controlling the sequence of events for a purpose that he has in mind. He is committing Dawkins' fallacy. EugeneS
Zachriel: I know your position. My example was trying to convey the idea that a new, complex function or meaning cannot evolve by gradual steps, simply because the function or the meaning is not present in simpler parts. You mention landscapes, but all the real observed examples we have of evolution by NS are examples of either simple changes or of optimization of an existing function. Your examples of "verses" evolved by designed software are, at best, irrelevant. As far as you have to "assign levels of fitness", you are designing. NS is a natural, spontaneous process where an existing function, by itself, confers a reproductive advantage in an existing system. Nobody assigns anything to anything. We have already debated the differences between intelligent selection and NS in another thread of mine, https://uncommondesc.wpengine.com/intelligent-design/natural-selection-vs-artificial-selection/ so I will not raise the subject again here. gpuccio
Zachriel: Just because something is functionally complex doesn’t mean there can’t be ancestors, as complexity can be built up over time. No one doubts that intelligent design is capable of building up complexity over time. Mung
Zachriel: If you can assign levels of fitness to words and phrases, then there’s no reason verse can’t evolve Yet we know from looking at the genomes of living species that they can evolve without the need for assigning levels of fitness to the "words" and "phrases" of the genome. Mung
gpuccio: Let’s take the initial verse of my favourite Shakespeare sonnet: “Why is my verse so barren of new pride?” If you can assign levels of fitness to words and phrases, then there's no reason verse can't evolve; e.g., "Why" > "xkw" "my verse" > "verse" These verses were evolved by the patented (not really) Phrasomatic®:
"a cold god soon berates" (23) "short zany theatre began" (25) "what fat agent may stare far" (28) "watery heart so thin beat apart" (31) "what hot and fat breast bears far" (33) "hate began here if a heart beat apart" (37)
gpuccio: If a piece of information is functionally complex (IOWs, if a great nubler of specific beats are necessary to convey the meaning or function implied), then as a rule there is no way to “deconstruct” it in simpler pieces of information with growing function. That is not necessarily correct. It depends on the landscape. Just because something is functionally complex doesn't mean there can't be ancestors, as complexity can be built up over time. At this point, you're supposed to add irreducibility to the mix, but even irreducible structures can evolve, such as by functional migration. Zachriel
bill cole: Thank you! :) You could be interested in this older post of mine about language: https://uncommondesc.wpengine.com/intelligent-design/an-attempt-at-computing-dfsci-for-english-language/ gpuccio
gpuccio Your language analogy is great. Thanks. It is interesting that the sequential space of language can be represented by the same mathematical equation for DNA and proteins. S=N^P S-Sequential space of a protein or sentence N-Numbers of letters available or amino acid types P-Length of the sequence or total amino acid count Alternative splicing also seems to follow the same math except you replace the amino acid with an exon in the above equation. bill cole
gpuccio @220
In a complex function, the specific function arises from the whole complexity: it cannot be found in partial pieces of it.
Very insightful. Dionisio
gpuccio @218
The sequence of a protein gene is a form of “hard” information, while epigenetics is about the procedures which can read that information in many different ways. Epigenetic procedures are certainly an extremely strong argument for design. The only problem is that they are so complex that we still don’t understand them as much as would be necessary to discuss how they originated, or how they differ in different species and different cell types. But we are making great progress, daily.
Very insightful. Dionisio
Adding to those short polypeptides would make them longer an unwieldy, ie unable to fold properly.
Hmm.. No! Titin is the largest known protein with 34,350 amino acids.It is the third most abundant protein in muscle. It has no problem unfolding at 30 pico-newtons (3e-11N)and folding at 2 pico-newtons. (2e-12 N)
Hmm.. Pfft. Titin is an existing protein doing exactly what it was intelligently designed to do. And there isn't any evidence that Titin evolved via NS, drift and neutral changes, from smaller sequences. There isn't any way to test the claim. Virgil Cain
Me Think:
Protein Domains are the evolutionary building blocks of all Proteins.
So you can't show that Titin evolved by incrementally adding on to a small protein. And yes, a common design expects repeat domains. Virgil Cain
Zachriel and others: My general point about deconstruction of complex digital information is very simple. If a piece of information is functionally complex (IOWs, if a great nubler of specific beats are necessary to convey the meaning or function implied), then as a rule there is no way to "deconstruct" it in simpler pieces of information with growing function. Let's take the initial verse of my favourite Shakespeare sonnet: "Why is my verse so barren of new pride?" It is a beautiful verse, a deep and moving verse. It conveys a lot. Now, let's consider the following hypothetical verse: "I have made a new error in copying that verse today" OK, we could rightfully consider this verse an intermediary form of our first verse, at sequence level. Why?, Because it contains some homologous pieces of sequence: "new" and "verse". But the question is: does verse 2 represent, in any way, a step to verse1, in the sense of meaning? And the simple answer is: absolutely not. There is absolutely nothing, in verse 2, of the meaning which is conveyed by verse 1. Not even a small piece of it. That's what I mean when I say that complex functions cannot be deconstructed into simpler functional pieces. In a complex function, the specific function arises from the whole complexity: it cannot be found in partial pieces of it. That's why we can, at most, describe pathways of optimization os osme functiona which already exist, by simple transformations. In some cases, that can be done. But we can never originate a new, original, complex function by randomly transforming simpler functional pieces of information. The concept should be simple, but unfortunately years of dogmatic reasoning seem to obstruct simple realistic reasoning in many otherwise intelligent minds. gpuccio
Me_Think: "Arbitrary examining a part of AA and claiming information jump without understanding that shorter sequence with favorable 3d structure can evolve is not scientific." Not sure that I understand your point, if you are making a point. Are you saying that we cannot reason scientifically on AA sequences? I certainly don't deny the importance of £d structure, when we have data about it, but what does that have to do with the reasoning here? A lot of evolutionary reasoning can be done on sequences, even if the 3d structure is not known. Variation at the genomic level knows nothing of the 3d structure: it just acts on the sequence. NS, obviously, selects the function, and structure os certainly important for that. But the simple point is: are you denying that a sequence which is highly conserved should be considered under purifying selection, even if we don't know the related structure? Because, you see, that is my point. And can you deny that a complex and specific sequence has functional restraints at the sequence level? Otherwise, why would it be conserved, in spite of neutral variation occurring all the time? And can you deny that, to get to some specific sequence through an evolutionary path implying positive selection, you need functional intermediaries at sequence level? Which should be detectable by homology? As I said, I am not sure I see your point. gpuccio
bill cole: "What role if any might alternative splicing have had in the protein sequence variation especially in the vertebrate differences?" The discussion here was about the genomic sequence. Alternative splicing is about how the same sequence can be used in different ways by slightly different transcription and post-transcriptional regulation. The sequence of a protein gene is a form of "hard" information, while epigenetics is about the procedures which can read that information in many different ways. Epigenetic procedures are certainly an extremely strong argument for design. The only problem is that they are so complex that we still don't understand them as much as would be necessary to discuss how they originated, or how they differ in different species and different cell types. But we are making great progress, daily. gpuccio
Virgil @ 216
LoL! Titin is an existing protein.
You are right !!!
Please demonstrate that it evolved by incrementally adding on to a small protein. Or shut up about it.
Protein Domains are the evolutionary building blocks of all Proteins. If interested, study 'Repeat domains' research by D G Higgins, S Labeit, M Gautel, T J Gibson, Abigail S McElhinny, Steven T Kazmierski, Siegfried Labeit and Carol C Gregorio Me_Think
LoL! Titin is an existing protein. Please demonstrate that it evolved by incrementally adding on to a small protein. Or shut up about it. BTW, once again your "response" did no such thing- ie it didn't address what you were responding to. Virgil Cain
Adding to those short polypeptides would make them longer an unwieldy, ie unable to fold properly.
Hmm.. No! Titin is the largest known protein with 34,350 amino acids.It is the third most abundant protein in muscle. It has no problem unfolding at 30 pico-newtons (3e-11N)and folding at 2 pico-newtons. (2e-12 N) Me_Think
Zachriel: Design Descent points to supposedly unbridgeable gaps, but when those gaps are filled, it either points to the two new gaps, or simply points elsewhere. This is false. DD posits a way to bridge gaps. Mung
MT:
You seem to have no idea of Protein structure.
Nice projection as that is all yours. Most proteins require at least one chaperone to reach their functional structure. The proteins that do not are short. Adding to those short polypeptides would make them longer an unwieldy, ie unable to fold properly. Virgil Cain
If Me_Think is arguing that sequence doesn't determine the positioning of the atoms I agree. Mung
Virgil @ 206
Buried under all of the new sequences that were added to the existing polypeptide. It would be inaccessible because it would be buried.
You seem to have no idea of Protein structure. Let’s take a short protein ' ABO' . There are about 2162 atoms with 3D Coordinate system as follows: {{1853.2 pm,4590.3 pm,1048.8 pm},{1930.7 pm,4482.5 pm,980.4 pm},{1861. pm,4429.6 pm,855.4 pm},{1923.6 pm,4418.4 pm,750.3 pm},{1956.4 pm,4366.9 pm,1076.7 pm},{1896.5 pm,4236.5 pm,1031.5 pm},{1813. pm,4150. pm,1164.6 pm},{1711.6 pm,4031.9 pm,1068.7 pm},,{328. pm,6439.7 pm,4331. pm},{222.6 pm,6492.3 pm,4243.9 pm},{275.4 pm,6561.1 pm,4118.7 pm},{199.8 pm,6628. pm,4047.7 pm},{148.2 pm,6589. pm,4336. pm},{259.8 pm,6644.6 pm,4418.9 pm},{337.5 pm,6519.6 pm,4454.8 pm}} The Corresponding Atom types are: {N,C,C,O,C,C,S,C,N,<>,C,C,N,C,C,O,C,C,C} Let’s see the Atom types of SP1 residue: {,[Alpha],,,[Beta],[Gamma],[Delta],[Epsilon],[Zeta],[Eta]1,[Eta]2,[Alpha],[Beta]2,[Beta]3,[Gamma]2,[Gamma]3,[Delta]2,[Delta]3,[Epsilon],11,12,21,22,1,2,3} We get the following Alpha- Carbon Atoms from the above residue: {[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha],[Alpha]} Based on the alpha-carbon positions protein backbone can be rendered: http://s14.postimg.org/3nct08plt/protein_Backgrd.png Atom occupy space around this backbone according to their Van Der Waals Radius. So there is no where that a sequence will ‘bury’. Me_Think
Virgil, you have the right idea. Darwinian GA's are such an oversimplification they are more like child's toys. With enough imagination they may look like the real thing, but to those who know better it is childish to believe that. GaryGaulin
mung: Somehow, magically, evolution just knows that they are intermediates and therefore they ought to be selected. Um. No. You are confusing evolution with ID. velikovskys
EugeneS: GAs are a search heuristic whereas NS is not even a search. And as you said you said GAs actively search for and direct secondary solutions towards a final solution. Neither natural selection nor drift is anything like that. Natural selection is like "did you survive? If 'yes', no problem, carry on." Virgil Cain
Virgil Cain #204, Absolutely. GAs use (typically explicit) sophisticated and finely controlled fitness function as well as heuristic search based on the human expertise of solving previous problems. Algorithmic control allows measuring the gradient of solution quality and finely controlling it. The key distinction between artificial and natural selection is that the level of sensitivity of the former is greatly higher than that of natural selection. It is a distinction between fine active control, on the one hand, and eliminative coarse passive control, on the other. EugeneS
Buried under all of the new sequences that were added to the existing polypeptide. It would be inaccessible because it would be buried. Virgil Cain
Virgil Cain @ 202
If that core is buried and cannot be reached it would be useless. Your response doesn’t even address what I said.
Buried where? Why would it be inaccessible ? Me_Think
Gary:
Genetic level intelligent causation would rapidly converge on solutions as is exemplified by the problem solving power of cognitive algorithms (i.e. David Heiserman, Beta and Gamma class machine intelligence).
True. I just love shoving genetic algorithms in the faces of evos as they actually think they support Darwinian evolution just cuz someone said they mimic natural selection. Of course anyone with any reasoning abilities can see GAs do not utilize blind and mindless processes- natural selection is both blind and mindless. Typically most evos cannot make that connection Virgil Cain
Zachriel:
Design Descent points to supposedly unbridgeable gaps,
Cuz you say so? Really? Seems they were bridged, by DESIGN. Virgil Cain
MT:
No if the ‘functioning substrate’ is in a hydrophobic core,
If that core is buried and cannot be reached it would be useless. Your response doesn't even address what I said. Virgil Cain
gpuccio: Wgìhat I mean is simply that those intermediaries do not exist for complex functions. Design Descent points to supposedly unbridgeable gaps, but when those gaps are filled, it either points to the two new gaps, or simply points elsewhere. Zachriel
Zachriel: I said: "I always say: complex functional digital information cannot be deconstructed into simpler functional steps, each of them increasingly functional, which may gradually “build” the final result." You commented: "You may keep saying it, but it’s clearly wrong. If there are selectable intermediaries, then evolution will rapidly converge on the solution." But you have misinterpreted my statement. I don't mean that, if there were selecrable intermediaries, evolution would not converge. Wgìhat I mean is simply that those intermediaries do not exist for complex functions. That is the meaning of my statement: "complex functional digital information cannot be deconstructed into simpler functional steps". gpuccio
Virgil Cain:
3- Intelligent design evolution would rapidly converge on solutions as is exemplified by the problem solving power of genetic algorithms.
Not all that bad. But to be more precise and informative I would say: Genetic level intelligent causation would rapidly converge on solutions as is exemplified by the problem solving power of cognitive algorithms (i.e. David Heiserman, Beta and Gamma class machine intelligence). Rodney Jr. demonstrates Beta level Machine Intelligence https://www.youtube.com/watch?v=R_2WAwZtMCQ http://cyberneticzoo.com/cyberneticanimals/1979-rodney-self-programming-robot-david-l-heiserman-american/ http://tnewton.solarbotics.net/robot1.html Some of my models: http://intelligencegenerator.blogspot.com/ GaryGaulin
Virgil @ 189
What allows that to happen? Why wouldn’t the functioning substrate be buried under the newly added segments rendering the polypeptide totally useless?
No if the 'functioning substrate' is in a hydrophobic core, it will be functional, which is why examining the 3d structure and atom position of sequence is important. For Eg, if we examine the KLKB1 protein data, the atom positions are: {{3931.5 pm,3311.3 pm,491. pm},{3817.8 pm,3403.5 pm,490.7 pm},{3715.7 pm,3346.3 pm,390.4 pm},{3749.9 pm,3321. pm,273.3 pm},{3867.5 pm,3545. pm,443.3 pm},{3973.3 pm,3602.9 pm,540.7 pm},{3745.2 pm,3638.9 pm,426.4 pm},{3926. pm,3644.3 pm,680.7 pm},<>,{6258.4 pm,4759. pm,2861.7 pm},{6341. pm,4691.5 pm,2959.9 pm},{6408.4 pm,4810.3 pm,3026.6 pm},{6473.2 pm,4889.5 pm,2955.2 pm},{6445.5 pm,4602.7 pm,2892.6 pm},{6392.5 pm,4527.4 pm,2783.6 pm},{6299.9 pm,4778.3 pm,2775.9 pm},{6303.2 pm,4501.6 pm,2812. pm}} Arbitrary examining a part of AA and claiming information jump without understanding that shorter sequence with favorable 3d structure can evolve is not scientific. Me_Think
Hi Gpuccio Very interesting post. I think you have successfully supported your thesis with evidence that intelligent cause may have been involved in the gene sequencing that lead to the differences in these proteins. While as Gary said, because of a lack of a mechanism this might not really qualify as a theory it certainly is a valid inference. What role if any might alternative splicing have had in the protein sequence variation especially in the vertebrate differences? bill cole
Zachriel:
If there are selectable intermediaries, then evolution will rapidly converge on the solution.
1- If pigs could fly... 2- Natural selection is eliminative and survival is the only solution- so it is solved just by living 3- Intelligent design evolution would rapidly converge on solutions as is exemplified by the problem solving power of genetic algorithms. 4- Yes variants of/from a designed archetype protein would form a phylogeny, a nice branching pattern Virgil Cain
Zachriel: If there are selectable intermediaries, then evolution will rapidly converge on the solution. Somehow, magically, evolution just knows that they are intermediates and therefore they ought to be selected. Um. No. Mung
gpuccio my friend, it's almost enough that the 'critics' agree with you that their mechanism can't get to 600 bits in large jumps. But I fear that if you were arguing that you could not possibly have large jumps like that they would argue against it. :) Keep blasting them! Perhaps find additional proteins involved in vertebral development. Mung
Zachriel: It predicts fossils with traits common to the ancestor and descendant. Fantastic. But we're talking sequences. Nucleotides or amino acids. Mung
Mung: But it can’t predict them, so it’s not scientific. It predicts fossils with traits common to the ancestor and descendant. gpuccio: An important point on which we may probably agree is that design and neo darwinian evolution point ad different scenarios, even if some aspects could be similar. You posited Designed Descent, so it will show a phylogeny by definition. We're trying to distinguish between the hypotheses of Biological Descent and Design Descent. A commenter at the Skeptical Zone once argued that the phylogeny alone could make this distinction. The counterexample was a tree that may branch naturally, forming a perfect phylogeny, but is pruned to create a design. Try to address the specifics @182. http://40.media.tumblr.com/299720b891b0396fffcdd65b24d69b15/tumblr_mocl4lllra1rw872io2_500.jpg gpuccio: I always say: complex functional digital information cannot be deconstructed into simpler functional steps, each of them increasingly functional, which may gradually “build” the final result. You may keep saying it, but it's clearly wrong. If there are selectable intermediaries, then evolution will rapidly converge on the solution. Zachriel
VC @ 190
All similarities are homologs to you because you cannot think beyond Common Descent.
My ass and a hole in the wall has a common homolog if one cannot think beyond common descent. Their arguments are not persuasive. And they're all gonna die anyway. It's beyond tedious, handling their idiotic ideology. mike1962
Alicia Cartelli:
If we had the genome sequences of the numerous species that existed early in vertebrate evolution between the agnathans and the chondricthyes, I’d wager that we would find homologs...
All similarities are homologs to you because you cannot think beyond Common Descent. Virgil Cain
MT:
What stops them from evolving in smaller segments over time?
What allows that to happen? Why wouldn't the functioning substrate be buried under the newly added segments rendering the polypeptide totally useless? Virgil Cain
Zachriel:
While it is certainly possible that particular gaps may have been due to Intelligent Intervention, there’s no evidence to support the claim, and substantial evidence that natural mechanisms are sufficient.
Design is a natural mechanism. and there isn't any evidence that natural selection, drift and neutral construction are capable. There isn't even any way to test the claim that they are capable. It is a vacuous and sterile claim. Virgil Cain
Mung: The absence of true naturally selectable molecular intermediates in natural history is one of the strongest arguments against neo darwinian theory. I have been discussing that point for years, but obviosuly neo darwinists in the end can always backpedal to the non scientific point that "they are extinct", or "they have been eaten" (as one of them once answered to my argument, maybe Felsenstein if I remember well). I always say: complex functional digital information cannot be deconstructed into simpler functional steps, each of them increasingly functional, which may gradually "build" the final result. This is not true as a general rule, and indeed it is not true even in single known cases. While this is obvious for complex functional objects as language and software, neo darwinists believe that for protein sequences, or in general biological information, the opposite may be true. Such a faith is based only on the desire to confirm a theory which has no reasonable support from facts, ans is maintained against fact only by appealing to what we still don't know and could some day discover. The simple fact is that positive selection, which should be the "great master" of neo darwinist evolutionary theory, is practically a ghost: the only realistic examples of it are those few cases of molecular microevolution of one (two at most) AA variations in organisms at very high reproduction rate (phages, bacteria, malaria parasites) under very strong selection pressure (like antibiotics). Positive selection is often posited (as Zachriel would say), and rarely observed. So, the "grand master" of neo darwinian evolution is indeed an absconder. Without positive selection, all neo darwinian theory is obviously beyond any possible credibility: a concept which seems to be ignored by the fans of neutral theory and of genetic drift, who are right in believing that selection is almost never positive, but don't understand that neutral or quasi neutral selection and genetic drift are irrelevant in modifying the probabilistic barriers which are evidence of the designed origin of biological information. gpuccio
Zachriel: You describe with honesty your point of view, and I appreciate that, although as you know I think differently. An important point on which we may probably agree is that design and neo darwinian evolution point ad different scenarios, even if some aspects could be similar. One objection often made to ID theory is that, in principle, a designer could design in any possible way, and therefore ID would be not falsifiable. But this is only a gross misunderstanding. Indeed, ID theory is not so much the theory that biological objects are designed, but rather the theory that biological objects exhibit clear properties which allow us to detect design by scientific inference. IOWs, while a designer could design without information gaps and without generating complex functional information, in those cases the design would not be detectable, and ID theory could not be applied. ID theory can be applied only to objects which exhibit complex functional information, and which cannot be explained by known natural algorithms. That's why the analysis of biological objects, like proteins, from an ID point of view, looks at high information and to information gaps: those two aspects allow an objective design detection. gpuccio
Me_Think: Just for clarification: If I blast a sequence of, say, 300 AAs, shorter homologies are found just the same, if they exist and if they are significant. I hope that answers your question. gpuccio
Zachriel: Biological Descent, however, posits the past existence of intermediates. But it can't predict them, so it's not scientific. Alicia, and now you, claim these intermediate sequences existed, but you can't tell us what they looked like so we can go search for them. Instead we are left with an assumption that lacks any actual content. Mung
"Experiments in silico also support theories of complex adaptation." They support the design hypothesis. Simply because they are done with intent. The more complex the desired result is, the more sophisticated and finer control it requires. EugeneS
gpuccio: “By the way, if I were like Alicia Cartelli I could simply argue that the data from extinct species would definitely support ID theory.” Let's consider the two hypotheses: Yours is sort of Design Descent, characterized by large, sudden jumps. The standard theory is Biological Descent with modification. Both hypotheses would predict a phylogeny of sorts. Biological Descent, however, posits the past existence of intermediates. While you might say Design Descent also posits intermediates, it can't say which intermediates should have existed. It points to gaps, but when those gaps are filled, it either points to the two new gaps, or simply points elsewhere. Biological Descent also can look to specific evidence in nature; the observations of • heredity • natural selection • natural variation • extinction The fossil evidence, in many cases, supports adaptation through natural selection, showing the efficacy of the mechanism; while molecular evidence shows how small variations in genes can lead to significant and relevant changes in morphology. Experiments in silico also support theories of complex adaptation. While it is certainly possible that particular gaps may have been due to Intelligent Intervention, there's no evidence to support the claim, and substantial evidence that natural mechanisms are sufficient. http://3.bp.blogspot.com/-jUU9FDeJBpw/Uko0LLj09eI/AAAAAAAAAC8/EwzBLu5WN8s/s1600/2001-a-space-odyssey-ape-monolith.jpg Zachriel
Mung @ 177: I guess it's possible to be too idiotic in a playground for idiots. Who knew? RexTugwell
Actually, in all honesty I think Alicia's argument has worth if there is at least one example of a fully reconstructed evolutionary path from A to B via some extinct fossilized intermediates, with monotonic increase of information. At least one can then appeal to analogy. Are there such examples that are fully documented, reliable and undisputed by a majority of specialists? EugeneS
Why should protiens evolve as a whole sequence? What stops them from evolving in smaller segments over time? Have you blasted, say, 'B2016020865RTHXAJ40' ? Me_Think
Mung: Is it narcissistic to repeat oneself? OK, I will do it: "By the way, if I were like Alicia Cartelli I could simply argue that the data from extinct species would definitely support ID theory." gpuccio
AC: Either come up with something intelligent or you will be re-relegated to the “too idiotic to respond to” category. LoL. And I just couldn't possibly bear that. What's next? If I don't behave you're going to make me eat ice cream? Mung
How clueless are you Mungy? "A protein involved in development of the spine evolved early during the evolution of organisms that first had spines" doesn't seem like much of a leap to me. If we had the genome sequences of the numerous species that existed early in vertebrate evolution between the agnathans and the chondricthyes, I'd wager that we would find homologs to human Prickle 1 with lower bit scores, and hence less of the jump that pucci is so obsessed with. But we don't have these sequences (conveniently for pucci) because these species are long extinct. You do not need to have complete or even close to complete sequence conservation in order to maintain the function of a protein. The ancestor would be some protein with partial sequence conservation, enough to carry out partial function of the protein as we know it today. Either come up with something intelligent or you will be re-relegated to the "too idiotic to respond to" category. Alicia Cartelli
Alicia can call me Mungy if she wants, as long as she doesn't take to calling gpuccio poochy. :) You have to admire Alicia. She doesn't know how it happened, but she knows when it happened. Right there where there's no evidence for it, that's when it happened! Protein evolution of the gaps. Mung
Alicia Cartelli: …like look for the evolution of a protein everywhere except where the protein is most likely to have actually evolved? Where did the protein most likely evolve and how do you calculate that likelihood? Also, I asked earlier and will ask again, what do you propose as the ancestor? It's ok to say: "I don't know." Really. Mung
Off topic: Please, see the posts @2 & @3 in the following link - do they really point to an error in the referenced paper? Thanks. https://uncommondesc.wpengine.com/peer-review/can-too-much-publishing-be-bad-for-science/#comment-595947 Dionisio
Comment #168 was just a gratuitous waste of electrons. RexTugwell
RexTugwell:
GaryGaulin, no one cares about your version of “ID Theory” so please give it a rest.
Quite actually the opposite is true: http://www.umc.org/news-and-media/denial-of-gc2016-booth-sparks-protest#comment-2499865149 You have no idea how foolish you look to those you have been claiming to speak for. P.S. all comments to the article must first be approved, anonymous posters are not allowed, therefore attempting to spam what I wrote will only make Methodists even more angry at you. It's in many more places than that anyway, and doing very well in both science and religion. GaryGaulin
"A real scientific journal?" You mean a crackpot Darwinist rag pretending to be a scientific journal. Mapou
"intelligent beings can certainly do non intelligent things" ...like look for the evolution of a protein everywhere except where the protein is most likely to have actually evolved? Yeah, you'd never be able to publish in a real scientific journal, but maybe BioComplexity will take you! Alicia Cartelli
jerry: The forces that produced this phrase in an example of how an intelligent cause works. The pressing of the keyboard symbols is an intelligent process. So you're saying the designer of life typed it out on a keyboard. How was the output of the keyboard converted into a biological form? Zachriel
Mung: "You just don’t have enough imagination." That's why I have not become a famous science fiction writer, which was one of my aims when I was young! gpuccio
jerry: Thank you for your contribution. Your pet rat was certainly intelligent in some measure, but his walk on the keyboard was not intelligently aimed at erasing your document (at least I hope so! :) ). Similar things happen with my cats, who are certainly very intelligent! OK, the point is: intelligent beings can certainly do non intelligent things (see Alicia Cartelli :) ) gpuccio
RexTugwell: Thank you for expressing so clearly what I think of GaryGaulin's theory. gpuccio
You have not scientifically explained how “intelligent cause” works
The forces that produced this phrase in an example of how an intelligent cause works. The pressing of the keyboard symbols is an intelligent process. Why a scientific explanation is necessary is beyond me. Intelligence as an explanation for an event is usually where the event cannot be explained as a result of the four basic forces of physics such as the pressing of keyboard symbols to effect a response from some unrelated entity. We once had a pet rat who we let loose on our desk. It proceeded to walk on the keyboard and erased a document we were working on. Now is that intelligent? My guess not. This rat was fairly smart and we taught it to do some fun things. jerry
GaryGaulin, no one cares about your version of "ID Theory" so please give it a rest. RexTugwell
gpuccio:
By the way, if I were like Alicia Cartelli I could simply argue that the data form extinct species would definitely support ID theory.
What "ID theory"? You have not scientifically explained how "intelligent cause" works, therefore you do not have an "ID theory". GaryGaulin
A -> B 600 bits A -> [missing sequence data] -> B 600 bits It's still 600 bits. Also, we're talking about a conserved sequence aren't we? So it's a reasonable inference that if it was present in the "missing intermediates" that it was also conserved there. Certainly more reasonable than ad hoc speculation with no supporting facts. Does Alicia care to at least speculate about the alleged ancestral sequence A and at least one supposed transitional sequence A', or are we just supposed to join her in wishful thinking? gpuccio, you'd never get published in a real science journal. You just don't have enough imagination. Mung
gpuccio:
The shameful manipulation by Alicia Cartellli (and apparently supported by you) is that, not having any observed data in favor of her theories, she assumes that such data could be found in extinct species if only we had those data available. And then she accuses Mung and me of having an untestable hypothesis (us!), because we base our hypothesis on existing data and not on non existing data, while she bases hers on imagined non existing data, and not on existing data.
You are the one sifting through the mountains of evidence for common descent, for anything that will make all the evidence against you seem to magically vanish. GaryGaulin
Oh Rexy, UD is just a playground for idiots and I treat it as such. Get over yourself Alicia Cartelli
Alicia, your use of cutesy names like pucci and mungy betrays an impotent fury that's just sad to watch. Whatever the reason for your bitterness, you should grow up. RexTugwell
Ignoring the fact that your experiment doesn't actually test your hypothesis? Another hallmark of "ID science." Good chat pucci. Alicia Cartelli
Ah, wonderful! Alicia Cartelli has gone back to merely stating platitudes, so I can go back to not discussing with her. gpuccio
mike1962: Thank you! :) gpuccio
Yes, let's use sequence data to look at the evolution of a protein, when there is no sequence data from the time that the protein evolved. Flawless logic. I can sleep easy knowing that's what "ID science" amounts to. Alicia Cartelli
gpuccio, thank you for your good work and patience. mike1962
Dionisio: An important point which should remain from this discussion, beyond the picturesque distractions provided by some, is that even in the protein coding part of the genome there are many sequences which are probably functional, which are probably regulatory, and which are at present not understood in terms of structure and specific function, and scarcely analyzed in terms of conservation and evolutionary history. Many of these sequences, IMO, could be interpreted in terms of what I have called 2b): functional sequences which can be very different in different sets of organisms, for functional reasons. gpuccio
Mung: I must really thank you for your contributions and for your company here. Your attitude is very positive, and you really don't deserve the infamous comments made by some here. gpuccio
Dionisio: I am very satisfied of the discussion, for its contents, if not for its tone. I believe that we must definitely go on bringing the discussion into biology, because ID is a precious tool to look at biological data and try to understand them. Neo darwinists definitely don't like that, and this thread is a good demonstration of this simple fact. gpuccio
Alicia Cartelli's post #146 obviously does not deserve any comment, but I invite all to read it and to judge for themselves. gpuccio
GaryGaulin: Mung is very serious and very reasonable. The shameful manipulation by Alicia Cartellli (and apparently supported by you) is that, not having any observed data in favor of her theories, she assumes that such data could be found in extinct species if only we had those data available. And then she accuses Mung and me of having an untestable hypothesis (us!), because we base our hypothesis on existing data and not on non existing data, while she bases hers on imagined non existing data, and not on existing data. A commendable scientific attitude indeed! Do you support that attitude? Please, take your responsibilities. By the way, if I were like Alicia Cartelli I could simply argue that the data form extinct species would definitely support ID theory. Well I do think that, but being serious (at least I hope) I have never made that argument. Why? Because nobody can seriously base his scientific arguments on data which are not available, imagining that those data would support his theory. gpuccio
gpuccio @139 Definitely I'm interested in the concepts explained in your OP and in your follow-up comments within this discussion thread. The papers you linked @127 are good illustrations of your OP concept 2b) which is fundamental to the important topic discussed here. Please, note that my comments @135 are intended to share the thoughts on that this highly important discussion just scratches the surface of the challenges science faces in the understanding of what's going on in biology. Some folks could believe that this discussion could resolve many remaining issues that hinder our full understanding of the biological complex complexity. That seems very far from reality, to say it nicely. The technical level of this discussion makes it harder for me (and perhaps a few others?) to understand it right away, but your detailed explanations with pertinent links and clear illustrations (plus the scary shark image presiding the OP) makes it easier to digest, assuming we try our best to understand it correctly. I'll be glad to see more of this kind of technical OPs in this forum. But with less of the distracting nonsense trolling that seems attracted to trying to derail the otherwise serious discussions. However, looking at the bright side of every situation, perhaps an unintended benefit of those annoying posts is the (sometimes) entertaining side of them. :) Dionisio
Oh pucci, I already explained that my choosing of homologs was random, and that any other random combination would have made my point. There are a whole bunch of different prickle-like protein genes in a whole bunch of species. In the end, as I already said, your "jump" in bit score occurs over some 50-100 million years, in species of which we have no sequence information. How convenient. You've come up with an untestable hypothesis. Congratulations. That is, unless mungy has a time machine he's not telling us about. Alicia Cartelli
Mung demands:
Produce the missing sequence data. Please.
If Mung is serious then (along with all else they have said in other threads) their demand for sequence data from all of the long gone living things that ever existed only leads to the conclusion that Mung is mentally ill. GaryGaulin
Mung: Alicia Cartelli is fully responsible of the followings sins: a) Cherry picking: as demonstrated #138 b) Intentional manipulation of the discussion: presenting her cherry picking without explaining in any way the methodology used, with the clear intention of suggesting a conclusion. c) Pitiful manipulation of the evolutionary theory itself: at post #112 she attributes a 600 bit homology between shark and humans to "convergent evolution", a concept which strangely is not restated in the following discussion, after my rather strong objections (including a desperate invocation to Popper). d) Further pitiful manipulation of the evolutionary theory, of scientific reasoning, and of the concept of chronological causation itself: in the last series of posts, she uses the range of homologies observed in vertebrates (from bony fishes on) to argue that there exists a reasonable evolutionary history of intermediates for the Prickle sequences we are debating, while all those homologies appear after the first appearance of our sequences (both the one in Prickle 1 and the one in Prickle 2) in cartilaginous fishes. She should be aware that usually a cause must precede an effect in a scientific explanation, and that the existence of a full range of homologues after the appearance of the functional sequences, while there is none before, is very strong evidence in favour of my interpretation, not of hers. OK, are those enough "present sins", for the moment? By the way, just as an aside, you may have observed that most of the different homologues which are observed in vertebrates fall grossly in three ranges of homology level: a) Two "high level" sets of homologues, let's say 500 - 700 bits and 300 - 450 bits), which can be explained as alignments of Prickle 1 like sequences with Prickle 1 like sequences (the first set) and Prickle 2 like sequences with prickle 2 like sequences (the second set). One "lower level" set of homologies (100 - 150 bits), which can be explained as cross alignments of Prickle 1 like sequences with Prickle 2 like sequences. As I have tried to explain in my posts #127 and #138. gpuccio
Oh of course Mungy, let me just jump in my time machine. Or were the jawless fish sequencing their own genomes 400 million years ago? Alicia Cartelli
Alicia Cartelli:
In the end, your argument is simply one of the gaps, because you take advantage of the 50-100 million years or so of missing sequence data...
Produce the missing sequence data. Please. Mung
My point was that there are many other homologs to the 2nd "region" ("domain" is commonly used colloquially to refer to a wide variety of protein regions, characterized or uncharacterized) of the prickle 1 protein, homologs which you were ignoring. So yes, the homologs I reported did not need to be specific, I could have picked any random combination from any of those species and gotten the idea across. You however, specifically picked the highest bit score, and ignored anything else. The bit score for the human prickle 2/C. milii prickle-like protein 2 is 464, a significantly smaller jump than what you chose to show, and which also suggests evolution through gene duplication took place. In the end, your argument is simply one of the gaps, because you take advantage of the 50-100 million years or so of missing sequence data between the extant jawless fish and the the earliest chondricthye lineage still living today. Alicia Cartelli
Alicia Cartelli has a real future as a cherry-picker. Mung
Dionisio at #135: Thank you, as always, for your observations. I think you can be interested in the different contributions of Prickle 1 and Prickle 2 (and other forms) to epigenetic regulation, for example as outlined in the paper I linked before: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427563/ where we can see that Prickle 1 and Prickle 2 have different cellular localizations during the regulation process. The idea that such specific tasks may be based, at least in part, on the differences between their "second part" is really appealing. That's what I mean with my 2b) category: differences in sequence between otherwise similar proteins which are the expression of differences in function. gpuccio
To Alicia Cartelli at #129: "And for the last time, none of my BLASTs are wrong, unlike yours." OK. Here is what you wrote in your post #104:
Bit score Species 107 Fundulus heteroclitus 130 Danio rerio 147 Alligator mississippiensis 165 Chrysemys picta bellii 294 Oryzias latipes 314 Ophiophagus Hannah 384 Esox Lucius 446 Salmo salar 480 Poecilia Formosa 516 Haplochromis burtoni 563 Clupen larengus (all vertebrates)
No comments, no explanations. So, you are offering 11 blasts of vertebrates, presumably representing a growing set of similarities with the sequence. Anybody can see that the bit scores are in ascending order. Now the question is, as you give no explanations regarding your methodology, we should assume that you used some consistent methodology to get those results. Let's se: 1) Fundulus heteroclitus: First hit: 481 bits Second hit: 318 bits Third hit: 317 bits Fourth hit: 107 bits You choose the fourth hit 2) Danio Rerio: First hit: 453 bits Second hit: 453 bits Third hit: 452 bits Fourth hit: 451 bits Fifth hit: 377 bits Sixth hit: 376 bits Seventh hit: 130 bits You choose the seventh hit 3) Alligator mississippiensis: First hit: 772 bits Second hit: 772 bits Third hit: 771 bits Fourth hit: 157 bits Fifth hit: 157 bits Sixth hit: 147 bits You choose the sixth hit 4) Chrysemys picta bellii: First hit: 775 bits Second hit: 165 bits You choose the second hit 5) Oryzias latipes: First hit: 477 bits Second hit: 295 bits Third hit: 294 bits You choose the third hit 6) Ophiophagus Hannah: First hit: 314 bits You choose the first hit 7) Esox Lucius: First hit: 455 bits Second hit: 384 bits You choose the second hit 8) Salmo Salar: First hit: 446 bits Second hit: 429 bits Third hit: 374 bits Fourth hit: 119 bits You choose the first hit 9) Poecilia Formosa: First hit: 480 bits Second hit: 323 bits Third hit: 323 bits Fourth hit: 118 bits You choose the first hit 10) Haplochromis burtoni: First hit: 516 bits Second hit: 327 bits Third hit: 85.5 bits Fourth hit: 85.5 bits You choose the first hit 11) Clupea harengus: First hit: 563 bits Second hit: 397 bits Third hit: 102 bits Fourth hit: 38.9 bits You choose the first hit Ah, what scientifically correct methodology! What honesty! Is it a problem of competence or simply ill faith? Or both? Have a good time. gpuccio
To Alicia Cartelli (#129): So, while I have to thank you for your work as an editor of my data, for the rest I completely disagree with you. You say: "What you’re essentially trying to do is show that there seems to be no intermediate forms for the 2nd domain of the prickle protein." Either you don't understand or you don't want to understand. What I am trying to do is to show: a) that the second part (Mung is right, it is not recognized as a domain) of the Prickle 1 protein has a sequence which is highly conserved from sharks to humans (can you deny it?), and therefore reasonably already present in the common ancestor of those two lines. b) that this conserved sequence has no detectable intermediate forms before the split between cartilaginous fishes and bony fishes (and therefore humans). Can you deny that? So, if you cannot deny either a) or b), all the rest of your "arguments" is useless. And I will happily stick to my "obsession". Moreover, with your help, we have demonstrated that: 1) The same can be said, in very similar terms, for the Prickle 2 protein. By the way, this "blue part" of the human Prickle 2 protein gives absolutely no hit either in Cephalochordata or in Tunicata, so we can all be happier. And, obviously, no significant hits in Drosophila, C. elegans or fungi or prokaryotes. You can check, and if you find other errors, I will be ready to correct myself. Here is the sequence: GSDSSDSAFQNARAKESRRSAKIGKNKGKTEEPMLNQHSQLQV SSNRLSADVDPLSLQMDMLSLSSQTPSLNRDPIWRSREEPYHYGNKMEQNQTQSPLQLLS QCNIRTSYSPGGQGAGAQPEMWGKHFSNPKRSSSLAMTGHAGSFIKECREDYYPGRLRSQ ESYSDMSSQSFSETRGSIQVPKYEEEEEEEGGLSTQQCRTRHPISSLKYTEDMTPTEQTP RGSMESLALSNATGLSADGGAKRQEHLSRFSMPDLSKDSGMNVSEKLSNMGTLNSSMQFR SAESVRSLLSAQQYQEMEGNLHQLSNPIGYRDLQSHGRMHQSFDFDGGMAGSKLPGQEGV RIQPMSERTRRRATSRDDNRRFRPHRSRRSRRSRSDNALHLASEREAISRLKDRPPLRAR EDYDQFMRQRSFQESMGHGSRRDLYGQCPRTVSDLALQNAFGDRWGPYFAEYDWCSTCSS SSESDNEGYFLGEPIPQPARLRYVTSDELLHKYSSYGLPKSSTLGGRGQLHSRKRQKSKN CIIS 2) The only weakly significant hit that I had found before the split (in Cephalochordata) was only an error of mine, as you kindly have pointed out. So, you an keep your ideas, and I will keep mine. Others can judge for themselves. gpuccio
To Alicia Cartelli (#128): These are the results in Tunicata, correctly reported: PREDICTED: uncharacterized protein LOC100180080 [Ciona intestinalis] Sequence ID: ref|XP_009858881.1|Length: 821 Score: 31.2 bits Expect 3.1 Identities 17/48(35%) Positives 24/48(50%) It's an alignment of only 48 AAs, with an expect of 3.1. An expect of 3.1, as anybody doing blasts should know, means that you can expect 3 matches of this kind by random chance. It is not significant at all. PREDICTED: uncharacterized protein LOC100186276 [Ciona intestinalis] Sequence ID: ref|XP_002125964.2| Score: 29.6 bits Expect 9.0 Identities 26/96(27%) Positives 45/96(46%) It's an alignment of only 96 AAs, with an expect of 9.0. An expect of 9.0, as anybody doing blasts should know, means that you can expect 9 matches of this kind by random chance. It is not significant at all. So, I did not consider those as homologies, because the results are not statistically significant, and in the range of random chance. I checked the results I posted for cephalochordata, and frankly it seems that I made an error, because here too the results are non significant: hypothetical protein BRAFLDRAFT_82601 [Branchiostoma floridae] Sequence ID: ref|XP_002602014.1|Length: 208 Score: 29.6 bits Expect 4.4 Identities 11/40(28%) Positives 21/40(52%) The problem is that in my OP I report correctly the number of bits, the identities and the similarities, but for some reason that I can't explain the expect value is wrong, and is reported as slightly significant: Expect 0.007 I apologize for the error, and I have no idea of how it came through. It is obviously an error in absolute good faith, because I had no reason to give a significant result for cephalochordata which was not rel, as it was against my reasoning, even is slightly. Indeed, in my OP I comment: "(the hit with Branchiostoma floridae can really be considered trivial, with an expect of 0.007)" So, for the sake of honesty I included it in the graph, because my methodology was to exclude all the result which did not reach any statistical significance, and to include the others. While an expect of 0.007 was in no way impressing, it could be considered slightly significant in the context, so for the sake of honesty I included it. By the way, I added the graph some time after posting the OP, and I did not check each individual result. So, I suppose I must thank you for checking everything, and making my results even better for my reasoning. I will correct the errors tomorrow. Of course, when I post data I expect that others check them, and I am ready to correct any error. But again, the point is not that I have "censored" significant data in Tunicata. Rather, I have erroneously added some slightly significant data in Cephalochordata, against my interest, and for a material error. gpuccio
gpuccio Now looking back after 130+ posts in this discussion thread, the comment posted @50 seems vindicated, validated, confirmed, proven. The topic you present here is quite interesting, and the way you explain it makes it more readable even for an uneducated person like me. However, having all the functional proteins at hand (one way or another) would resolve just part of the gigantic problem we face when trying to put together the spatiotemporally elaborate molecular and cellular choreographies orchestrated within the biological systems. The main issue is not to guess how we got all the required functional components. Guessing past events that did not get accurately recorded is always an extremely difficult (should I say almost impossible?) task, hence discussions on those topics tend to go forever unsettled. The question is how exactly one could make all the observed systemic complexity, assuming one has all the needed components and full-blown labs with the required toolkits and materials. Some famous folks have managed to shuffle genetic material between cells, thus prompting euphoric headlines in the mainstream media and pop-sci journals. But no one has explained how exactly to build a prokaryote cell. Let's not even bother asking about the eukaryotic cells. Forget about morphogenesis, organogenesis, interconnection, for the multicellular systems. Simply put all that aside for now. Still, one would have the enormous advantage of knowing the end result to guide the building process. Does anyone out there want to take that challenge? This is comparable to trying to swim across the Mediterranean Sea and the Atlantic Ocean from Fiumicino to Boston. The discussion about which, when, how functional proteins were available is like having a discussion -before jumping into the sea- about whether the swimmer should wear fins right from the start, or when passing near Ibiza or through the Gibraltar strait. At the end of the day it won't matter, because either way the guy will need to get pulled out of the water completely exhausted before crossing the strait between Corsica and Sardegna. :) Dionisio
I am treating the 2nd part of the protein as a single domain, of which there is no known structure. Everything I have said refers to this domain. We are ignoring the first part of the protein because as Pucci has already admitted, there is an evolutionary trail of this protein sequence, so it doesn't fit his "science." Really not that confusing if you know what you are talking about, Mungy. Try to keep up. Alicia Cartelli
Alicia Cartelli:
I’m saying that if you find a highly conserved protein domain present in a diverse group of species and want to reconstruct the evolution of that protein domain, then you have to look for the intermediates, not ignore them.
Alicia, you are being unclear. gpuccio identified four protein domains and admits they are all conserved. according to Uniprot, in the first part of the molecule we can recognize 4 domains: His argument has nothing to do with those domains. Mung
Mungy, I'm saying that if you find a highly conserved protein domain present in a diverse group of species and want to reconstruct the evolution of that protein domain, then you have to look for the intermediates, not ignore them. You can't just take the protein sequences that are very similar, then take some species that are +100 million years older with no homologs, graph them, and claim that intermediates don't exist. You should probably actually look for the intermediates (or the leftovers of them) in more closely related species before drawing that conclusion. No? Alicia Cartelli
gpuccio: I am without words. That's about as likely s Zachriel being without words. ;) Mung
Alicia, so if A and B both exist in humans, and A and B both exist in sharks, then I need to look at both A and B in humans because in humans B could have evolved from A rather than B being present in humans by descent from B in sharks? Is that your point? Mung
"The cross alignments between form 1 and form 2 and between shark and human confirm all that has been said" No. Don't you see that when you start taking the other protein variants into account, that you start to see higher bit scores and therefore less of this "jump" you're obsessed with? What you're essentially trying to do is show that there seems to be no intermediate forms for the 2nd domain of the prickle protein. But you tried to do this by only looking at the protein in a few species that is most similar to the human form. You can't do this when trying to reconstruct the evolutionary history of a protein. You have to account for any significant sequence homology. You are essentially "looking for intermediates," but ignoring the actual evidence for them. And for the last time, none of my BLASTs are wrong, unlike yours. Alicia Cartelli
Did you not read what I just wrote Mungy? You can't just ignore other copies of the gene in a certain organism when trying to reconstruct the evolution of a protein. Also, when I BLAST the 2nd domain in Tunicates, I get hits: PREDICTED: uncharacterized protein LOC100180080 [Ciona intestinalis] 31.2 31.2 9% 3.1 35% XP_009858881.1 PREDICTED: uncharacterized protein LOC100186276 [Ciona intestinalis] 29.6 29.6 18% 9.0 27% XP_002125964.2 While both hits are similar to that of the cephalochordates, they are certainly not zero ("no homologies"). So, pucci, any comments on your wrong BLASTs? Alicia Cartelli
I am without words. So your blasts were wrong, from all points of view, and you still have the arrogance to stick to your position (whatever it is) instead of having the honesty to admit it, or simply the smartness to remain silent? So, according to you, I cannot take the highest bit score, which is perfectly consistent with what I am looking for and arguing, while you can take a much lower score from another protein and just post it, without any other comments, as thought is were the result of the blast in question? If your argument had been that my blasts were correct, but that there were other sequences in the same organisms which has lower homologies with my sequence, you could just say that. Obviously it's not coincidence that there are other lower homologies with the sequence in organisms which already have high scoring sequences. But the point is, none of those can be used to say that they are intermediaries, because they all happen after the appearance of the sequence in cartilaginous fishes. Let's clarify better the question of Prickle 2. As it is clear form my OP, there are at least 2 main functional forms of the Prickle protein, usually called Prickle 1 and Prickle 2. My analysis, as explicitly stated in the OP, focused on Prickle 1. "The protein is called “Prickle”, and we will consider in particular the one known as “Prickle 1”." The paper quoted in my OP is about Prickle 1, too. But Prickle 2 (and other isoforms) is an important and functional protein too. For example, see this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530445/ or this one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427563/ IOWs, we are in front of a set of functional proteins, related and partially different. A perfect example of my 2b) concept in the OP. Now, the question is: what is the relationship between Prickle 1 and Prickle 2 in humans? First of all, they are very similar in length (831 and 844) and they very strongly share the 4 domain part (the red sequence): 542 bits Expect 0.0 Identities 246/311(79%) Positives 274/311(88%) And the second part? Well, the two "blue parts" in the two human sequences, when blasted one against the other, give the following result: 150 bits 8e-44 Identities 192/548(35%) Positives 278/548(50%) So, partial homology, but also big differences. In two proteins which are both functional and regulatory in humans. Again, clearly a case of 2b). The most interesting thin is that, if we blast each of the two "blue sequences" against shark, these are the results: Blue sequence from human Prickle 1: Best hit: prickle-like protein 1 [Callorhinchus milii] Sequence ID: ref|XP_007892833.1|Length: 832 597 bits Expect 0.0 Identities 350/526(67%) Positives 429/526(81%) (which is the result given in my OP) Second (and last) significant hit: prickle-like protein 2[Callorhinchus milii] Sequence ID: ref|XP_007893374.1|Length: 895 159 bits Expect 4e-41 Identities 192/542(35%) Positives 283/542(52%) Just to avoid further tricks from you, I mention that you also get a few minor hits, the best of which is 37.7 bits with an expect of 0.022, with other isoforms, which I have not considered significant. Now, just to have a further check of what that means, let's blast the blue sequence from human Prickle 2 protein against shark: These are the result: Bets hit: prickle-like protein 2 [Callorhinchus milii] Sequence ID: ref|XP_007893374.1|Length: 895 464 bits Expect 6e-153 Identities 295/531(56%) Similarities 375/531(70%) Second (and last) significant hit: prickle-like protein 1 [Callorhinchus milii] Sequence ID: ref|XP_007892833.1|Length: 832 175 bits Expect 8e-47 Identities 191/537(36%) Similarities 281/537(52%) Must I really explain what that really means? OK: a) There are at least two main forms of Prickle, let's say Prickle 1 and Prickle 2 b) Both are functional regulatory proteins in vetebrates, including humans c) Both share, vastly, what we have called the "red" sequence (the 4 domain part) d) They have significant homology, but also big differences, in the "blue" part. e) Both forms are already present in sharks, and extremely conserved up to humans. f) Both forms share approximately the same level of homology between them (in the blue part) both in sharks and in humans. g) The cross alignments between form 1 and form 2 and between shark and human confirm all that has been said. I leave it to you (and to all readers here) to judge how these data (facts) support your interpretations or mine. One final note, and believe me, I am very sincere here: I think that it is really a pity that this discussion, which is certainly interesting and stimulating, must go on without any reciprocal respect merely because of of your discussion "style". gpuccio
gpuccio: Any other case should be discussed before getting to conclusions. Sure there are gaps. You conclude from this particular gap that it represents an unbridgeable jump. As many such gaps have been filled in before, it would seem premature to assume that this gap is special in that way. Extinction is a fact of biology, and is a more parsimonious explanation. Zachriel
Alicia Cartelli: Your analysis is simply too rudimentary to support your conclusions. Could you say why and offer some suggestions on how to improve the analysis? Mung
Sure you can take the highest bit score, but you can’t just ignore the other hits based on the genome sequence of the species. My BLASTs are not wrong, you just have no idea how to deal with even a small amount of data. You point to this huge jump in bits based on only part of the story. Do you think it’s just coincidence that the gator, for example, has four predicted prickle-like proteins encoded in its genome with varying sequence identity/homology to the human prickle protein? PREDICTED: prickle-like protein 1 [Alligator mississippiensis] 771 771 100% 0.0 84% XP_006269157.1 PREDICTED: prickle-like protein 2 [Alligator mississippiensis] 157 157 100% 3e-40 35% XP_006262189.2 PREDICTED: prickle-like protein 3 isoform X1 [Alligator mississippiensis] 30.8 30.8 10% 5.5 36% XP_006261340.2 PREDICTED: prickle-like protein 4 [Alligator mississippiensis] 47.4 47.4 5% 4e-05 65% XP_006278833.2 We are looking at the leftovers of various evolutionary processes at work. Your analysis is simply too rudimentary to support your conclusions. Alicia Cartelli
One of the simplest of all the defining novelties of any major taxon is the enucleate red blood cell of mammals. This is a homolog shared by monotremes, marsupials, and placentals, and so must be assumed to be an ancient novelty which originated in the common ancestor of all extant mammalian species. - Denton, Michael. Evolution: Still a Theory in Crisis.
Mung
nite gpuccio! Mung
OK, goodnight everybody! gpuccio
Again, any comments on your apparently wrong blasts? I should go to bed, it's late here in Italy... gpuccio
You have achieved a great purpose: you have defied all my attempts to defend Common Descent. All homologies are not indicators of CD, they are convergent evolution. All differences are not a sign of neutral variation, they are non convergent evolution. Popper, where are you? gpuccio
"has since convergently evolved in each lineage to have the similar sequences we now see." So, the 600 bits of homology between sharks and humans are the result of convergent evolution? Is that your theory? My compliments, really! gpuccio
Again, any comments on your apparently wrong blasts? gpuccio
"the huge amount of missing sequence data from both extinct and extant species" ??? To which, I suppose, you have privileged access? Not like us, poor laymen? gpuccio
If there had been homologies in the Prickle-2-like proteins, my blasts would have shown it. I did not put any limitations to my blasts. I just filled in the sequence, as you can find it in my OP, and restricted the class of organisms or the organisms. I did not exclude the Prickle-2-like proteins from the search, or any other protein, for that. Can you understand these simple principles? gpuccio
By the way, I can blast and keep the highest bit score. The 600 bits of homology between sharks and humans are a fact. There is 0 probability (approximation) to get that result by chance in the available proteome. So yes, if you can understand anything of scientific methodology, I can blast and keep the highest bit score. And I do it. gpuccio
Any comments on your apparently wrong blasts? gpuccio
The last common ancestor of humans, sharks, and bony fishes had this "proto-prickle-protein" which originally played a role in the development of the spine and has since convergently evolved in each lineage to have the similar sequences we now see. This makes sense as the protein carries out an important function during development. And you can't just BLAST it and pick the highest bit score. You can't just ignore the Prickle-2-like proteins, because we don't know which evolved first. It's just not as simple as you try to make it, not to mention the huge amount of missing sequence data from both extinct and extant species. Alicia Cartelli
Alligator Mississipiensis: hypothetical protein Y1Q_031085 Sequence ID: gb|KQL86178.1|Length: 900 Score 772 bits Expect 0 Identities 436/522(84%) Positives 476/522(91%) gpuccio
Danio Rerio: Prickle-like 1 Sequence ID: gb|AAI62516.1|Length: 793 Score 453 bits Expect 8e-150 Identities 301/536(56%) Positives 363/536(67%) gpuccio
By the way, how did you do your blasts? I have just checked the first: PREDICTED: prickle-like protein 1 [Fundulus heteroclitus] Sequence ID: ref|XP_012735872.1|Length: 846Number of Matches: 1 Bit score: 481; Expect: 3e-160; Identities: 318/542(59%) Positives: 382/542(70%) Can you explain where did you find your 107 bits value? gpuccio
I blasted the vertebrates. But the information jump is between the common ancestor of vertebrates and humans. gpuccio
What do you mean? Those are vertebrates, with different levels of homology, which is perfectly normal. The fact remains that 600 bits of sequence are conserved between sharks and humans. You cannot bring bony fishes as intermediaries to explain the conservation of a sequence between cartilaginous fishes and humans. Where is the logic? As you should know, the split between cartilaginous fishes and bony fishes is older, and humans derive from bony fishes. Again, grabbing at straws? gpuccio
Why wouldn't you BLAST the vertebrates? They're the species that actually use Prickle's new domain, aren't they? Alicia Cartelli
Zachriel: Are we at this point? Of course I meant in this case. Any other case should be discussed before getting to conclusions. I am always ready to discuss your examples, as you know. gpuccio
Bit score Species 107 Fundulus heteroclitus 130 Danio rerio 147 Alligator mississippiensis 165 Chrysemys picta bellii 294 Oryzias latipes 314 Ophiophagus Hannah 384 Esox Lucius 446 Salmo salar 480 Poecilia Formosa 516 Haplochromis burtoni 563 Clupen larengus (all vertebrates) Alicia Cartelli
By the way, I have blasted that sequence against all organisms except vertebrates, finding nothing significant (except the 30 bits already mentioned). gpuccio
gpuccio: a) No intermediaries have been observed in the proteome, as we can see from the results of my blasts. Of course intermediates have been observed in the proteome. Just not necessarily in this case. Zachriel
What if somebody showed them? What if neo darwinists started to do science, instead of imagining things? gpuccio
For all those interested: Pickle 1, as already said, is nothing special, just an example from hundreds or thousands of other possible examples. I believe in making practical examples, because that helps visualize the concepts and clarify the methodology. It also helps to kill time while we wait for some example of true neo darwinian evolution of functional complexity from our brilliant interlocutors. gpuccio
What if there were other species with bit scores varying from 30 to 600 when BLASTing the 2nd domain of Prickle? Alicia Cartelli
Everything is possible. Neo darwinists could gain 30 bits. My compliments. They are in the clear now, certainly. gpuccio
Grabbing at straws? gpuccio
So there's no chance it's some leftover of an intermediate during the evolution of Prickle 1 as we know it in vertebrates? Alicia Cartelli
There is nothing to explain. With an expect of 0.007, the result is barely, if at all, significant. And 30 bits make no significant difference in a 600 bit jump. gpuccio
Interesting. The evolution of cephalochordates, tunicates, and vertebrates is anything but settled and in fact hotly debated. You could just as easily put the tunicates before the cephalochordates, shortening the jump in bits. If not, then going by your current figure, how do we explain the slight homology seen in the cephalochordates, that then disappears in the tunicates? Alicia Cartelli
Well, I respect faith, Alicia Cartelli respects the effort... This thread is definitely full of respect. Too much respect, maybe. Well, after all I am a layman, not a priest! :) gpuccio
https://en.wikipedia.org/wiki/Chordate Image: "A consensus family tree of the chordates" gpuccio
What can I say, I enjoy reading anything that has to do with biological sciences, even extremely poor attempts at research carried out by laymen who have no idea what they are doing. I respect the effort though! Anyways, why was cephalochordata put before tunicata in the graph? Alicia Cartelli
Zachriel: OK, I respect faith. Just a comment about "assuming". In my simple mind, things are this way. a) No intermediaries have been observed in the proteome, as we can see from the results of my blasts. b) I acknowledge that simple fact: no intermediaries have been observed. Therefore, in my simple mind which tries to make some simple scientific reasoning, I don't build explanations based on intermediaries which have never been observed. I am assuming nothing, just using my scientific method according to my reason. c) You may assume that intermediaries of our protein existed and were destroyed. That's fine. But you have to offer some support from facts to get my attention. d) If you insist that I am "assuming the lack of intermediaries", it's fine with me. There is freedom of thought. I simply disagree. gpuccio
gpuccio: The quantitative argument, as I have tried to show, can be applied both to cases where no selectable intermediaries are observed, and to cases where they are observed. If there are selectable intermediaries, then evolution can occur very rapidly. Your "jump" wouldn't be implausible for adaptive radiation over millions of years. gpuccio: The important point is that those intermediaries must be observed, and not only hoped for. Make up your mind. Are you assuming the lack of intermediaries or not? As for the existence of intermediaries, your limited search can't be considered exhaustive. It's like asking, if humans evolved from primitive apes, where are the intermediates. Whenever someone fills in a gap, two new gaps open up! gpuccio: The apparent position of neo darwinists is that all those intermediaries have vanished. Frankly, I find that position absolutely dogmatic and foolish, speaking of proteins in the proteome, where even slight homologies are well detectable at huge distances in time. Let's see we have evidence of extensive extinction. The transitions are extremely ancient, and proteins leave few fossils. When fossil proteins are found, they confirm the overall phylogeny. Zachriel
Mung: No problem in forgiving past sins: it's present sins that I find annoying! :) I will read Denton's book in the future. In the meantime, if you can give me some interesting preview, that would be certainly appreciated. By the way, I have corrected the graph. gpuccio
p.s. I read about some more interesting cases in Denton's latest book. I'll try to remember to post a couple here to get your opinion. Mung
gpuccio, we can always hope that Alicia has a change of attitude and we can always forgive past sins. Mung
Mung: Ooops! Should I say thank you? :) gpuccio
gpuccio: This is simply a refusal to accept what is in the data. :) Mung
Mung: It seems that Alicia Cartelli has found a material error in my graph. I have exchanged the bit numbers of Drosophila and Cephalochordata. My fault! That certainly changes things a lot! I must say that I am really honored of the attention Alicia Cartelli dedicates to my work, even if I seem to ignore her. Life is certainly strange. OK, I will correct the graph as soon as I have time. gpuccio
Zachriel: The quantitative argument does not assume that there are no selectable intemediaries. The quantitative argument, as I have tried to show, can be applied both to cases where no selectable intermediaries are observed, and to cases where they are observed. The important point is that those intermediaries must be observed, and not only hoped for. Moreover, we are discussing sequences in the proteome, not morphology or fossils. As you know, I have been discussing the lack of intermediaries for protein superfamilies as an argument for ID for years. The apparent position of neo darwinists is that all those intermediaries have vanished. Frankly, I find that position absolutely dogmatic and foolish, speaking of proteins in the proteome, where even slight homologies are well detectable at huge distances in time. This is simply a refusal to accept what is in the data. gpuccio
Mung: He searched for intermediates. That's correct. And not finding them, he assumed they didn't exist. Evolution posits that intermediates went extinct. There is ample evidence of extinction for other biological forms, so he would have to show why his search is exhaustive in this case. That is, he has to justify the assumption. - Assume gravitational force varies by the inverse square. Assume two bodies in motion... Zachriel
Zachriel: The quantitative argument assumes that there are no selectable intermediaries. This is simply false. He searched for intermediates. Zachriel: You might try to argue this assumption is reasonable due to lack of evidence of selectable intermediaries. LoL. Like I said, your first statement was false and you know it. If there's a lack of evidence, as you say, then it's not an assumption. Grow up Zachriel. Mung
"Drosophila melanogaster: no homologies ... Cephalochordata (Branchiostoma floridae): 11 identities, 21 positives, expect 0.007 (29.6 bits)" Is it just me, or is the graph saying something different? Alicia Cartelli
gppucio: “The quantitative argument acknowledges that there is no evidence of selectable intermediaries.” The quantitative argument assumes that there are no selectable intermediaries. You might try to argue this assumption is reasonable due to lack of evidence of selectable intermediaries. However, there is ample evidence of transitions in many other cases. We have a strongly supported theory of common descent, so you would have to show why it doesn't apply in this case. Sort of like if tetrapods evolved from fish, where are the fishapods. Zachriel
Mung: You certainly know the answer, but if you allow me (again, if I remember well) to use you as a comfortable interlocutor to answer questions made by others, I would like to clarify that the bit scores I used are those computed by the Blast online service. The documentation can be found here: http://www.ncbi.nlm.nih.gov/BLAST/tutorial/ gpuccio
GaryGaulin: I appreciate your post, but I am still ill at ease with what you say. First of all, I definitely do not agree with your comment about classical ID. ID is not an argument from ignorance. It is an argument from facts and reasonable inference. If you don't understand that, you are no better than dogmatic neo darwinists. Regarding your "definitions", I find them tragically biased. In essence, it seems to me that you, like materialists, try to ignore the role of consciousness in conscious activities, first of all intelligence. For example, you solve with the introduction of a RAM what can only be explained by conscious representations. That said, I suppose that there is really no point going into further detail, if we don't clarify the fundamental differences in our way of thinking. gpuccio
From my lack of understanding: classical ID is an argument from ignorance: Fixed that fer ya! Mung
So random numbers were punched into a calculator until pucci's fingers got tired or what? Alicia Cartelli
It was calculated with a precisely crafted and carefully calibrated bit-score calculator. Mung
Does anybody know how the "bit score" was calculated? Keep in mind, I am the lay-est of laymen. Alicia Cartelli
gpuccio at 57:
I am not sure that I understand what your position is, and how it differs from classical ID.
From my understanding: classical ID is an argument from ignorance:
https://en.wikipedia.org/wiki/Argument_from_ignorance Argument from ignorance (Latin: argumentum ad ignorantiam), also known as appeal to ignorance (in which ignorance stands for "a lack of contrary evidence"), is a fallacy in informal logic. It asserts that a proposition is true because it has not yet been proven false (or vice versa). This represents a type of false dichotomy in that it excludes a third option, which is that: there may have been an insufficient investigation, and therefore there is insufficient information to prove the proposition be either true or false. Nor does it allow the admission that the choices may in fact not be two (true or false), but may be as many as four, 1. true 2. false 3. unknown between true or false 4. being unknowable (among the first three). In debates, appeals to ignorance are sometimes used in an attempt to shift the burden of proof.
What I have given this forum to study is a testable theory that this forum should now be helping to test. The lack of interest in doing so indicates that the ID movement is happy promoting a logical fallacy. In that case I'm best off to not waste what little free time I have with those who honestly look to me that they are arguing that a magical Santa Claus (of new species) has a hidden workshop somewhere (possibly the North Pole or even outer space) and once a year (or so) secretly flies around delivering presents. I provided a very nice scientific operational definition for intelligence that's based on machine intelligence and cognitive theory 101:
Behavior from a system or device qualifies as intelligent by meeting all four circuit requirements for this ability, which are: [1] Something to control (a body, either real or virtual representation) with motor muscles (proteins, electric speaker, electronic write to a screen). [2] Random Access Memory (RAM) addressed by its sensory sensors where each motor action and its associated confidence value are stored as separate data elements. [3] Confidence (central hedonic) system that increments the confidence level of successful motor actions and decrements the confidence value of actions that fail. [4] Ability to guess a new memory action when associated confidence level sufficiently decreases. For flagella powered cells a random guess response (to a new heading) is designed into the motor system by the action of reversing motor direction causing it to “tumble”. At all biological intelligence levels whatever sensory the system has to work with addresses a memory that works like a random access memory chip used in a computer. It is possible to put the contents of a RAM into a Read Only Memory (ROM) but using a ROM instead of RAM takes away the system's ability to self-learn, it cannot form new memories that are needed to adapt to new environments. The result is more of a zombie that may at first appear to be a fully functional intelligence but they are missing something necessary, a RAM in the circuit, not a ROM. Behavior of matter does not need to be intelligent, a fully trained (all knowing) ROM could be used to produce atomic/molecular behavior. But a ROM would not work where intelligent behavior is needed. Unless the ROM contains all-knowing knowledge of the future and all the humans it will ever meet in its lifetime it can never recall memories of meeting them, or their name and what they look like. For machine intelligence the IBM Watson system that won at Jeopardy qualifies as intelligent. Word combinations for hypotheses were guessed then tested against memory for confidence in each being a hypothesis that is true and whether confident enough in its best answer to push a button/buzzer. The Watson platform had a speaker (for vocal muscles) and muscles guiding a pen was simulated by an electric powered writing device. For computer modeling purposes the behavior of matter can be thought of as being “all-knowing” in the sense that the behavior is inherent, does not have to learn its responses. A computer model then starts off with this behavior already in memory and has no GUESS or CONFIDENCE included in the algorithm, as does intelligence. Memory contents then never changes. Only a GUESS can write new data to memory and GUESS must here be taken out of the algorithm. But it is possible to leave the CONFIDENCE in the algorithm, it will still work the exact same way. Where this in time proves to be true for real matter it would be a valuable clue as to how consciousness works and possibly how to model it, which may in turn help answer the “big questions” including those pertaining to afterlife. Reciprocal cause/causation between levels goes in both the forward and reverse direction. These communicative behavioral pathways cause all of our complex intelligence related behaviors to connect back to the behavior of matter, which does not necessarily need to be intelligent to be the fundamental source of consciousness. Multicellular and cellular level individuals are born then die while the genetic molecular level lives on, by this self-replication of itself. We are part of a molecular learning process that keeps itself going through time by replicating previous contents of genetic memory along with good (better than random) guesses what may work better in the next replication, for our children. The resulting cladogram shows a progression of adapting designs evidenced by the fossil record where never once was there not a predecessor of similar design (which can at times lead to entirely new function) present in memory for the descendant design to have come from.
If anyone is serious about writing a scientific theory then that is the operational definition for intelligence to study and test: http://intelligencegenerator.blogspot.com/ I'm always happy to answer good questions but science does not obligate me to entertain a logical fallacy that attempts to argue for what sounds more like Santa Claus. GaryGaulin
Zachriel: "The quantitative argument assumes that there are no selectable intermediaries." Well, I would rather say: "The quantitative argument acknowledges that there is no evidence of selectable intermediaries." Maybe you assume that there could be selectable intermediaries, but unless you find trace of them, that is just your unsupported assumption. I think we must work with the facts we have. gpuccio
gpuccio: Neo-darwinists are strange people: they always complain that IDists are never quantitative, that they do not offer scientific analyses, that CSI or its similar concepts is never measured, and so on. Then, when one tries to do exactly that, they suddenly become disinterested, distracted, dismissive, and they don’t seem at all happy. The quantitative argument assumes that there are no selectable intermediaries. Zachriel
I'd be satisfied seeing a land mammal with a fluke and a blowhole. Mung
Alicia Cartelli:
Wow! Groundbreaking!
I know! Isn't biology fun! Mung
"Sort of like, if whales evolved from land mammals, where are the whales with legs." We should remember that what we are discussing here is sequences, digital information, and that allows to be much more quantitative. After all, we cannot blast legs or body forms. Neo-darwinists are strange people: they always complain that IDists are never quantitative, that they do not offer scientific analyses, that CSI or its similar concepts is never measured, and so on. Then, when one tries to do exactly that, they suddenly become disinterested, distracted, dismissive, and they don't seem at all happy. How strange is human nature. gpuccio
Sort of like, if whales evolved from land mammals, where are the whales with legs. I see whales with legs at the beach all the time. :D mike1962
EugeneS, Dionisio: Thank you for your very kind attention, which makes the effort to go into details absolutely worth! gpuccio
Zachriel: "To be fair, the point raised concerns the supposedly large gap." Thank you for being fair! :) I suppose that's the difference between you and Alicia Cartelli. And it is a big difference (a jump? :) ). gpuccio
gpuccio @58 Clear explanation! Even I understood it*! BTW, #58 seems to nicely expand what you wrote @46 in response to #43. This thread looks like what the doctor prescribed to help me learn quite a few technical issues. Mile grazie caro Dottore! (*) perhaps struggled trying to grasp a few details though. :) Dionisio
GP, Many Thanks. No need to apologize. I just needed a bit more detail. It is clear. My take on UPB is a bit different. I got it from David Abel's paper of 2009. His approach is broadly the same, but his point (unless I misinterpret it) is given the system and a certain type of interactions in it, we can derive a max number of bits bound for these interactions irrespective of all possible combinations of factors interplaying. I take it to mean that regardless of whether chance and necessity act on their own in sequence or in combination, the net effect is only so many bits of information (under certain assumptions), not more. Essentially, this is saying that all natural processes can provide is little more than information noise. But as you said, the probability of a series of consecutive successful steps can be significantly higher than that of a single sudden jump (again, under certain assumptions). EugeneS
Alicia Cartelli: So during the same time that some of the chordates were evolving a bony spine, a protein now known to be involved in spinal development also evolved? That seems to be it. To be fair, the point raised concerns the supposedly large gap. Sort of like, if whales evolved from land mammals, where are the whales with legs. Zachriel
GaryGaulin: You ask: "The question is now: how do you know you are not seeing a genetic memory for a working solution to a morphological design problem that was figured out by a billions of years old intelligent (and possibly conscious) system that has always been inside of all of us, which has a mind that works using the same systematics as our brain?" I am sorry, but "how do you know you are not seeing" is not a good scientific question, IMO. The right question is: why should I think that I am seeing what you describe? What are the empirical facts which support your explanation? gpuccio
EugeneS: You raise an important point, which deserves some in depth discussion. It is true that the absolute probabilty of finding a specific functional sequence (assuming for the moment a target space of 1) is 1/search space. Therefore, for both sequences, red and blue, we have the same absolute probability of finding a single functional sequence in the time span which goes from prokaryotes to sharks, because both sequences exhibit about 600 bits of information in sharks which are then conserved in vertebrates. As we have to consider the probabilistic resources of the system, the computation would go this way: a) Absolute probability of finding the sequence by a random search: 2e-600 (for both red and blue sequence) b) Probabilistic resources from prokaryotes to sharks: let's say 2e140 (240 bits, which is more or less the number of bacterial reproductions in 1 billion years. This is opbviously an approximation, but it will do for our discussion). These resources are again the same for the red and the blue sequence. So, the absolute probability of finding a functional sequence of A or B in 1 billion years would be, at most, 2e-466 (466 bits, which comes from 2e-600 / 2e140) So, where is the difference? Why is the "information jump" so important, and whu does ot make a design inference muck more necessary fpr the blue sequence? The point is, our adversaries, IOWs "smart" neo-darwinists, will argue that positive NS can lower the probabilistic barriers (beware, now we are talking of positive NS, which is completely different from negative, purifying NS. Purifying NS is an important concept. Positive NS ia practically almost a myth). Now, is true that positive NS, if and when it happens, can lower the probabilistic barriers, but what is needed is the demostration (real demonstration) of intermediates at sequence level which are naturally selectable. IOWs, we need scientific evidence of positive NS, not only wishful thinking and personal faith. But, in the case of the red sequence, our adversaries can argue that the "gradual" forms of the sequence, in which the similarity to the human sequence "gradually" increases, can be considered as functional intermediates, expanded by positive NS. Now, I don't believe that such a concept is true: IMO, the differences here are due to both random neutral variation and different functional constraints in different species. However, it is difficult to exclude a role of positive NS, ans so we must take seriously the possibility that those different forms can be considerate as functional intermediates expanded from time to time by positive NS. OK, but we are still discussing "jumps" which are rather big: of the order of 100 - 200 bits each. Now, I will show that if we can decostruct a transition into intermediate steps, assuming that each step undergoes perfect expansion to the whole population by positive NS and in a very short time, then probabilistic barriers are significantly lowered (but in no way cancelled). Let's make an example. Let's say, for the sake of simplicity, that our functional target are the 600 bits which both sequences exhibit in sharks. Let's say that the blue sequence goes from 0 to 600 bits in one step (let's even assume that the time window is the same, 1 billion years, even if it is not true). The red sequence, instead, reaches the same target in 4 intermediate steps, and each step is supposed to undergo perfect positive NS. In this scenario, the probability to get the blue sequence in that time span is, as explained, 2e-466: IOWs, the functional information of the transition in that system is 466 bits. What is the probability of the transition of the red sequence from 0 to 600? With our assumptions, it is equal to the probability of having 4 successes, each with a probability of 2e-150, in 2e140 attempts (the probabilistic resources). That can be computed by the binomial distribution, and the total probability of the transition (under those extremely favourable assumptions) is: 2e-129 (129 bits). As you can see, there is a very big difference: from 466 bits to 129 bits. OK, our assumptions are obviously too favorable to darwinism. OK, those forms of the red proteins are probably not really selectable intermediates. OK, I would still infer design for the global transition of the red sequence, with a probability which is still 2e-129 after taking into account maximal probabilistic resource. OK. But still, we can see that the case of the blue sequence, where no intermediate form can be shown, and the time span is certainly shorter (one thing which I have not considered in this reasoning for the sake of simplicity), is much stronger as an example of design inference. I apologize for the technical details, but your question was important, and it was important to answer it. gpuccio
GaryGaulin: I have given a look, many times, at your pages, but I must confess that, like Virgil Cain, I am perplexed. I am not sure that I understand what your position is, and how it differs from classical ID. Maybe you could try to explain the main points in simple words, just to start. If you are really interested in the discussion. And, if possible, give the empirical support for your theories, as I have tried to do. gpuccio
I know this is "ID". That's why I had to title it "Theory of Intelligent Design". GaryGaulin
GaryGaulin:
The question is now: how do you know you are not seeing a genetic memory for a working solution to a morphological design problem that was figured out by a billions of years old intelligent (and possibly conscious) system that has always been inside of all of us, which has a mind that works using the same systematics as our brain?
That is still design, Gary. Organisms designed to evolve is still ID, Gary. Not sure of your point. Virgil Cain
I have given the facts that support the design inference based on dFSCI.
The question is now: how do you know you are not seeing a genetic memory for a working solution to a morphological design problem that was figured out by a billions of years old intelligent (and possibly conscious) system that has always been inside of all of us, which has a mind that works using the same systematics as our brain? GaryGaulin
What facts have you given to support any other kind of explanation? Just to know.
Start here: http://theoryofid.blogspot.com/ GaryGaulin
GPuccio, It occurred to me. As you obviously refer to a universal plausibility bound, the crucial piece of evidence is not so much the jump, but the number of bits acquired (be it gradually or abruptly). The reason I am asking is because from the UPB perspective, as far as I understand it, it does not really matter what the graph is. Judging by that, the red graph is also displaying design because it reaches the same magnitude in bits. Am I right? Thanks. EugeneS
Alicia Cartelli:
So during the same time that some of the chordates were evolving a bony spine,...
How can we test that claim? My bet is that Alicia doesn't have a clue. Virgil Cain
gpuccio @48 Agree. Your time is too precious to be squandered on senseless discussions that lead nowhere. I'd rather see you investing part of your limited spare time on preparing an insightful article on the mysteriously hidden 'procedures'. :) Dionisio
gpuccio @46 I see what you mean. Thank you. Dionisio
Someone will probably remember that I don't discuss with Alicia Cartelli. Happy to have drawn her attention, however. gpuccio
So during the same time that some of the chordates were evolving a bony spine, a protein now known to be involved in spinal development also evolved? Wow! Groundbreaking! Alicia Cartelli
Dionisio: The first part of the protein, with its domains, shows a rather "gradual" increase in its similarity to the human sequence as time splits become shorter. As discussed, in that case it is more difficult to distinguish between neutral variation and functional tweaking of the molecule in different species. There are tools, obviously: a detailed study of structure and function of the different forms, Ka/Ks analysis, and so on. However, I have not looked at those aspects (and I am not sure at all that we have enough information to get reasonable inferences about that issue), because my focus here was mainly on the evolutionary history of the second part of the protein. gpuccio
GaryGaulin: Alternative exlanation to what? I have given the facts that support the design inference based on dFSCI. You may agree or not, but I have given facts, and in great detail. What facts have you given to support any other kind of explanation? Just to know. gpuccio
Gpuccio, as you say: An alternative explanation (what you call “dFSCI”) should be supported by explicit facts to be scientifically considered. And it is not. GaryGaulin
gpuccio @24 I think I understood your explanation about the conclusion inferred from the big jump seen so clearly in your graph related to the protein second part (blue lines). However, my long (mouthful) question @21 is in reference to the first part of the protein that you described in the graph using the red lines. Dionisio
Your ID argument seems to be that because we can’t point to a plausible evolutionary history (given the supposed time constraints and complexity of the sequence) of a section of protein in primitive vertebrates, that it must have been designed.
Grow up Zachriel. Please. Mung
Zachriel: OK to your OKs. Many million years is fine with me. Many. Not "too many", however, in an evolutionary sense. Certainly less than the 400+ million years of evolution of vertebrates. You say: "Genomes sequencing is not nearly as complete as made out to be. Also, it’s possible that the sequence was present in the common ancestor, but lost in a particular lineage." OK, that's the standard defense. Is that your best? "Your ID argument seems to be that because we can’t point to a plausible evolutionary history (given the supposed time constraints and complexity of the sequence) of a section of protein in primitive vertebrates, that it must have been designed." You know my argument very well. My argument, which is essentially the ID argument, is that high levels of dFSCI (functionally specified information, in digital form) arise empirically only from design, and point to a design inference. In all the cases we know about. My argument is that 600 bits of functional information is vastly, vastly beyond the 500 bit threshold which is usually considered as Universal Probability Bound. My argument is that, in the presence of such facts, design is the best inference. An alternative explanation (what you call "a plausible evolutionary history") should be supported by explicit facts to be scientifically considered. And it is not. Therefore, dFSCI at its best is exhibited by the sequence we are discussing, and a design inference remains by far the best explanation for its origin. This is my argument, and always has been. gpuccio
gpuccio: a, b, c, d, e Okay. gpuccio: f We don't claim any particular expertise. Early chordates left few fossils, though vertebrate fossils have been found during the Cambrian Explosion. The split between protostomes and deuterostomes apparently occurred well before the Cambrian Explosion. Molecular clocks show a divergence of urochordates long before the Cambrian Explosion. See Blair & Hedges, Molecular Phylogeny and Divergence Times of Deuterostome Animals, Molecular Biology and Evolution 2005. Molecular clocks are probably not terribly accurate at that distance, but it's safe to say there were many millions of years involved. gpuccio: g) Genomes sequencing is not nearly as complete as made out to be. gpuccio: h) Your ID argument seems to be that because we can’t point to a plausible evolutionary history (given the supposed time constraints and complexity of the sequence) of a section of protein in primitive vertebrates, that it must have been designed. Zachriel
Mung: Zachriel is doing his best. The fact that this is his best, however, is really significant. :) gpuccio
Zachriel: The point is: conservation is a matter of sequence homology. Of course it is a matter of degree: that's why in a blast it is measured in bits, and expressed as a bit score and an expect value, which are exactly the measures that I have considered in mt reasoning. And of course it is a matter of time: that's why I have compared blasts with different organisms which are references to specific times in natural history. But the main point is: conservation is conservation of the sequence, and the results of a blast measure the degree of conservation between two sequences. Do you agree? Let's go to my argument. The correct way of describing it is the following: a) We have a sequence which is highly conserved in vertebrates, and apparently not present before. b) It is part of a protein which, instead, is present before, and whose first part shows, well recognizable homologues in all eukaryotes. c) As the sequence in the second part is highly conserved in vertebrates, it is very reasonable to infer that it is functional, and under purifying selection, from its appearance in vertebrates up to humans (about 400 million years of evolution). d) As the sequence is functional and conserved, we can reasonably infer that its functional complexity is very high: in particular, we can take the difference in bit score between two specific times of natural history as a gross measure of the functional complexity, IOWs of the improbability to get that sequence by chance. e) The highest difference in bit score, for our sequence, is observed at its appearance, at the split between tunicata and vertebrates. At that point, and before the following split between cartilaginous fishes and bony fishes, the sequence has already acquired about 600 bits of its functional complexity. That's what I have called an "information jump". f) That information jump happens in a rather narrow window time: I leave it to you, who certainly are more expert than I am of these things, the task to suggest how wide it is (between the tunicata - vertebrates split and the cartilaginous fishes - bony fishes split). g) There is obviously no trace at all in the proteome of any intermediate sequences, as shown by the results of the blasts, least of all of "a plausible evolutionary history ". h) And so it is: the appearance in natural history (a rather sudden appearance) of a functional sequence, which is then highly conserved, and whose functional complexity at its appearance can be quantified at about 600 bits of specific functional information, is a very strong argument for a design inference. This is correct. gpuccio
Reading further, your ID argument seems to be that because we can’t point to a plausible evolutionary history of a section of protein in primitive vertebrates, that it must have been designed. Is this correct?
Grow up Zachriel. Please. Mung
gpuccio: I think there is great confusion in what you say. Perhaps. We'll reboot. gpuccio: When we say that a sequence is conserved, we mean just that simple fact: the sequence is conserved. Conservation is a matter of degree and time. Take a gene under purifying selection. The gene duplicates, and the copy experiences some modest changes, undergoes directional selection, then stabilizes with a different function under purifying selection. We look at the sequence and recognize the homology and the phylogeny. Reading further, your ID argument seems to be that because we can't point to a plausible evolutionary history of a section of protein in primitive vertebrates, that it must have been designed. Is this correct? Zachriel
Zachriel: I think there is great confusion in what you say. "If the function can change, then they aren’t conserved." ??? What do you mean? When we say that a sequence is conserved, we mean just that simple fact: the sequence is conserved. The statement that a sequence is conserved between two species simply means that you find strong homology between two or more sequences in the two species. The fact that a sequence is conserved through enough evolutionary time points, according to evolutionary theory, to purifying selection. Purifying selection implies function in terms of reproductive fitness. Function linked to a conserved sequence implies functional constraint in that sequence: it means that, if the sequence changes, reproductive fitness is reduced. That's how purifying selection works. So, you must distinguish between the different consepts: a) Sequence conservation is just sequence conservation. You observe it by observing sequences, not by reasoning about function (in science, that is called an observed fact). b) According to evolutionary theory, we infer function for the sequences which are conserved, in terms of reproductive fitness. That is how purifying selection is supposed to work. We infer function because we know that a sequence, if not functional, changes through time because of neutral variation. c) For my reasoning here, it is irrelevant what the function is. The only relevant point is that the sequence is conserved, and therefore functional, and therefore under functional constraints. You say: "Yes. Paralogs form by gene duplication, so one or both can drift, contrary to your statement that the “sequence cannot be significantly transformed by random variation”. Hemoglobin is such an example." But that's exactly because globins are less functionally constrained at the sequence level, and therefore can undergo sequence variation retaining function. Indeed, in my discussion with Eric Anderson here: https://uncommondesc.wpengine.com/atheism/ba77-and-a-vid-on-foxp-123-molecular-trees-vs-dawkins-claim-of-you-get-the-same-family-tree/ I have used exactly myoglobin as an example of protein which changes at sequence level, while retaining the same function. I post here, for your consideration, the pertinent part from my post #30 in that thread:
I have said many times that, IMO, the strongest argument at the molecular level for CD is not the homologies, but the differences. My point is: I accept that neutral variation happens, if there is not a strong functional constraint which translates into negative (purifying) selection. IOWs, take histone H3, a 136 AAs protein which is practically the same in all eukaryotes: it does not change, except for really trivial differences, throughout something like 1 – 2 billion years (impossible to say exactly when eukaryotes first appeared). Is that an argument for CD? Yes and no. It is an argument for a very strong functional constraint on histone H3, and if we accept CD it is an argument for extremely strong purifying selection on the protein. IOWs, it is an argument for the designed origin of the protein (a sequence of 136 AAs which has to be, in some way, almost exactly that specific sequence has a lot of functional information in it). But the fans of common design could simply argue that, exactly because there is such a functional constraint, a designer who redesigns each living species can only use that sequence. So, simple strong homology and conservation is not the best argument fro CD. Now, take myoglobin. Human myoglobin is 154 AAs long. Globins are rather “simple” globular proteins, whose 3D structure is rather well conserved even in presence of great differences in sequence. Now, if we blast human myoglobin against chimp, we have 153/154 identities (99%), expect 2e-108. IOWs, almost the same sequence. And a few million years of chronological split. Let’s go to mouse. Against human, we have 129/154 identities (89%), expect 1e-89. The two proteins are still very similar, but less. And we have 80 – 100 million years of chronological split. Let’s go to bony fishes. We have 71/149 identities (48%), with an expect of 6e-37. And a time split of about 400 million years. And so on. Now, my point is: these molecules are rather similar. They do more or less the same thing in different species. They have similar 3d structure. OK, there could be different functional constraint to explain some of the sequence differences, but… frankly, the best explanation for the growing differences at sequence level between homologue molecules with the same function and 3d structure is simply: neutral variation through time. And indeed, as the time split grows, so grows the sequence difference. This is a good argument for CD: not the homologies, but the differences in similar molecules, differences which are proportional to time separation between species.
I hope that helps. Finally, you say: "2b is standard adaptation. A protein which might be under strong purifying selection in one context may evolve when put in a different context, e.g. angiogenin. Not sure how you distinguish this from design." 2b means that the sequence changes, and acquires a new function (or simply a function). The design inference in that case is linked to the functional complexity of that function. In a sense, the appearance of a new functional sequence, like the second part of the Prickle molecule sequence in vertebrates, is a case of 2b: that sequence did not exist in previous species, indeed other sequences were present in previous species associated with the conserved "first part". Then, suddenly, in vertebrates, a new long sequence appears, and then it remains highly conserved, which proves that it is unsed purifying selection, and therefore functional. It's as simple as that. gpuccio
Zachriel: If the function can change, then they aren’t conserved. Sure it is. You're making an assumption and begging the question. Mung
gpuccio: Remember that proteins with different general functions can share conserved domains, whose strict function, however, usually remains similar. If the function can change, then they aren't conserved. gpuccio: However, do you agree that if a sequence resists change by neutral variation, it can only be because it is under purifying selection, and therefore functional? Yes. Paralogs form by gene duplication, so one or both can drift, contrary to your statement that the "sequence cannot be significantly transformed by random variation". Hemoglobin is such an example. gpuccio: 2. Differences between homologues, instead, can have two completely different meanings: 2a) They can be the result of accumulating neutral variation in parts of the molecule which are not functionally constrained 2b) They can be the expression of differences in function in different species and contexts 2b is standard adaptation. A protein which might be under strong purifying selection in one context may evolve when put in a different context, e.g. angiogenin. Not sure how you distinguish this from design. Zachriel
Mung: Thank you! I don't know if the process can be automated (probably yes), but the method is not too complex. I would look preferentially at regulatory proteins, especially Transcription Factors, which often have large parts of the molecule which are unexplained, while the DNA binding site is usually conserved and corresponds to well known motifs. The important point is to verify if the non explained parts are conserved, and in what range of natural history. That can easily be done with a few blasts with reference organisms or groups of organisms. I will try to look for some more examples, in the future. The Prickle protein is in no way special: it's just an example which I looked at recently. gpuccio
Nice post. Any opinion on whether it would be possible to automate a process to identify other similar sequences? Would we first search for sequences of some minimum length? Then look within that sequence for a sub-sequence of some minimum length where there is no known something but where the same sequences also contains one of more sub-sequences of some known something? Mung
EugeneS: Thank you for the kind comment. gpuccio
KF: I have just given one example, but that kind of information jump is rather common. Both eukaryotes versus prokaryotes, and vertebrates versus other metazoa, are critical nodes where a lot of information is gained at sequence level. And there are many others. A common mistake is to underestimate information jumps which happen just in parts of a molecule, and that is one point that I wanted to stress in my post. gpuccio
Zachriel: My #1 is that homologues with sequences which are strongly conserved can only be explained as the result of purifying selection, and therefore of functional constraints on the sequence. Do you disagree? Paralogs can be different things, and I don't see how they contradict the principle I have stated. Could you maybe give examples? Remember that proteins with different general functions can share conserved domains, whose strict function, however, usually remains similar. However, do you agree that if a sequence resists change by neutral variation, it can only be because it is under purifying selection, and therefore functional? It seems that this is a fundamental principle in evolutionary theory. gpuccio
gpuccio: I know you love cryptic and deep statements, but could you please be kind and explain better what you mean? Not sure if it is so cryptic, much less deep. A paralog is a homolog that has a different function than the ancestor, which seems to contradict your #1 above. Zachriel
GPuccio, As usual, a very good and very plainly written OP. Could I suggest to the people who run the blog to develop the search functionality a bit further e.g. to be able to look for OPs written by an author. That would be really handy. EugeneS
GP, a 500+ bit info jump is of course just what the doctor ordered; dear (and most gentle) physician. KF kairosfocus
Dionisio: I believe that strong functional constraints which point to a strict target space are the best indicator of design. In the case of the second part of the Prickle proteins, the sudden jump in informational content in a relatively small evolutionary time is a very reliable indicator of a designed origin. I am not aware of any other reasonable explanation for such a scenario. gpuccio
Zachriel: Welcome to the discussion: after all, one word is better than nothing! :) I know you love cryptic and deep statements, but could you please be kind and explain better what you mean? Thank you in advance. gpuccio
gpuccio: 1. Given those premises, homologies through natural history are certainly an indicator of functional constraints, because they mean that some sequence cannot be significantly transformed by random variation. Paralogs. Zachriel
gpuccio As far as you know, what would be the most detailed illustrated explanation of at least a hypothetical scenario for the different functional constraints and neutral evolution that occurred on the protein prickle from Prokaryotes to fungi, then to c. elegans, an later to Drosophila melanogaster, that I could look at to learn about this? Thank you. Dionisio
Dionisio at #19: Yes. gpuccio
gpuccio @17
[...] those known domains show some “graduality” of modification in eukaryotes [...]
is the above quoted statement associated with the below one taken from your OP?
[...] it can be explained as a mixed result of different functional constraints and neutral evolution in different time splits [...]
Dionisio
The added graph does illustrate what you explained so well. Definitely a picture is worth a thousand words. :) Thank you. BTW, that impressive jump could easily win an Olympic gold medal, but also it could raise suspicion about doping, thus prompting some serious folks to demand an investigation to search for a valid explanation. :) Dionisio
Dionisio at #15: No, obviously there is probably no clue about the appearance of those domains, as there is usually no clue about the appearance of any new domain. However, my point here is that, at least, those known domains show some "graduality" of modification in eukaryotes, while the second sequence "arises" suddenly in vertebrates, and is very well conserved afterwards. gpuccio
I have added a graph to the post. I hope it shows more clearly the point I am discussing here. gpuccio
Before the OP gets to what is mentioned @10 & @14, it states this:
The first part of the sequence (AAs 1 – 313) shows no homologies in prokaryotes. So, we are apparently in the presence of domains which appear in eukaryotes.
Their functionality is well known, but how much is it known about how exactly they appeared? Can someone point to serious literature that explains it well? Thanks. Dionisio
Dionisio at #10: As soon as I have time, I will look for that. But probably there is not much: blast does not recognize any domain in the sequence, which usually means that there is no information about the 3D structure. The protein function is not really well understood, but its regulatory role in many contexts is well proven gpuccio
Dionisio: Yes, the shark is there because cartilaginous fishes are the oldest vertebrates (except for lampreys, which are jawless vertebrates). But you are right, a little bit of aggression could be helpful, sometimes... :) gpuccio
Dionisio at #6: Correction made! :) gpuccio
gpuccio You have answered satisfactorily my question about the E value. Thank you. BTW, one of my children -who works on something related to cancer research- has used that Blast program, but I prefer to ask you publicly about the E value, so that others readers here -who might be as technically challenged as I am- could benefit from your clear explanation too. :) Dionisio
So, we have a steep informational jump from non chordates and non vertebrate chordates, where the sequence is practically absent, to the very first vertebrates, where the sequence is already highly specific. We have here a very good example of a part of a protein which practically appears in vertebrates while it is absent before, and which is reasonably highly functional in vertebrates.
Is anyone aware of any literature that explains the appearance of this highly specific sequence? In the meantime, would it help to look for papers on any known functionality associated with that vertebrate-only sequence? Dionisio
Dionisio: Your questions are most welcome! :) In Blast, the expect value (E value) is a measure of the improbability of finding the observed homology by chance in the existing sequence database. Here is the description from the Blast FAQ page:
Q: What is the Expect (E) value? The Expect value (E) is a parameter that describes the number of hits one can "expect" to see by chance when searching a database of a particular size. It decreases exponentially as the Score (S) of the match increases. Essentially, the E value describes the random background noise. For example, an E value of 1 assigned to a hit can be interpreted as meaning that in a database of the current size one might expect to see 1 match with a similar score simply by chance. The lower the E-value, or the closer it is to zero, the more "significant" the match is. However, keep in mind that virtually identical short alignments have relatively high E values. This is because the calculation of the E value takes into account the length of the query sequence. These high E values make sense because shorter sequences have a higher probability of occurring in the database purely by chance. For more details please see the calculations in the BLAST Course. The Expect value can also be used as a convenient way to create a significance threshold for reporting results.
The bit score is another way to express the same concept. The lower the expect value, the higher the bit score. When the expect value is very low, it is simply given as "0.0", but the bit score can still be used to evaluate differences between different blasts. gpuccio
BTW, impressive shark image at the top of the OP. Why did you choose that particular picture? Does it have to do with the shark being an allegedly ancient species? Or was it intended to impose certain level of discipline in the follow-up discussion, so everyone must stick to the discussed topic or else... :) Thank you. Dionisio
Sorry for asking so many distracting irrelevant questions. I prefer to understand most technical terms encountered within the text before trying to understand more deeply what the whole article actually means. What does the following expression mean?
The best hit is an expect of 2e-21.
I'll try to refrain from asking too many questions though. Please, delete any of my posts that you deem irrelevant, distracting or off topic. Thank you. Dionisio
The protein is called “Prickle”, and we will consider in particular the from known as “Prickle 1”.
What does that mean? Thank you. Dionisio
[...] we have to try to bring the discussion into some biological detail.
Yes, agree. Thank you for taking the time to write this insightful OP, which should lead to a serious discussion on some related biological details. Dionisio
Dionisio: Thank you for the revision! :) Yes, I know, the post is rather technical. But I think that we have to try to bring the discussion into some biological detail. Thank you for taking the time to consider it! gpuccio
(hihly conserved from LUCA to humans) Dionisio
This is a very important point. because it means that stron homologies thorugh time point to high functional complexity, and therefore to design.
Dionisio
Very insightful article. Thank you. Haven't digested it entirely yet, though. It'll take me some time to process it completely. Dionisio

Leave a Reply