BA77 and a vid on FOXP “1/2/3” molecular trees vs Dawkins’ claim of “You get the same family tree”

_{kairosfocus

January 23, 2016

Atheism, Genetics, rhetoric}

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BA77 often posts clips of citations and links here at UD. ~~After a recent noticeable break (we missed you),~~ he has ~~just~~ [–> correction: he posted in a thread some time ago which just got a comment from TJG . . . ] posted a link to a video on objections to prof Dawkins’ claims that FOXP 2 (let me be exact) etc trees give the same structure:

Key clips include a transcript:

Plus, several family trees, such as FOXP1, showing:

With FOXP2:

FOXP3:

The three trees seem to be quite divergent, one putting chimps with squirrels and the like, another putting gorillas on a different branch, and only one putting the three on neighbouring twigs.

This seems to be consistent with the objection that molecular trees are both inconsistent with traditional trees and that they are mutually inconsistent.

So, has Mr Dawkins erred, or is this the grand-daddy of all elaborate Creationist quote mines and hoaxes?

If you assert or imply the latter, what is your evidence? END

Comments

Eric: OK, I think of physical continuity in the sense that design happens, more or less gradually, or even suddenly, by modifying information in existing species while those species go on reproducing. IOWs, even if design is realized by the input of information, the continuity of reproduction is not interrupted. This has many advantages on designing new living beings from non living parts, even if we reuse design features. I think it's also the way we would act, in modifying living cells: just input the modifications in the existing cells, and then relying on their reproduction. And again, the point is that my argument for CD is based on the heredity of neutral variation. Now, the important issue is that neutral variation happens mainly because of random errors in reproduction: it is not part of the original design. So, let's say that the designer design A. Then A lives for a few million years, and in that time some of the proteins in A undergo neutral variation, and some of those modifications survive in the population, or even become fixed by genetic drift. That's what happens to neutral variation. Now, the designer designs B, which is in part similar to A, but has many new features. Now, the point is: if the designer rebuild B physically from scratch, even reusing his plans for A, there is no reason why we should observe in B, in the proteins which are common to A, any neutral variation. Why? Because the neutral variation has accumulated in A through time, after the initial design. But, if the designer inputs his new information in some member of the A population, and then lets it reproduce, then the neutral variation which was present in that organism will be inherited by the new species. And that is exactly what we observe in the proteome, at least IMO. By the way, I have posted an OP which is in some way an expansion of our discussion here. I would be happy if you could give it a look: https://uncommondescent.com/intelligent-design/homologies-differences-and-information-jumps/gpuccio_{February 3, 2016
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gpuccio: Your example of (a) building from scratch versus (b) transforming into a new engineering work is well stated. Indeed, with anything even semi-complicated, design is typically done as a transformative work, as in (b). I think I'm in agreement with you there, and you may well be right that this could account for some of the interesting data. Definitely an approach worth considering. I just want to press a little bit, however, on your definitions. You mentioned that in case (b) there is physical continuity. But is there really physical continuity? In what sense? If there is meaningful redesign between A and B (which you seem to agree is likely, as opposed to Darwin's slight, successive modifications), then presumably we aren't suggesting that -- to give a grossly-oversimplified example -- a dinosaur gave birth to a bird, thus preserving the physical continuity, as well as the common descent. Meaning, we could indeed have a situation in which a designer takes an existing species and significantly modifies it, accounting (as you note) for some of the genetic continuity. But surely we wouldn't be proposing that there was an actual, physical parent-child relationship between A and B? In other words, perhaps we are dealing with continuity of design or continuity of features, rather than what is commonly referred to as "common descent" -- a physical, parent-child relationship from A to B.Eric Anderson_{February 1, 2016
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Eric: Your comments at #58 are very interesting, and I certainly agree with many of the things that you say. Still, I think that the concept of Common Descent has its importance, even if we agree that new species are (maybe mostly) the result of new design. Let's simplify the problem. Let's say that there is species A, and at some time, a new species, B, appears. Let's say that B has many new features: differences in body plan, new proteins, new networks. And yet, it also reuses many basic biological structures which were already in species A. I have also discussed that simple fact that there is strong evidence that events which happen in species A along time, like neutral variation in many of its already existing proteins, are often "inherited" by species B, where the same proteins will again undergo further neutral variation which will be "inherited" by some future species C, and so on. That is, IMO, the best explanation for a significant part of the similarities and differences which we can observe in the proteome. OK, Common descent, even in the context of new engineering and design, mean one important thing: there is physical continuity between species. Not only the continuity of the reuse of some software which was written in some non physical world, but rather the reuse of biological software as written in the physical bodies of existing species. Let's simplify again, and suppose that we have a human biological designer who has succeeded in engineering from scratch a new species, maybe even a simple one, let's say a new form of prokaryote, in his lab. Let's say that this new species, that we call A, has its new proteins, engineered in the lab, and it is a satisfactory achievement for our biological engineer. Now, our engineer plans a further advancement, a new new prokaryote, with even more surprising abilities, which will be, in part, based on what he has already achieved. Let's call this new project species B. Now, even admitting that B will be a new example of original design, there are two different ways for the engineer to bring B into existence: a) He designs B from scratch, if necessary by reusing some notes that he has in his lab. b) He works on A, transforming it into B by new engineering work. The two scenarios have different implications, and are recognizable from the results. In a) there is no common descent, only common design. In b), there is common descent (physical continuity) and new design. My point is that the aspects which I have discussed in my previous posts definitely point to b, and not to a). That's what I mean when I say that observations in the proteome strongly favor Common Descent. I am convinced that there are many patterns which cannot be reasonably explained by the a) scenario. As my only commitment, in this kind of reasoning, is to scientific facts and good inferences from those facts, I remain convinced that CD is at present the best explanation for those patterns. It's as simple as that.gpuccio_{January 30, 2016
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Eric Anderson @59 Thank you for the insightful analysis of such an important aspect of the current state of affairs in scientific research: how to approach the object of study. Please, help me with organizing/streamlining/refining/correcting these (overlapping/colliding/redundant/senseless/vague/ambiguous?) thoughts: Could we dare to say that -at least in part- the "unfortunate" situation you have pointed at and so concisely described may have to do with our natural human condition that makes us lose the sense of wonder we had (in different degrees) in our childhood? Can we say that such a natural loss of our infantile sense of wonder be partially associated with our lack of humility (any chicken-egg dilemma here?), which may lead us to narrow-minded thinking that keeps us from putting everything to test and thinking out of any box others might have established previously? Perhaps an additional (and kind of more earthly 'pragmatic' and less philosophical) reason for that "embarrassingly" confusing approach seen through the recent history of scientific research is the university undergrad students' lack of exposure to at least basic courses on math logic, systems theory, set theory, (regardless of what they're majoring on) that could help them look at certain things from a slightly different perspective? Could we risk much by saying that the above situation might explain -at least partially- the cases where outsiders, who in most occasions lack the required deep technical knowledge and expertise, end up noticing and pointing at obvious basic things the experts could not or did not want to see? In any case, you have brought up very important points that provide much food for thoughts that could lead to very interesting extensive discussions. However, in all this there's an important caveat: we should ask honest questions -whatever that means according to a distinguished professor from the U. of Toronto who has commented here in this forum. :)Dionisio_{January 30, 2016
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Dionosio @49: gpuccio has already provided a good response, but just wanted to add a few thoughts.
When the term ‘code’ is mentioned, can we make any association with the multiple layers of different code that is seen in computers?
Absolutely. Indeed, one of the unfortunate side effects of all the emphasis for decades on the "genetic code" is that it has really hampered some people's ability to think clearly about what is required for an integrated, functional system. In hindsight we are starting to see that the Central Dogma of "DNA makes RNA makes protein makes us" is not just incomplete, not just too simplistic, but in very substantive ways is fundamentally misguided. Notwithstanding the value of hindsight, it is nevertheless rather embarrassing that it has taken so long for the scientific community in general to catch up to what should have been anticipated and predicted long before, just by thinking through in detail what might be required to build an organism. And I am convinced that a researcher today with the tools and the willingness to look has the opportunity to make many profound discoveries in biology by going through a design exercise beforehand. Unfortunately, we still see biological science being dragged down by the simplistic and naive evolutionary baggage of yesteryear, with its creation story focused on happenstance tweaks to DNA, as though nucleotide sequences alone were the be-all-and-end-all of biology. Might as well try to build a new server by making random changes to files on the hard drive . . . That is not an exaggeration. If anything, it is probably still an underestimation. There are layers upon layers of functional integration and feedbacks and sensors -- nearly all of which require coding, not to mention precisely interconnected physical systems. We are barely scratching the surface and will one day look back on the "protein-coding DNA determines the organism" idea as a reflection of an incredibly backward and primitive time in biological science. The sooner we shed the "tweak nucleotides and build a new organism" school of thought and start approaching biology with a real eye toward design -- including by going through detailed design analysis exercises -- the better off the whole of biological science will be.Eric Anderson_{January 29, 2016
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gpuccio: I know this thread is getting a little old, but I'm finally getting a few moments to continue our discussion and wanted to offer a couple of additional thoughts for consideration. 1. There is a logical separation between common descent and design. We know that design can either incorporate prior elements or not, at the decision of the designer. 2. Building an organism requires significant integrated complexity and functionality. When thinking of common descent we need to consider the whole organism. We can't follow the naive approach that seems to be taken by some evolutionary proponents of considering each gene as though it were some independent, isolated construct. A gene doesn't descend from generation to generation in a vacuum. Although a gene may change over time, we have to remember that the mental picture we sometimes have of a gene descending through time is essentially a hypothetical construct. The only thing that ever descends is a complete, functional organism, with all its code, parts and functions intact. 3. If we look at organism A and organism B and note that (a) some gene or other small element is highly similar, and (b) there are a host of other elements that are unique, then, under your proposal, we are looking at significant redesign. But in that case, and considering #1 and #2 above, what sense does it make to say that the small element came about by common descent? If there were a piece of code in the latest iPhone that was also in the first iPhone and, before that, even in the iPod, it still wouldn't make sense to say the latest iPhone came about by common descent from the iPod. Of course not. Rather, we are dealing with a new design, a massive exercise in building integrated functional complexity that took years and hundreds of millions of dollars. Yes, it happens to incorporate an element that was in an earlier entity, but by any rational use of language the latter entity came about through design, not common descent. Furthermore, it wouldn't make sense to say that most of the iPhone came about by design, and a small part came about by common descent. The prior coding element (in our example) was included as part of the new entity and integrated into the functionality of the new entity on purpose, not via some parallel accidental development process.* It would stretch common sense to say that an element was included by accident, but integrated on purpose. Finally, in a situation like this it just confuses things to refer to common descent, particularly when that term typically carries an implication of purely natural and material causes. ----- I'm not saying there is a simple, satisfactory answer to all this. You have provided some interesting and intriguing examples. There might even be some valuable clues to be found. But perhaps we still have no clear answers. ----- * It is possible that a designer might include a piece of old code by accident, but that would be unusual, particularly if the piece of code performs an essential function in the new entity. Most of the cases don't seem to be of that sort and would not support an accidental-inclusion hypothesis.Eric Anderson_{January 29, 2016
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gpuccio @ 56
[...] this is one of the most interesting aspects which are coming out from recent research. As you know, it seems that many “decisions” about cell fate, especially in stem cells, happen as “events” which are superimposed to some basic oscillating state. That is really very interesting. So, that could really be a basic procedure in cell differentiation: the establishment of oscillations in time and space of important patterns (TFs and other epigenetic components), whose purpose would be to generate a range of possible states from which the cell can “choose” at appropriate times. Of course, both the ways that oscillations in time and space are established, and the mechanisms of control and choice, remain vastly unknown. :)
Esattamente eccellente mio caro Dottore!Dionisio_{January 29, 2016
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Dionisio: Thank you for your always careful interest! Yes, probably I should collect some of these ideas in a thread. I am thinking about these things almost daily, and always checking the literature for pertinent news (with your precious help, obviously :) ). Regarding your questions at #53, this is one of the most interesting aspects which are coming out from recent research. As you know, it seems that many "decisions" about cell fate, especially in stem cells, happen as "events" which are superimposed to some basic oscillating state. That is really very interesting. So, that could really be a basic procedure in cell differentiation: the establishment of oscillations in time and space of important patterns (TFs and other epigenetic components), whose purpose would be to generate a range of possible states from which the cell can "choose" at appropriate times. Of course, both the ways that oscillations in time and space are established, and the mechanisms of control and choice, remain vastly unknown. :)gpuccio_{January 29, 2016
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gpuccio, Thank you for the clear explanation you wrote @51. BTW, would it be reasonable to associate the last paragraph of your comments @51 (related to TFs) with any of the things you explained @52 and my follow up questions @53? Sometimes my visible ignorance makes me ask questions that may not make too much sense (if any). But that's how I learn some things. :)Dionisio_{January 28, 2016
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gpuccio, would it help to open a separate thread for this discussion related to your post @52?Dionisio_{January 28, 2016
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gpuccio, Thank you for the very insightful explanation. Here are a few additional questions -which might sound kind of senseless: 1. Are all the "coding"/"controlling" mechanisms stochastic? IOW, are there any spatiotemporal cases of "coding"/"controlling" mechanisms? If there are spatiotemporal "coding"/"controlling" mechanisms, then 2. what would be the spatial component(s)? Could it be (for example) the location of certain things relative to other things within each given scenario? 3. what would be the temporal component(s)? Could it be (for example) the timing for certain biochemical/biological events to take place? 4. What mechanisms of spatiotemporal control could determine the occurrence of certain biochemical/biological events in the right place at the right time? Mile grazie! again for taking your time to explain things here.Dionisio_{January 28, 2016
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Dionisio at #49: Very good points! Let's try to make an example with what we know. a) The classical genetic code allows to write proteins sequences by a strict link between the symbolic sequence of codons in the gene and the sequence of AAs in the protein, which is the main cause of some biochemical activities. So, if I want to change the activity, I can change the coded nucleotide sequence and that will change the protein and its activities. b) Histone post translational modifications contribute strongly to determine chromatine status, and therefore transcription (what is usually called the "histone code). Let's say that we understand well what parts of DNA or else controls different histone modifications, and how the code works. That is not yet completely true, but we know something about those mechanisms. So, let's say that I am an engineer, and that I want to change some transcriptional scenario from species A to species B. I can act at least in two different ways: 1) I change the sequence of some transcription factor, so that it interacts differently with other transcription factors, and the different combinatorial effect changes what is transcribed. As trasncription factors are proteins, to do that I can simply change appropriately the sequence of my TF, not so much the part which binds DNA (the DNA binding site), but rather the part which interacts with other TFs (the "rest"). To do that, I must change the nucleotide sequence in the coding gene of my TF, so that the modified TF will have a different AA sequence and interact differently with other TFs. IOWs, I write my variation by changing the nucleotide sequence in its gene: I am writing my new code in the language of the classical genetic code. 2) In alternative, I can change histone modifications in the appropriate situation, so that different chromatin configuration will be active at the appropriate time. To do that, I can act on those parts of the genome which control histone modifications at different times. While we don't know well what those parts are and how they work, it is reasonable that much of the information is not in the gene coding part, and does not work by coding AA sequences. DNA sequences which act as signals in the non coding part of the genome, for example, could have important roles to "guide" histone modifications in different states. That is already known in part. So, if I choose to act in this way, I will change sequences of nucleotides in the appropriate non coding parts of the genome, and I will not use the classical genetic code, which only serves to build proteins, but rather the biochemical code which allows to guide histone modifications by non protein coding DNA sequences, and therefore to achieve modifications of the histone code active at particular times. IOWs, I am using a different language to achieve the same result. 3) In alternative, I can do both things. That can give me functional redundancy, and allow finer levels of regulation which benefit of the interaction between the two levels. That is what commonly happens in epigenetic regulation, and we already know that it happens: only, the levels are not just two, but many more (just add alternative splicing, microRNA control, long RNAs control and all the other forms of RNA control, DNA methylations, chromatine modifying enzymes, post translational modifications of proteins, regulation of transport between nucleus and cytoplasm, differences in localization, and many others which are all coming out as our understanding grows).gpuccio_{January 28, 2016
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drc466: I have not been clear enough. My reasoning about neutral variation is similar to the general reasoning about neutral variation in evolutionary thought, because that is the only part of traditional evolutionary thought that I accept as credible (with the differences that I have tried to highlight in my previous posts. Therefore, the reasoning is not that the sequence does not change in one species and changes in the other: that would be unreasonable, as you correctly point out. Let's take the myoglobin example in mouse and humans. We observe similarities, and also differences. The 3d structure and the function are very similar, while the sequence is 89% identical. There are some differences. If instead we compare myoglobin in humans and bony fishes, we still have a strong homology, but it is only, at best, 48%. Now, let's say for simplicity that the time split between mice and humans is about 100 million years, while between fishes and humans it is about 400 million years. And let's say that the "relationship" between differences in that homologue protein and time from the split is consistent in most species (which, for myoglobin, seems to be the case). The question is: how so we explain that pattern? The best explanation. IMO, is CD (probably, the only credible explanation that I can think of for this particular pattern). It goes this way. We assume CD, and we assume that the species we consider shared a common ancestor up to the moment of the split. We also assume, reasonably, that the function and 3d structure of myoglobin do not change significantly in species, and that most differences observed between species are due to neutral variation. That means that in the last common ancestor of mouse and human, myoglobin had a certain sequence, which was perfectly compatible with its 3d structure and function. In the time from the split, both lines undergo neutral variation at a rate which is more or less "proportional" to time, and retain the same 3d structure and function (with possible slight adaptations). So, the difference we observe between mice and humans is the result of neutral variation acting on both evolutionary lines in 100 million years. While the difference we observe between bony fishes and humans is the result of neutral variation acting on both evolutionary lines in 400 million years. Therefore, it is much greater. This explanation is good. Can you offer a better one? Of course, myoglobin is a good case for this reasoning, because it apparently satisfies the premises: its 3d structure and function do not vary much in time and between species, and the 3d strucutre and function are compatible with big sequence variation (IOWs, myoglobin is a protein which allows big neutral sequence changes). Histone H3 is not a good case for our reasoning, because its structure and function do reamin the same, but its sequence also remains the same. As we know that neutral variation happens (when it can happen), the only possible explanation for that is that the molecule is under such functional restraints that purifying (negative) selection keeps it the same. IOWs. it tells us all about similarities, and nothing about differences. Transcription factors are not a good case for our reasoning, because they reasonably change their function in different species: they are regulatory proteins, and they have to regulate different things in different contexts. In this case, it is reasonable that most of the differences we observe are due to different functions. However, the DNA binding site in TFs (which is often a minor part of the sequence) usually is much more conserved, because it works in the same way in different species. I hope that I have been more clear.gpuccio_{January 28, 2016
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bill cole: "Do you think this makes trying to form a tree bush etc of life premature?" Probably. And I believe that trees and bushes should always be considered tentative, as should be all scientific inferences. We should always be looking for the best available inference. And just avoid making the worst available inference ! :)gpuccio_{January 28, 2016
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Eric, bill cole, gpuccio When the term 'code' is mentioned, can we make any association with the multiple layers of different code that is seen in computers? For example, in a laptop an engineer could enter a code written in some kind of specialized engineering language, which would be understood and translated by an engineering design program in order to adapt its general procedures to the given engineer's conditions, standards and methods. The engineering design software might have been written in C# linked to some utility libraries written in C++, all compiled/assembled on .NET framework, which runs on Microsoft Windows 10, running on the Intel microprocessor code and the drivers for separate devices. All that still requires an external source of energy to run. But most importantly, it depends on the actions of someone to start it. The biological systems might not be comparable to the described computer software, but perhaps some analogies could be made for illustration? As gpuccio stated so clearly, in the biological systems we still don't understand well enough their entire controlling architecture. However, as more data keeps coming at an accelerated pace out of the ongoing research, perhaps more light could be shed on the details in order to have a better idea of the big picture?Dionisio_{January 27, 2016
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gpuccio @43
Of course alternative splicing is a big part of the picture, and so are all epigenetic regulation mechanisms. [...] while much is known of the different final procedures which contribute to those mechanisms, very little is still understood of the general control of those mechanisms. [...] For proteins, at least, we have the sequence data and understand a little (sometimes too little) of the sequence – structure – function relationship. Much less is understood of transcriptional regulation, [...] For example, regarding alternative splicing, it is still not clear what regulates the different splicing in different situations [...]
esattamente eccellente mio caro Dottore!!!Dionisio_{January 27, 2016
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gpuccio further, I'm not expressing my concern very well, so let me try to elaborate further. In order for your mouse-human myoglobin correlation to be valid, you must assume that modern mouse myoglobin is identical to that of a mouse 80-100 million years ago. In other words, that myoglobin is immutable in mice (if not, the % difference between mouse/human myoglobin is...irrelevant). But, if we assume that mouse myoglobin is a foundation for, or an evidence of CD for human myoglobin, we must admit that myoglobin can change neutrally - that merely changing myoglobin is not a death warrant for a species. This leads us to a logical conclusion that if myoglobin evidences change, then there MUST be a corresponding species change - e.g. a mouse of 50million years ago shared identical myoglobin with modern and 100myo mice, but for a 50myo descendant of mice, myoglobin evidences 50my of neutral change. Further, since a single data point doesn't make a trend, you must make this same argument for any other protein that supposedly shows the same time/change correlation between mice and humans - the mouse version is immutable from 80-100my ago, but the human version evidences 100my of neutral change. How can this be? As a logical argument: 1) Mouse myoglobin is immutable in mice - changes in myoglobin must result in either a species change or evolutionary dead-end. (see above) 2) Non-mouse myoglobin shows "neutral" changes corresponding to evolutionary time (assertion required for CD) 3) All similar proteins that are evidence for CD have the same pattern - immutable in original species, but evidencing gradual change in descendants. (logical expansion of 1st two points from myoglobin) Forced Logical Conclusion: Descendants of ancient species accumulate neutral changes in synchronization with their change in species - all proteins that evidence CD simultaneously change when, and only when, the species changes. True or False? This seems like an incredible stretch to me. Further - for myoglobin (and other similar proteins) to be a valid indicator of CD, you should be able to plot the differences of myoglobin over time for ALL mammals and show a direct correlation between change accumulation and time of evolutionary appearance, using a rodent like the mouse as your starting point. Otherwise, mouse/chimp/human simply represent cherry-picked data - in this case, 3 points out of thousands don't make a trend. The logic doesn't make sense to me - what am I missing?drc466_{January 27, 2016
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Gpuccio @38, I have a question. You make some good points regarding common descent but I don't understand why some genes would remain in stasis for 80 - 100 million years while others undergo large changes. For your mouse human comparison to work, you must assume that that particular genetic code is the same in modern mouse as a mouse of 100 million years ago. If the modern mouse has not changed, then all its genetic code should have the same relationship to human genetic code. By pointing to one piece of code and saying look this has not changed in a long time and shows the proper amount of neutral evolution while ignoring other genetic code that has changed a lot and shows much greater variation, are you guilty of cherry picking code to support your common descent assumption?drc466_{January 27, 2016
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gpuccio Good points regarding how little is known about transcriptional regulation and alternative splicing codes. Do you think this makes trying to form a tree bush etc of life premature?bill cole_{January 27, 2016
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If you think GA's are powerful now, just think what they will be able to do once they are programmed to use epigenetic and natural genetic engineering techniques!Mung_{January 27, 2016
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bill cole: Thank you, and thank you for the very interesting link. Of course alternative splicing is a big part of the picture, and so are all epigenetic regulation mechanisms. Unfortunately, while much is known of the different final procedures which contribute to those mechanisms, very little is still understood of the general control of those mechanisms. This is a very important field for the application of ID theory, but we really need to understand more. For proteins, at least, we have the sequence data and understand a little (sometimes too little) of the sequence - structure - function relationship. Much less is understood of transcriptional regulation, which is the key to everything. For example, regarding alternative splicing, it is still not clear what regulates the different splicing in different situations (even if there are interesting data about a "splicing code" in the paper you linked). I think that, when we understand more of the general control of those mechanisms, we will be able to apply a quantitative design detection analysis to the codes and sequences implied. And that will be bad news for the neo-darwinian theory. Again.gpuccio_{January 27, 2016
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Hi Eric gpuccio Thanks to both you guys for the interesting posts. I think we need to keep in mind that DNA protein sequences are a small part of the genome and that how genes are expressed and how RNA is alternatively spliced may be a bigger part of the story. www.sciencemag.org Science 21 December 2012: Vol. 338 no. 6114 pp. 1587-1593 DOI: 10.1126/science.1230612 From this paper you will see very different alternative splicing sequences among vertebrates which may tell us more about evolution then the DNA sequences.bill cole_{January 27, 2016
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Eric: Ah, I forgot to answer your last question! "Asked perhaps another way, do you view the design as being introduced (i) in tiny incremental variations, (ii) in somewhat larger creative events throughout the history of life, or (iii) as front-loading only?" I don't believe in front loading. It is a possibility, but I am not aware of any real empiric support to it. That said, I believe in active design interventions throughout natural history. Only data and good inferences can distinguish between gradual and rather sudden interventions. I think that what we know at present data support both scenarios, even if the second seems more common.gpuccio_{January 27, 2016
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Eric at #37: Well, I can agree with much of what you say here, but... My reasonings are always about molecular data, and molecular data are digital information. In digital information, development by continuity is often the rule. That's why I offered the example of Windows 11. In digital information, it is rather easy to distinguish, at the level of the source code, whether a new software was designed independently from an existing one, or if it is simply derived from an existing one. That kind of "design detection" can also be used in legal trials. There are simply a lot of signatures of the precious design which would never have occurred in a new design from scratch. Wheels can be redesigned independently, but if you build a new computer with new components, but you reuse the same video card, maybe adding just a couple of new features, the old video card will be easily recognizable. Indeed, software design is usually object oriented now. Why? Because that allows to reuse the precious parts of the software more easily, in new contexts and with the minimum quantity of modifications. That's what we usually observe in the biological scenario: reuse of the software, with designed modifications. OK, that was certainly a very interesting discussion. I really thank you for your points, and obviously I remain open to new ones! :)gpuccio_{January 27, 2016
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Eric at #36:
Homology has an extremely poor track record as a tool for determining common descent. It is essentially a circular definition with as many exceptions as rules, is fraught with subjectivity, and is salvaged only with a host of ad hoc rationalizations, such as convergent evolution and the like.
OK, but even in the field of darwinian biologists, descent is not usually based on homology alone, rather on homology and differences. For example, at the molecular level the common principle is to compare differences in homologues. I am not saying that there are not inconsistencies. I am not a big fun of trees, either morphological or molecular. However, at the molecular level, definite techniques can be used, with all their limits, for example the Ka/Ks ratio. I agree with you that homology should never be used alone to infer CD. There is also the HGT issue which complicates things!gpuccio_{January 27, 2016
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Eric at #35:
OK, but if I read the rest of your first post correctly, you are talking about differences within a similar structure, correct?
Yes.
In other words, what we might call “small differences in a similarity,” rather than stark differences. I was more focused on the latter, but let’s see where else we agree
Well, as I have tried to show with the example of myoglobin, we can have rather big differences due to neutral variation. However, I agree with you that big functional differences can only appear by design.
How is the chronological split determined?
From known facts about natural history: fossils, reasonable morphological inference, and so on. IOWs, independently from the molecular issue itself. In my reasoning, I have used only very obvious splits: I think we cannot argue about the different times of appearance of mammals and bony fishes, for example. And it seems obvious that single celled eukaryotes like fungi appeared before metazoa. We also know that primates and humans are very recent in natural history. So, if I compare mouse and humans, I assume a split of about 80 - 100 million years, because mammals first appeared at that time, while humans only a few millions years ago. So, I compare two different mammals, one of them certainly very recent, and the chronological split between possible common ancestors in mammalian line (which is the assumption we are reasoning about) should be approximately that. I think this kind of reasoning is absolutely acceptable.
I think that is a reasonable position, if (a) the time split is independently known, at least to a reasonable level,
I have tried to show that in my reasoning it is independently determined, to a reasonable level.
(b) we are confident that the sequence differences do not meaningfully impact function and are not necessary to the particular organisms in question.
That should be reasonably evaluated from case to case. In the case of myoglobin, which is very well studied, it is IMO very reasonable that most of the differences are not functional, even if part of them can be functional. In other cases, it is not so obvious. But again the point is: we certainly have neutral variation, and where we can reasonably recognize it, it points to continuity and CD.
I presume you mean “is so different” rather than “changes so much.”
Yes, that's what I meant.
I would tend to agree, if (a) we know that variation is actually neutral (probably much less clear in most cases than we might be inclined think),
OK, I have already discussed that, and I think we agree.
(b) we assume that there was only one original single sequence. This brings in the whole issue of how we define similarity-by-descent versus independent/convergent origins.
No, here the point is different: it's the growing difference in time between similar sequences which points to continuity and CD. I can't see how you can explain it in other ways. In the case of independent/ convergent origins we would expect convergence towards function in time, but that is not what we observe: function is there from the beginning. Myoglobins are functional. ATP synthase is functional. In all species. And the functional parts are conserved at sequence level (in the case of some chains of ATP synthase, even for billions of years, as I have often debated). Histones are the same in all eukaryotes, which gives us a reasonable time span of at least one billion years. One of the great unsupported points of neo darwinian theory is that function gradually increases. That is not what we observe in the general case. We observe highly optimized proteins which often share almost the same sequence between distantly related organisms. And in those sequences, we observe often differences which increase with time, and which seem not to affect the function, which remains essentially similar. That's the correct argument for CD.
What I mean is that we don’t know how to build an organism. We don’t know the details. No-one has any reasonable level of knowledge about how all the various structures work together, or how tweaks to DNA could possibly lead to large-scale changes. Thus, it is simply factually false for a Darwinist to claim that something like random mutations and natural selection can change an organism from A to B. They have no idea, even in principle, whether it is possible.
Agreed!
If a similar gene counts as evidence for a descent relationship, then unique genes suggest something else entirely.
Yes. New genes with new functions suggest design from scratch. I absolutely agree with that, and with the rest of what you say here. But I would add that the assumption of common descent + design allows us to test some interesting possibilities about design procedures in natural history. For example, as I have discussed many times, there are many clues which seem to suggest that, at least in some cases, new functional genes arise from non coding DNA, often by the working of transposone activity. Now, if that is confirmed (and I believe it will be), we can find homologies between the functional sequence in the more recent species (let's say humans) and the non coding sequence in older species (let's say primates). If probabilities can well exclude sheer luck, in the light of the CD hypothesis that can mean only one thing: gradual design which prepares a functional sequence in non coding form, and at some point, when it is requested, activates it in coding form. By transposone activity, which is a very good candidate for a consciousness - matter interface at quantum level.gpuccio_{January 27, 2016
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#3: You mentioned getting from organism A to B is a matter of common descent and design. I wanted to push on the design aspect, if perhaps just definitionally. Specifically, when we look at designed systems, we can find many similarities across systems of the same domain (transportation, for example), but that does not necessarily mean there is a descent relationship. For example, compare the wheels on my car and the wheels on the Space Shuttle. Lots of similarities. We could argue that there is a descent relationship. We could analyze various characteristics and come up with a tree. We could create nested hierarchies to show where my wheel and the Space Shuttle wheel each lie in the tree. We could call them part of a family. We could make claims about one giving rise to the other or about some common wheel giving rise to both. But it would all be nothing more than an analogy, a creative description, a made-up tree and a made-up hierarchy and a made-up story of descent. Because design does not work that way. Design is not, fundamentally, a process of descent from A to B to C. Yes, products change over time, but they do so not on the basis of some natural process. Design works by understanding the field, being aware of and analyzing various options, considering prior systems, applying principles, re-using parts or approaches, and so on. A new design might bear striking similarity to something that came before. Or it might scrap everything and start all over with a wildly different approach. That is how design works. It is an intellectual, creative effort. Any attempt to create a genealogy or a tree or a nested hierarchy is just a matter of descriptive convenience. So . . . When you say that organisms came about through common descent plus design, what does that really mean in practice? If, despite the similarities between organism A and B, organism B exists only as a result of additional engineering, including, we must not forget, making sure that even the similarities are properly integrated into the new functional whole – if it requires a substantial re-engineering exercise to get from A to B, then how does that differ from design generally? Does it even make sense to say that there is a descent relationship between A and B? Is the only reason to refer to common descent in such a case just to give lip service to the concept? Or are we really talking about regular injections of design tweaks over time? Keeping in mind that the fossil record is largely discontinuous, is the design process one of “slight, successive modifications” or one of larger-scale, discreet creative bursts? Asked perhaps another way, do you view the design as being introduced (i) in tiny incremental variations, (ii) in somewhat larger creative events throughout the history of life, or (iii) as front-loading only?Eric Anderson_{January 26, 2016
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#2: Homology has an extremely poor track record as a tool for determining common descent. It is essentially a circular definition with as many exceptions as rules, is fraught with subjectivity, and is salvaged only with a host of ad hoc rationalizations, such as convergent evolution and the like. Personally, I am very unimpressed with a tool that claims similar structures point to common descent . . . Except when they don’t. Thus, given that everyone seems to recognize that similar structures might be due to common descent but might not, when presented with a similarity between organisms that is supposed to demonstrate some common descent relationship, I feel perfectly comfortable asking, “Perhaps. But what if it doesn’t?” This is not to say that we just throw the whole enterprise out the door. Some interesting facts can be collected, some interesting similarities can be noted, we might even learn some biology in the process. But as a general matter, I think we have to view the collection, cataloging, and relationship-tree-drawing exercise as highly tentative and subject to massive error bars.Eric Anderson_{January 26, 2016
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gpuccio:
I have said many times that, IMO, the strongest argument at the molecular level for CD is not the homologies, but the differences.
OK, but if I read the rest of your first post correctly, you are talking about differences within a similar structure, correct? In other words, what we might call “small differences in a similarity,” rather than stark differences. I was more focused on the latter, but let’s see where else we agree . . .
My point is: I accept that neutral variation happens, if there is not a strong functional constraint which translates into negative (purifying) selection.
Agreed.
So, simple strong homology and conservation is not the best argument [for] CD.
Agreed.
[Talking about various splits in time between humans and other organisms] . . . we have [x] million years of chronological split.]
How is the chronological split determined?
… 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.
I think that is a reasonable position, if (a) the time split is independently known, at least to a reasonable level, and (b) we are confident that the sequence differences do not meaningfully impact function and are not necessary to the particular organisms in question.
But many other differences are due to different functional constraints in different species. That is the case, IMO, with transcription factors. . . . So, while the DNA binding site works in similar ways in different species, the “rest” regulates different procedures in different species. That’s why the “rest” changes so much: not because it is not functional and neutral variation acts on it, but because its functions vary from species to species.
I presume you mean “is so different” rather than “changes so much.” Again, the source of the change or whether there has been a “change” is the question at issue. :)
So, restricting function to conserved sequences is a potential error. Different functions require different sequences.
Absolutely.
However, we cannot deny that neutral variation happens: we see it happening even in the human genome, and generating functional polymorphisms, exactly as negative variation generates genetic diseases.
Agreed.
So, neutral variation, when it is really neutral variation, tells us that proteins pass from one species to another, and bring with them the neutral differences which have accumulated through time.
I would tend to agree, if (a) we know that variation is actually neutral (probably much less clear in most cases than we might be inclined think), and (b) we assume that there was only one original single sequence. This brings in the whole issue of how we define similarity-by-descent versus independent/convergent origins.
I must disagree. I believe that I have a very good knowledge about what it takes “to get from organism A to organism B”: it takes design, the input of new original functional information. And you may probably agree with that.
Of course! :) What I mean is that we don’t know how to build an organism. We don’t know the details. No-one has any reasonable level of knowledge about how all the various structures work together, or how tweaks to DNA could possibly lead to large-scale changes. Thus, it is simply factually false for a Darwinist to claim that something like random mutations and natural selection can change an organism from A to B. They have no idea, even in principle, whether it is possible.
The point is: when I say that there is strong evidence for CD, in no way I am saying that CD explains the evolution of species. What I am saying is: a) There is CD and b) New species appear by design, and reuse some previous information by CD. IOWs, CD is guided CD, engineered CD.
I would say that is certainly a reasonable position to take. And is far stronger than the purely naturalistic story. ----- I think you have some reasonable and well-considered thoughts on the topic. You’ve probably followed some of the issues around common descent more closely than I, but to the extent I’ve looked into them, I think we are largely on the same page. If you’ll permit me, I just wanted to clarify my earlier comment about dissimilarities. We can look at it from a high-level perspective as follows: Organism A and organism B share a similar structure, say, a similar gene, based on genetic sequence. We look at this and conclude that there is a descent relationship between A and B (or, from a common ancestor). Yet at the same time, A and B have a number of unique genes, say, a dozen of them. What do we make of that? If a similar gene counts as evidence for a descent relationship, then unique genes suggest something else entirely. I can’t just say that a similar gene in organism B came from organism A (explained by the alleged descent relationship) and at the same time ignore the many more genes that don’t have similarities in organism A. After all, where did they come from? From the same descent relationship? Obviously not. Unfortunately, if an answer is given it is usually some vague claim about horizontal gene transfer and the like. More often than not, the point is simply ignored. Yet it is precisely the differences that evolution is supposed to be able to explain. Similarities from generation to generation are not a smoking gun for evolution. As you well point out, we can explain small differences in the same gene by neutral variation. It is precisely the claim of novelty, the claim of ability to generate new, specified, functional structures that lies at the heart of evolutionary theory – at least the grand claims of the theory. So we might be able to explain a few tweaks in the same gene accumulating by neutral variation over time, but where did all the unique new stuff come from? You have proposed an answer in the claim of design – if not a completely satisfactory answer, at least a rational one. The materialist creation story has no rational answer. (Two further points to follow.)Eric Anderson_{January 26, 2016
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Windows 11, like the humanatee, is a mythical creature.Mung_{January 26, 2016
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