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Kirk Durston: A common either-or mistake both Darwinists and ID theorists make

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Biophysicist Kirk Durston of the New Scholars Society offers an explanation below:

Note: Kirk Durston is back and this post has been stuck to the front page until late this evening EST, so that further comments and his responses may be noted. – News

There is a common either-or mistake made by most Darwinists and, quite frequently, by ID theorists as well. The mistake, which is an example of the fallacy known as the false dichotomy, can be described as occurring when one assumes that either no functional information encoded in the genomes of life can be produced by natural processes, or all of it was produced by natural processes. A closely related mistake made by Darwinists is the assumption that if natural processes can produce a trivial level of functional information, then we can safely conclude that natural processes can produce all biological information.

There are still challenges in mathematically defining functional information or functional complexity. For my purpose here, however, I will simply use the mathematical descriptions published by Hazen et al., and Durston et al. Both approaches cited are very closely related to an earlier equation published in 1951 by Leon Brillouin, which can be simply represented as

FI = -log nf/nt

Where nf = number of sequences that are functional and nt = the total number of possible sequences. It should be clear from the above equation that if nf is large enough for examples to be generated by random recombinations, then functional information (FI) can be generated by random natural processes, albeit a trivial level. For example, it is clear from work done at the Georgia Institute of Technology, that nf for simple binding pockets is pretty high, which entails that the FI required to code for binding pockets is relatively trivial.

Reflection on the above equation reveals that the FI required for a given function can range anywhere from zero to some very high number. It is, therefore, a mistake to assume that FI can only be generated by intelligence; a trivial level of FI can be produced by completely mindless processes, as should be obvious from the above equation, and as the Georgia Tech results illustrate.

It is also a mistake to assume, as many Darwinists do, that because mindless processes can generate a trivial level of FI, therefore mindless processes can generate high levels of FI. Again, reflection upon the above equation (or the more detailed equations published by Hazen or Durston) reveal that the higher the FI required, the less probable it becomes (i.e., the nf/nt ratio approaches zero).

The fatal mistake made by Darwinists at this point is to invoke what has become the Darwinist god-of-the-gaps, namely selection. As we can illustrate from evolutionary algorithms, selection requires a fitness function which, itself requires FI to encode. Of course, it follows from what I am arguing here that trivial levels of selection can be produced with trivial levels of FI. The question is whether natural selection has sufficient information to locate stable, functional, biological proteins. All our work to date seems to falsify that option and verify the need and actual role for intelligent design (in this case human) when producing artificial proteins of any significant structure. To clarify, recent building of artificial proteins is an example of intelligent design in action.

The Georgia Tech work has led some Darwinists to believe that because binding pockets are relatively trivial to encode in a sequence that, therefore, we have somehow explained how natural processes could have encoded biological proteins. In real life, however, proteins are about a lot more than simple binding. Binding to the right molecule is important, at the right time, at the right location and with the right binding strength so that the bond can be broken at the right time and place, etc. This can often require a larger 3D structure for proper functionality, that has a nf/nt ratio approaching zero. For example, if we take the results published for 35 protein families by Durston et al., and solve for nf/nt, we observe that it is extremely small for many protein families.

My contention is that the ability to generate statistically significant levels of functional information is unique to intelligence. It follows from this that if a function can be achieved with a statistically insignificant level of FI, then intelligence is not required. Statistical significance, therefore, is the safeguard against false positives and can be measured in a variety of ways, such as measuring the adjusted residual of the outcome and choosing a cutoff that represents a very high confidence level, such as 99.9% or greater. With this in mind, an executive summary of my own case for intelligent design in biological life is available here.

Comments
Jerad, in spite of this consistent evidence, of which I’m sure you are well aware, you still believe in evolutionary theory, to which I can only ask, ‘Are you sure you’ve really understood evolutionary theory?’
Yup. The mutual support given by multiple lines of independent evidence. over 150 years of research and data collection, the fact that the theory has withstood various and sundry criticisms and attempts to knock it down. In fact, some of the strongest evidence in support of the theory has come in the last 60 years with the discovery of the structure of the DNA molecule and the genetic evidence of transposons, ERVs and the coding redundancies. For any other phenomena the incredible volume of confirmatory evidence would be more than enough. Still I've thought long and hard about it. And, I admit, it seems fantastical at times. But there is no better explanatory model. There's no hypothesis that comes close to lining up with ALL the data. It's elegant and it works. And it requires no assumption of some undefined, undiscovered agent. It has predictive power, it lines up with all the data, it's supported by multiple lines of evidence, we are even starting to see it 'in action'. I'm just glad I was born at a time when we are figuring out how we came to be. Its fascinating. It helps me to appreciate the wonders of nature and how lucky we are to be around at a time when the structures beneath the surface are becoming discernible.Jerad
July 26, 2013
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Though I did think disqualifying human beings as designers was a bit rich.Axel
July 26, 2013
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From your #11, JLAfan2011: 'Show me on natural thing by experimant in the lab or in the field that a designer was invloved in. I don’t want human made examples and I don’t want evidence after the fact.' I can't afford to visit a beaver-lodge construction site on my own, never mind organise a field trip for you, fer goodness sake.Axel
July 26, 2013
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If you don’t know what it says then how do you know you disagree with it?
Well we don't know if we disagree with something we have never seen. We do disagree with several basic conclusions of modern evolutionary theory based on the evidence we have seen. But maybe there is something we are not aware of. That is what the comment about "alleged" evolutionary theory was referring to. Is there something we are not aware of. You are presenting the "overwhelming evidence" argument and we have seen that before but science does not work that way. A lot of what you present does not indicate any specific mechanism for evolution. So I suggest that you present the best case for how major changes happened. One of the necessities for major changes is the origin of new proteins which is what this OP is about. New proteins are not the only thing necessary but it is one of them. What determines where these proteins go and in what sequence is unknown as of this moment so is another major issue. New proteins however, present a very thorny problem.jerry
July 26, 2013
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'And exactly what does cumulative Natural Selection accumulate?' First of all, a blueprint, Philip, a design? Then it's all random systems go! Like working out a rubik cube by accidental fiddle-faddling. It'll all fall into place just as per the blueprint. Apparently, there's a strange, little-understood affinity between designs and randomness.Axel
July 26, 2013
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Hence significance of 500 - 1,000 bit thresholds as a barrier to blind search for novel islands of function, starting with the first. Where discussing incrementalism within an island begs the pivotal question, finding islands. And how do we know, isolated islands? Multipart function depending on specific arrangement, interfacing and coupling, in a world where otherwise, ever so many arrangements are possible. KFkairosfocus
July 26, 2013
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Jerad you state:
"Natural selection is cumulative and not random."
And exactly what does cumulative Natural Selection accumulate?
Climbing Mount Improbable - Evolution Vs. Functional Proteins - Doug Axe & Stephen Meyer - video http://www.metacafe.com/watch/4018222/
Hmm it's not proteins that it accumulates,, In fact the overwhelming tendency of Natural Selection is to eliminate (purify) a genome of non-functional elements,,
Natural Selection, Genetic Mutations and Information - EXPELLED - video "...but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have..." Maciej Marian Giertych - Population Geneticist - member of the European Parliament - EXPELLED http://www.metacafe.com/watch/4036840
To the extent Natural Selection can be said to accumulate anything Jerad, it can be said that Natural Selection is excellent in accumulating slightly detrimental mutations long before any rare island of functionality will ever be stumbled upon:
Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load: Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space. http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle - "Haldane's Ratchet" - Christopher L. Rupe and John C. Sanford - 2013 Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage. Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as "Haldane's Dilemma" is very real. Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon "Haldane's Ratchet". http://creationicc.org/more.php?pk=46 Sanford’s pro-ID thesis supported by PNAS paper, read it and weep, literally - September 2010 Excerpt: Unfortunately, it has become increasingly clear that most of the mutation load is associated with mutations with very small effects distributed at unpredictable locations over the entire genome, rendering the prospects for long-term management of the human gene pool by genetic counseling highly unlikely for all but perhaps a few hundred key loci underlying debilitating monogenic genetic disorders (such as those focused on in the present study). https://uncommondescent.com/darwinism/sanfords-pro-id-thesis-supported-by-pnas-paper-read-it-and-weep-literally/
the evidence for the detrimental nature of mutations in humans is overwhelming for scientists have already cited over 100,000 mutational disorders.
Inside the Human Genome: A Case for Non-Intelligent Design - Pg. 57 By John C. Avise Excerpt: "Another compilation of gene lesions responsible for inherited diseases is the web-based Human Gene Mutation Database (HGMD). Recent versions of HGMD describe more than 75,000 different disease causing mutations identified to date in Homo-sapiens." I went to the mutation database website cited by John Avise and found: HGMD®: Now celebrating our 100,000 mutation milestone! http://www.hgmd.org/
Also of note;
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
Jerad, in spite of this consistent evidence, of which I'm sure you are well aware, you still believe in evolutionary theory, to which I can only ask, 'Are you sure you’ve really understood evolutionary theory?'bornagain77
July 26, 2013
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Upright Biped
Dr Liddle, for a replicator to be “Darwinian capable” it must have the capacity to translate a genotype into a phenotype.
Well, it must have heritable variation in reproductive success. The thing that has reproductive success is the phenotype. The thing that makes it heritable is what you might call the genotype, but at its simplest, the genotype is the phenotype. For example if you had a double stranded polymer that tended to split into two single strands (as the Szostak lab has suggested), and those single strands then bonded with corresponding monomers in the environment to produce two versions of the original double strand, you'd have a self-replicator with a genome that was also the entire phenotype. And if, for example some monomers are more prevalent in the environment than others, then those polymers whose segments frequency most closely matched the distribution in the environment would tend to reproduce most successfully. So you've got a Darwinian-capable self-replicator already. Szostak also suggests that the combination of such polymers and lipid vesicles that enclose them provides a slightly more complex phenotype, where again, very simple properties of the enclosed polymers, length, for intance - could affect reproductive success - for instance by optimising osmotic pressure gradients. So while I agree that a phenotype-genotype relationship is important, and that, specifically, the genotype needs to affect the reproductive success of the phenotype ("heritable variance in reproductive success") to be capable, by definition, of Darwinian evolution, there is no need for that relationship to involve a "translation" process as we now know it. Nor even, once we are talking about RNA, do we need even to involve proteins - RNA is a double polymer capable not only of self-replication but of self-catalysis, offering the possibility, again, of catalysing compounds within the vesicle that could make it more robust, for instance. I'm not saying these things did happen, just that they are hypotheses currently being investigated, and which do not involve the modern DNA-RNA-Protein pathway and yet would be Darwinian-capable.
We do not know how simple a self-replicator has to be to be Darwinian-capable. It might be very simple indeed, and within reach of chemistry and physics, or it might not be.
You pose the question in a manner to avoid the answer. We do not know “how simple” it can be, but we do know how complex it must be – at least at a minimum, in order to accomplish Darwinian evolution.
I'm not trying to "avoid the answer" - I don't know the answer. No-one does. That's why there is active research going on. We don't know how complex it must be at a minimum. That's why I said we don't know how simple it could be. It's the same question, and we don't know the answer.
Those requirements have been explained to you in a coherent physical model which has been verified by both experiment and logic.
Not in any way that persuades me that the DNA-RNA-protein process is the simplest Darwinian-capable process. You have explained your case, but that doesn't mean your explanation holds water. I don't think it does.
Exactly none of the key hurdles in that model have been shown to be associated with mere “chemistry and physics”. What is gained by ignoring these facts? To simply repeat “I do not believe the model” is insufficient for empirical discourse. If you cannot demonstrate it to be false, and if you choose not to accept it provisionally, then you are left to simply ignore it. There are no other alternatives.
Because they aren't facts, Upright Biped. I know that you think that there is something other than "mere chemistry and physics" going on, but I see no reason to think so. We know that what goes on in the cell requires nothing other than chemistry and physics of the molecules. They are certainly very fancy molecules, and I understand that IDers think they can only have come into existence by means of some kind of intelligent agent, but they are, nonetheless, biochemical molecules and they do what they do because of physical and chemical forces in the cell, not anything else. And nothing you have said persuades me that there is some necessary barrier between a Darwinian-capable pre-DNA system and a DNA system. Indeed there is a body of research on the evolution of the ribosome, for instance. There might be a barrier, but I see no reason to infer one, just because the DNA-RNA-ribosome pathway is the way it is.Elizabeth B Liddle
July 26, 2013
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And BTW, could you please link to this alleged “evolutionary theory” so we can all read what it says. Thanks.
If you don't know what it says then how do you know you disagree with it?Jerad
July 26, 2013
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Evidence please. Cumulative selection = ID
The fossil record, the DNA evidence, bio-geographic distributions, morphology. Cumulative selection is just one round of environmental culling on top of another, on top of another, etc. You know, I'm sure you've heard all the explanations before and so your asking for another round of clarification is just time wasting really. No matter what I say you're going to claim that my evidence isn't adequate. BUT you won't have any good, positive counter evidence and you'll assert that finding gaps in our current knowledge is enough to call the whole of evolutionary theory into question. I think there are ID proponents who really are interested in having a dialogue and considering the actual evidence. But, sadly, there are others who just look to score immediate points on blogs which have nothing to do with the real evidence or research. When can we get past the endless repetition of restating what evolutionary theory does and doesn't say? And, more importantly, can we please give up the notion that the Uncommon Descent forum is the proving ground? I might argue my case badly but it doesn't mean my 'side' has lost. IF you all really are interested in the best case for evolutionary theory then you won't find it here, or in Dr Dawkins books, or at any one website. You'll find it in the accumulated knowledge generated by 150 of work done by biologists probing and testing and expanding on the basic framework. Darwin's idea survived the insight given by Mendel. It survived, and was upheld, by the discovery of the structure of DNA. Modifications to the basic theory have had to be made as one would expect. All knowledge is provisional. But the core is very solid. And to be asked for evidence now that natural selection is not random is just showing a wilful and intentional ignorance about the model. If you want to be taken seriously then stop making ignorant arguments. Show some insight and some knowledge and make some real criticisms. Like Dr Margolis. Goodness knows, that woman had to fight hard to get her ideas accepted. But she did because she did the work and had the evidence and really understood the basic theory. And asking questions that have been addressed many, many, many times before is not understanding the basic idea. It's just wasting time and trying to score points. And I wish some of the more insightful ID proponents would call their fellows on such pointless behaviour. But you won't. You all have this conspiracy theory mindset and we're 'the enemy' against who you all must strive. And even bad counter-arguments are good because they uphold the side.Jerad
July 26, 2013
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And BTW, could you please link to this alleged "evolutionary theory" so we can all read what it says. Thanks.Joe
July 26, 2013
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Jerad:
Natural selection is cumulative and not random.
Evidence please. Cumulative selection = IDJoe
July 26, 2013
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Please tell us the difference between darwinian processes and a random draw.
Natural selection is cumulative and not random. Are you sure you've really understood evolutionary theory?Jerad
July 26, 2013
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Elizabeth:
But I will say that perfectly reasonable people are perfectly capable of being persuaded, by evidence, that Darwinian evolution i.e. adaptation by means of heritable variance in reproductive success in the current environment, not only works, but can be observed to work, in lab, in field, and in silico.
Unlike you, perfectly reasonable people understand what darwinain evolution entails. And it is more than just "heritable variance in reproductive success in the current environment".Joe
July 26, 2013
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Elizabeth:
Therefore Darwinian processes, not random draw, must considered as possible non-design origins for them.
Please tell us the difference between darwinian processes and a random draw.
The minimum system required for Darwinian evolution is a population of self-replicators that replicate with heritable variance in reproductive success in the current environment.
Well Tracy and Lincoln had a population of self-sustained replicating RNAs that had heritable variation. But nothing new evolved.
The virtual organisms in an evolutionary algorithm satisfy some criteria for life, but not others.
Evolutionary algorithms are evidence for intelligent design evolution, not darwinian evolution. Ya see Lizzie, EAs have a goal or goals and darwinian processes do not.Joe
July 26, 2013
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Dr Liddle, for a replicator to be “Darwinian capable” it must have the capacity to translate a genotype into a phenotype.
We do not know how simple a self-replicator has to be to be Darwinian-capable. It might be very simple indeed, and within reach of chemistry and physics, or it might not be.
You pose the question in a manner to avoid the answer. We do not know “how simple” it can be, but we do know how complex it must be - at least at a minimum, in order to accomplish Darwinian evolution. Those requirements have been explained to you in a coherent physical model which has been verified by both experiment and logic. Exactly none of the key hurdles in that model have been shown to be associated with mere “chemistry and physics”. What is gained by ignoring these facts? To simply repeat “I do not believe the model” is insufficient for empirical discourse. If you cannot demonstrate it to be false, and if you choose not to accept it provisionally, then you are left to simply ignore it. There are no other alternatives.Upright BiPed
July 26, 2013
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Actually it is better to think of the information in a gene pools as opposed to specific proteins. I am sure Durston has a much better answer. But the basic answer is yes, information can be increased by some small amounts and happens quite frequently. By the way information decreases from gene pools quite frequently as certain alleles/genes get eliminated.jerry
July 26, 2013
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gpuccio:
a) I, like many other people, have dedicate much time here to “considered rebuttals” of current OOL “theories”. I dismiss them as fantasy, but I have explained many times why I do that.
OK.
b) All science is made of inferences. Some are good, some are bad. But there is nothing else in empirical science. Only inferences to explain facts.
Or models to fit data :) I agree.
c) I do deny that darwinian processes account for “macroevolution” at all. They can generate no complex functional information. They have a minor role in microevolution and simple adaptations. If, after all the time we have discussed, you have not yet understood that this is my position, there is really no hope.
I thought it was your position, but your post seemed to contradict that. Thanks for clarifying.
d) I do believe and maintain that your “perfectly reasonable people” stick, for reasons that are completely mysterious to me, to perfectly unreasonable convictions and ideas. Is that an unpopular belief? Probably. But it’s exactly what I believe.
OK.Elizabeth B Liddle
July 26, 2013
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Mung
Tell us Dr. Liddle, what is the minimal system required for Darwinian evolution? Is such a system “alive,” and if so, according to which definition of “life”?
The minimum system required for Darwinian evolution is a population of self-replicators that replicate with heritable variance in reproductive success in the current environment. I do not know - no-one does - what the simplest molecular assembly is that can do this is. If we were to find one (for example, Szostak's populations of lipid vesicles containing self-replicating double polymers), I don't know whether you'd call it "alive" or not. It would satisfy some traditional criteria for living things, anyway - growth, reproduction and nutrition.
Are genetic algorithms alive?
The virtual organisms in an evolutionary algorithm satisfy some criteria for life, but not others.
Are they capable of Darwinian evolution?
Yes.Elizabeth B Liddle
July 26, 2013
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Elizabeth: We can certainly leave it there. Just a few clarifications: a) I, like many other people, have dedicate much time here to "considered rebuttals" of current OOL "theories". I dismiss them as fantasy, but I have explained many times why I do that. b) All science is made of inferences. Some are good, some are bad. But there is nothing else in empirical science. Only inferences to explain facts. c) I do deny that darwinian processes account for "macroevolution" at all. They can generate no complex functional information. They have a minor role in microevolution and simple adaptations. If, after all the time we have discussed, you have not yet understood that this is my position, there is really no hope. d) I do believe and maintain that your "perfectly reasonable people" stick, for reasons that are completely mysterious to me, to perfectly unreasonable convictions and ideas. Is that an unpopular belief? Probably. But it's exactly what I believe.gpuccio
July 26, 2013
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Could natural selection add to the FI of the complex protein by some incrementally small amount? If so, why. If not, why not?
Absolutely, yes. I explained why in my answer to you but it is better to think of alleles instead of proteins and to think of populations instead of an individual protein. A population could have several different versions of the protein, each slightly different and this represents an increase in information. I haven't read all the other replies but I doubt they say something different.jerry
July 26, 2013
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gpuccio
Yes, but “a posteriori”, from all that we know, the only self-replicators that have ever been observed in the natural world are, at present, prokaryotes. You are free to imagime “a priori” any possible darwinian self-replicator, be it stone, air or RNA, but as far as I know there is nothing that can help those myths to “evolve” from their status of pure imagination to the status of scientific hypothesis.
There are plenty of hypotheses that can be tested, and are. In any case, ancient prokaryotes are themselves putative - we don't have any to observe! They are an inference, from perfectly valid data and data analysis. The same techniques can potentially take us back further. Obviously you are entitled regard such work as "fantasy" but many scientists beg to differ, and for good reason. I think it needs a more considered rebuttal than mere dismissal as "fantasy".
It’s not a misunderstanding. I am not interested in phyla or species here. New proteins simply emerge. That is a fact. They emerge in new species (or phyla, or whatever), and they do have new sequences and new functions.
Well, as you say, they emerge in populations of organisms, and yes, they have new sequences and functions. My point is that you do not need new proteins for either speciation or adaptation to occur.
At OOL (let’s say in LUCA, that for me, and for all reasonable people, is the only OOL empirically known)
"LUCA" is not "empirically known" to be the Origin of Life. It is merely an inferred organism, or population, regarded as the Last Universal Common Ancestor. That inference does not imply that it was also the First. And while you might regard anyone who does not regard the LUCA as the FUCA as not "reasonable", there are plenty of them. There is simply no reason to make that assumption.
less than half of protein superfamilies were present. The others emerged after that. Are you denying this simple fact?
Well, it's not a "simple fact" - it's an inference. But I'm certainly not denying it. It supports my case, not yours - that the majority of protein superfamilies emerged after Darwinian-capable organisms are inferred to exist. Therefore Darwinian processes, not random draw, must considered as possible non-design origins for them. The more interesting problem is how the protein superfamilies that were present at LUCA got there. Most biologists would say they evolved - i.e. assume that there were many many populations ancestral to LUCA, all capable of evolving. Again, you may disagree, but there's nothing intrinsically "unreasonable" about this.
Must? That is funny indeed!
Not really. Obviously you can't invoke something that doesn't yet exist to account for itself.
I will never invoke darwinian processes to account neither for the first living replicators nor for for what evolved after. I still have some respect for reason and science.
You deny that Darwinian processes account for evolution at all? Really?
I maintain That OOL and the following evolution of species should suggest the need for a similar explanation to all reasonable people who are not committed by faith to give unwarranted room to the neo darwinian theory “a priori”.
Well, I think we'd better just leave it there, gpuccio. I didn't realise that you denied Darwinian evolution completely. I thought you just thought it insufficient. But I will say that perfectly reasonable people are perfectly capable of being persuaded, by evidence, that Darwinian evolution i.e. adaptation by means of heritable variance in reproductive success in the current environment, not only works, but can be observed to work, in lab, in field, and in silico.Elizabeth B Liddle
July 26, 2013
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RodW: I am afraid that still your question is not completely clear, but I will assume that it corresponds to my interpretation a) in my post #34. Is that correct? However, I think I have tried to answer both possible meanings of your question, in that post.gpuccio
July 26, 2013
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An interesting fact as to the universal RecA protein, which Dr. Durston mentions here in these videos,,
Functional Information In Molecular Biology - Kirk Durston - video (RecA is at the 8:15 minute mark) http://www.metacafe.com/watch/3995236/ Intelligent Design - Kirk Durston - entire video http://vimeo.com/1775160 Proteins - Kirk Durston - short video http://www.metacafe.com/watch/4171853
and which Dr. Durston also mentions here in this paper,,
(A Reply To PZ Myers) Estimating the Probability of Functional Biological Proteins? Kirk Durston , Ph.D. Biophysics – 2012 Excerpt (Page 3-5): ,,,This method was applied to 35 protein families, including the universal protein RecA,,, The Probabilities Get Worse This measure of functional information (for the RecA protein) is good as a first pass estimate, but the situation is actually far worse for an evolutionary search. In the method described above and as noted in our paper, each site in an amino acid protein sequence is assumed to be independent of all other sites in the sequence. In reality, we know that this is not the case. There are numerous sites in the sequence that are mutually interdependent with other sites somewhere else in the sequence. A more recent paper shows how these interdependencies can be located within multiple sequence alignments.[6] These interdependencies greatly reduce the number of possible functional protein sequences by many orders of magnitude which, in turn, reduce the probabilities by many orders of magnitude as well. In other words, the numbers we obtained for RecA above are exceedingly generous; the actual situation is far worse for an evolutionary search. http://powertochange.com/wp-content/uploads/2012/11/Devious-Distortions-Durston-or-Myers_.pdf
Adding to the 'context dependency' of aa sequences for RecA (and other proteins) which Dr. Durston mentioned in the preceding paper, it is now found that his "universal RecA protein" is also found to be involved in a rather 'miraculous' feat of extreme genome repair which takes this 'context dependency' issue to a whole other level!
The World’s Toughest Bacterium - 2002 Excerpt: Several recent studies of the bacterium's DNA repair pathway have focused on one protein that is now known to be essential for radiation resistance—the RecA protein.,, "When subjected to high levels of radiation, the Deinococcus genome is reduced to fragments," they write in Proceedings of the National Academy of Sciences. "RecA proteins may play role in finding overlapping fragments and splicing them together." http://www.genomenewsnetwork.org/articles/07_02/deinococcus.shtml Extreme Genome Repair - 2009 Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal.,,, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319128/
i.e. How can RecA proteins possibly know how to reconstruct 'shattered' DNA? If the Genetic/Molecular reductionism model of neo-Darwinism were actually true this should not be possible? Clearly the information for how the DNA is to be reconstructed must reside elsewhere than within the shattered DNA or even within the RecA protein.bornagain77
July 26, 2013
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RodW, It is STILL a matter of EVIDENCE. Also what "evolution" are you referring to?Joe
July 26, 2013
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Elizabeth: We have been there before...
We do not know how simple a self-replicator has to be to be Darwinian-capable. It might be very simple indeed, and within reach of chemistry and physics, or it might not be. But we can’t assume one way or the other a priori.
Yes, but "a posteriori", from all that we know, the only self-replicators that have ever been observed in the natural world are, at present, prokaryotes. You are free to imagime "a priori" any possible darwinian self-replicator, be it stone, air or RNA, but as far as I know there is nothing that can help those myths to "evolve" from their status of pure imagination to the status of scientific hypothesis.
In addition, we can’t assume that the simplest Darwinian-capable selfreplicators had proteins at all. So there is no a priori reason for saying that Darwinian processes can’t have led to functional proteins, and that therefore the only non-design pathway was random draw.
Please, refer to the previous point. I am trying to discuss science here. Although I like fantasy fiction, this is probably not the place to discuss it. By the way, I have just begun the "Wheel of time" series! :)
I think this is a misunderstanding. There’s nothing special about phyla – all lineage divergences, under the Darwinian hypotheses, are speciation events, and speciation can happen without radically new proteins emerging. And we simply do not know that “new original proteins” are needed for OoL.
It's not a misunderstanding. I am not interested in phyla or species here. New proteins simply emerge. That is a fact. They emerge in new species (or phyla, or whatever), and they do have new sequences and new functions. At OOL (let's say in LUCA, that for me, and for all reasonable people, is the only OOL empirically known), less than half of protein superfamilies were present. The others emerged after that. Are you denying this simple fact?
It’s possible that peptides were part of the pre-biotic scene, but possibly not. It’s a question worth asking but not one to which we can assume we have an answer.
An answer that we certainly do have is that functional proteins, hundreds of them, were part of LUCA, the only OOL empirically known. For me, that is a very interesting answer, and not one that is based on pure imagination.
They must require completely different solutions, because you can’t invoke Darwinian processes to account for the first Darwinian-capable self-replicator! Whereas you can invoke Darwinian processes to account for things that evolved as a result of there being Darwinian-capable self-replicators.
Must? That is funny indeed! I will never invoke darwinian processes to account neither for the first living replicators nor for for what evolved after. I still have some respect for reason and science. I maintain That OOL and the following evolution of species should suggest the need for a similar explanation to all reasonable people who are not committed by faith to give unwarranted room to the neo darwinian theory "a priori".
So the interesting OoL question is: how simple did that first Darwinian-capable self-replicator have to be, and (for IDists), was it within reach of non-Darwinian processes, such as the physical and chemical processes on early earth?
To that, we have very simple and reasonable empirical answers: the only biological self-replicators that we know to exist are prokaryotes, and the first prokaryote of which we can empirically know anything is LUCA. And even prokaryotes are not "Darwinian capables", if not for trivial cases of microevolution. And no, LUCA was not within reach of neo darwinian processes. But, as for that, neither were all the following species that emerged.gpuccio
July 26, 2013
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Elizabeth, How Dr Nim came into existence directly affects how it operates from that point on. Go figure. The same can be said for computers, automobiles, TVs, blenders, microwaves, etc.Joe
July 26, 2013
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My apologies for not proofing my post. As it is my question is vague..so I'm reposting here with correction: I have a question for KD when he gets back..or anyone else for that matter. Consider a complex protein with a great deal of FI. Lets ignore for the moment how this protein came into existence. Durston suggests that small amounts of FI can be produced by evolution. Could natural selection add to the FI of the complex protein by some incrementally small amount? If so, why. If not, why not?RodW
July 26, 2013
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Elizabeth:
But we do not know this – it’s the subject matter of OoL research. We do not know how simple a self-replicator has to be to be Darwinian-capable. It might be very simple indeed, and within reach of chemistry and physics, or it might not be.
Lizzie, scioentists have been working on this issue for many decades. Therefor if it is simple then you are calling all of those scientists imbeciles.
In addition, we can’t assume that the simplest Darwinian-capable selfreplicators had proteins at all.
You are still living in a fantasy world and confusing it with the real one.
So there is no a priori reason for saying that Darwinian processes can’t have led to functional proteins, and that therefore the only non-design pathway was random draw.
Evidence, Lizzie, you don't have any evidence to support anything you say.
They must require completely different solutions, because you can’t invoke Darwinian processes to account for the first Darwinian-capable self-replicator!
Nope, blind and undirected chemical processes are still blind and undirected chemical processes. Also Tracy and Lincoln's experiment with a self-sustained replication of RNAs refute your claims. I take it that is why you ignore their results and prattle on anyway.Joe
July 26, 2013
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gpuccio
a) First of all, it seems rather odd that you try to separate so strongly two problems that are, indeed, strictly connected. OOL needs living beings to come into existence, and living beings do need a lot of biological information to exist.
But we do not know this - it's the subject matter of OoL research. We do not know how simple a self-replicator has to be to be Darwinian-capable. It might be very simple indeed, and within reach of chemistry and physics, or it might not be. But we can't assume one way or the other a priori. In addition, we can't assume that the simplest Darwinian-capable selfreplicators had proteins at all. So there is no a priori reason for saying that Darwinian processes can't have led to functional proteins, and that therefore the only non-design pathway was random draw.
New species have similar requirements: a lot of new biological information. Even if we keep it proteins (which certainly are not the whole story), new original proteins are needed both for OOL (certainly at least a few hundreds of them) and for the emergence of new phyla, orders, species, and so on.
I think this is a misunderstanding. There's nothing special about phyla - all lineage divergences, under the Darwinian hypotheses, are speciation events, and speciation can happen without radically new proteins emerging. And we simply do not know that "new original proteins" are needed for OoL. It's possible that peptides were part of the pre-biotic scene, but possibly not. It's a question worth asking but not one to which we can assume we have an answer.
The two problems are obviously similar, and it would be very strange indeed that they require two completely different solutions.
They must require completely different solutions, because you can't invoke Darwinian processes to account for the first Darwinian-capable self-replicator! Whereas you can invoke Darwinian processes to account for things that evolved as a result of there being Darwinian-capable self-replicators. So the interesting OoL question is: how simple did that first Darwinian-capable self-replicator have to be, and (for IDists), was it within reach of non-Darwinian processes, such as the physical and chemical processes on early earth?Elizabeth B Liddle
July 26, 2013
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