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Evolution needs a library of Platonic forms?

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Well, then it sure isn’t “evolution” as National Geographic understands it.

This just in from Andreas Wagner at Aeon:

How do random DNA changes lead to innovation? Darwin’s concept of natural selection, although crucial to understand evolution, doesn’t help much. The thing is, selection can only spread innovations that already exist. The botanist Hugo de Vries said it best in 1905: ‘Natural selection can explain the survival of the fittest, but it cannot explain the arrival of the fittest.’ (Half a century earlier, Darwin had already admitted that calling variations random is just another way of admitting that we don’t know their origins.)

A metaphor might help to clarify the problem. Imagine a giant library of books containing all possible sequences of letters in the alphabet. Such a library would be huge beyond imagination, and most of its texts would of course be pure gibberish. But some would contain islands of intelligibility – a word here, a Haiku there – in a sea of random letters. Still others would tell all stories real and imagined: not only Dickens’s Oliver Twist or Goethe’s Faust, but all possible novels and dramas, the biography of every single human, true and false histories of the world, of other worlds as yet unseen, and so on. Some texts would include descriptions of countless technological innovations, from the wheel to the steam engine to the transistor – including countless innovations yet to be imagined. But the chances of choosing such a valuable tome by chance are minuscule.

Just think, even in the age of National Geographic, someone is actually looking at the problems seriously.

But then, didn’t Aeon also publish “Die, Selfish Gene, Die”?

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Comments
Another pearl of wisdom from Joe. "FREQUENCY = WAVELENGTH"not_querius
March 20, 2015
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Joe, You have a long record of showing the world your "understanding" of nested hierarchies and getting pwned. Apparently some people can't resist returning to their follies, like a dog returns to its vomit. Let me remind you that you still owe $10,000 to one of your former opponents, Andreas Schueler: http://www.skepticink.com/tippling/2013/04/07/cdesign-proponent-joeg-loses-10000-bet-and-chickens-out/Piotr
March 20, 2015
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Piotr is just upset because I proved he doesn't understand what a nested hierarchy is nor what it entails. Piotr is a joke as his position can't explain genomes, proteomes, nor regulatory networks. He just doesn't get it...Joe
March 20, 2015
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Box, Gpuccio and me are having a civil and interesting discussion. You are welcome to join it with some real arguments, but cheap satire is... well... just cheap satire. Mercifully, Joe G. seems to have taken a temporary leave, sparing us hoots from the peanut gallery. Can't we keep it like that?Piotr
March 20, 2015
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Piotr, I'm sorry to hear that. Maybe my mistake was putting in too much reality.Box
March 20, 2015
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Wagner reparaphrased for the IDer Given the astoundingly unlikely gift that there are multiple adjacent "synonymous texts" from which to choose, there has to be some sort of huge library, which contains all the information of life, available for organisms. peacefifthmonarchyman
March 20, 2015
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Box, Thanks for the stand-up show; your skills as a parodyist are on a par with Wagner's skills as a pop-science author.Piotr
March 20, 2015
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Wagner paraphrased:
Given that materialism is true and therefor evolution is true, there has to be some sort of huge library, which contains all the information of life, available for organisms. Yes ppl you are perfectly right, I have indeed no idea of what I'm talking about but in my opinion there is no other way - given that unguided evolution is true. Next, in order to be able to find anything in this gigantic library it has to be housed by a vast multidimensional hypercube. Quiet please! Again, please don't ask me what the heck I'm talking about, I'm simply telling you that there is no other way - given that unguided evolution is true. Lastly we need some sort of network which acts as a guide from genes to phenotype. Yeah I know I know ... but as I see it, there is no other way ladies and gents.
Box
March 20, 2015
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gpuccio:
a) is scarcely possible unless Wagner’s “networks” really exist (and believe me, they don’t). Why? Because the powerful effect of negative selection is completely against it. Negative selection is very powerful in restricting variation to an existing functional island, if the process takes place in a functional, active gene. We have a lot of evidence of that, especially the very high conservation at sequence level which can be observed in a lot of proteins (shall I quote again ATP synthase?).
Nobody questions the fact that there are "highly conserved" genes/proteins whose evolution is kept in check by negative selection. But there are many less conserved ones as well. Even the "death" of a protein because of a disabling mutation in the gene (never mind reduced functionality) need not be fatal to the phenotype, or there would be no pseudogenes. GULO was surely quite an important gene, but we, together with other haplorhines (as well as some bats and cavies), can survive without it. In a typical genome there are thousands of genes that can be knocked out without doing much harm to their carrier. Many of them have duplicates, but Wagner's (and others') experiments with yeast (and other test organisms) show that 40-90% single-copy genes can be disabled without any visible phenotypic effect. As Zachriel has already remarked, promiscuity is one reason for that. There will often be other proteins fortuitously capable of doing the same job. If they have duplicates, one copy is free to specialise and improve its secondary functionality. Metabolic networks are functionally interconnected in the sense that many metabolites can be produced by alternative processes. Wagner argues that the phenotype is much more robust to disabling mutations than used to be thought, and that numerous proteins, even "important" ones, may evolve under nearly-neutral conditions, which prevents them from getting trapped in local peaks of fitness.
The Gauger – Axe paper shows that direct transitions are difficult even in the case of two very similar structures and functions. The rugged landscape paper shows that even different functional islands for the same function are really isolated. Those difficulties are exactly the reason why the b scenarios have been proposed, and have definitely greater empirical support from data.
The Gauger--Axe paper is a joke -- comparable to a demonstration that since a bat can't evolve into a whale or vice versa, they can't be related. The "splendid isolation" of functional islands is exaggerated. As I have already argued, the "rugged landscape paper" doesn't address the effectiveness of long quasi-neutral walks (not to mention recombination, changing landscapes, and so on). These things have been studied in other papers. By the way, phages and other viruses, with their small and highly "streamlined" genomes, evolving under extremely strong selection, are much more vulnerable to deleterious mutations than "true" organisms. Andreas Wagner's ideas make a lot of sense to me. The "Platonic" stuff should not be taken literally: is just a literary device which tends to spin out of control. Wagner doesn't seem to be particularly talented as a popular science writer, which in no way diminishes his credibility as a researcher. Maybe he should team up with Carl Zimmer ;)Piotr
March 20, 2015
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gpuccio: In present biology, there are different models about how new proteins could emerge. Another model is enzyme promiscuity, and it turns out that many if not most enzymes have some level of promiscuity.Zachriel
March 20, 2015
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Box: My point is rather simple: there is no sense in what Wagner says.gpuccio
March 20, 2015
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Piotr: I agree with what you say about Wagner's "style". OK, back to the discussion. I have not much time, so let's try to be precise and discuss a thing at a time. I would like to go deeper about the role of variation, recombination and NS. Wagner seems to "put all his eggs" in variation which can easily find a target because platonic networks exists. So, his "position" depends critically on the true existence of those networks. I am not sure that most neo darwinists would agree, and abandon the familiar comfort of NS as the main actor in the game. One point that is easily overlooked in the discussion is the following: What is the model we are referring to? I will try to be more clear. In present biology, there are different models about how new proteins could emerge. I will try to reduce them to two main scenarios: a) A functional proteins changes until it becomes a new, different functional protein. This scenario can be about one proteins giving birth to another one, let's say A -> B, ore one functional precursor giving birth to two different functional proteins, let's say A -> B1 and B2. And, obviously, there can be n functional and selectable intermediates, let's say A -> A1... An -> B. However, the important point is that the transition happens from functional sequences to functional sequences. This seems to be also Wagner's idea, even if he seems to abandon the need for functional intermediates, invoking platonic networks to make miracles happen by a "slip of the tongue". b) However, this is not the only scenario, and probably not the most popular in modern biology. The second scenario can take two different forms: b1) Some functional gene becomes duplicated and then inactivated, so that it can vary freely until it becomes the new functional proteins. Here, again, we can adjust possible selectable intermediates. b2) Like in b1, but the transition starts from some non coding sequence. Now, the two scenarios are quite different, and have different problems. a) is scarcely possible unless Wagner's "networks" really exist (and believe me, they don't). Why? Because the powerful effect of negative selection is completely against it. Negative selection is very powerful in restricting variation to an existing functional island, if the process takes place in a functional, active gene. We have a lot of evidence of that, especially the very high conservation at sequence level which can be observed in a lot of proteins (shall I quote again ATP synthase?). The Gauger - Axe paper shows that direct transitions are difficult even in the case of two very similar structures and functions. The rugged landscape paper shows that even different functional islands for the same function are really isolated. Those difficulties are exactly the reason why the b scenarios have been proposed, and have definitely greater empirical support from data. The b scenario, in both forms, has a great advantage: the sequence is free to change in any possible way, because it is not functional. In that way, negative selection is no more a constraint. But that's exactly the problem, isn't it? Is any transition is allowed, all states (or at least, all states which have no sequence similarity with the starting state) become quickly equiprobable, and the imaginary networks suggested by Wagner become useless, even in their imaginary condition. And yet, the best examples we know of new genes seem to be of this kind. In particular, new genes seem to originate from (apparently) random transposon activity, and then become functional. Non coding DNA is certainly the best repository of starting sequences for future genes. And, of course, while that is perfectly compatible with ID, it is perfectly incompatible with all forms of neo darwinism.gpuccio
March 20, 2015
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Gpuccio, Piotr, //on the meaning of the analogy "synonymous texts"//
By creating safe paths through the library, genotype networks create the very possibility of innovation. Let me put this point as strongly as I can. Without these pathways of synonymous texts, these sets of genes that express precisely the same function in ever-shifting sequences of letters, it would not be possible to keep finding new innovations via random mutation. Evolution would not work. [from the blog article, linked in OP]
Wagner [AOTF, ch.3]: Genotype networks guarantee that evolving populations can explore the library. Without them the lethal punishment of losing viability would be inevitable. But without diverse neighborhoods in this library, exploring a genotype network would be pointless: The exploration would not turn up many texts with new meanings.
Okay, so by "synonymous texts" Wagner means "genotype networks". So what are genotype networks?
Wagner et al: Genotype networks are a concept used in systems biology to study sets of genotypes having the same phenotype, and the ability of these to bring forth novel phenotypes. [source]
-- edit: Maybe it's just me, but I have yet to come up with a reason why "genotypes having the same phenotype" constitute a set or a network in the real world...Box
March 20, 2015
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As soon as I find a few free moments, I will answer your points. For now, I just want to say that I used “synonymous” because it was in the Wagner article where, if I understand it well (with Wagner, I am never sure!), it means “having the same meaning or function”...
I see. Indeed, his use of "synonymous" in this blog article (and also in Arrival of the Fittest, where he uses the same "librarian" metaphor) is confusing. I much prefer Wagner's matter-of-fact style in technical prose to these literary flourishes in popular books and articles. He tries to convey rather difficult messages using figurative language and somewhat mixed poetic metaphors, often making himself harder rather than easier to understand (some German-language stylistic habits lurking underneath the surface don't help either). All right, let's agree that by "a synonymous text" he means "another protein capable of performing the same function(s)", and let's be more precise ourselves whenever it matters (leaving "texts" and "books" to philologists, and "meanings" to linguists).Piotr
March 20, 2015
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Piotr: "Our old discussion got buried deep in the archive, so how about restarting it here?" Sure! With great pleasure. :) As soon as I find a few free moments, I will answer your points. For now, I just want to say that I used "synonymous" because it was in the Wagner article where, if I understand it well (with Wagner, I am never sure!), it means "having the same meaning or function": "Random DNA changes in some members of a population could disable an essential protein such as haemoglobin and lead to death, but because genotype networks exist, other mutations can create a synonymous text that preserves the protein’s function and saves the organism." I understand that it is not the same thing as "synonymous mutation" in genetics.gpuccio
March 20, 2015
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// Andreas Wagner on what the theory of evolution lacks // A.Wagner: (...) the puzzle of how new phenotypes come into being has stymied science for more than a century. It’s one thing to recognize that phenotypes are like enormous pointillist paintings, created one molecular change at a time. It’s another to use that insight to understand how those paintings are actually created. The challenge is daunting, even on the smallest scale of proteins like the alcoholdehydrogenase that stands between you and Death by Happy Hour, since there are more ways to string amino acids together than there are hydrogen atoms in the entire universe. Referring to random change, recited like a mantra since Darwin’s time, as a source of all innovation is about as helpful as Anaximander’s argument that humans originated inside fish. It sweeps our ignorance under the rug by giving it a different name. This doesn’t mean that mutations don’t matter, or that natural selection isn’t absolutely necessary.54 But given the staggering odds, selection is not enough. We need a principle that accelerates innovation. Until a few years ago this principle was not merely unknown but beyond reach, and this book could not have been written. Because life is built of molecules, we need to understand molecules to understand innovation: not only the genotype embodied in DNA, but how this genotype helps build a phenotype. And a phenotype like that of a human body is not just a string of DNA. It is a hierarchy of being that descends from the visible organism, its tissues and cells, to the molecular webs formed by metabolic molecules, signaling molecules, and many others, extending down to the level of individual proteins. New phenotypes can originate at each level. A mere thirty years ago, we knew little of this staggering complexity. And if we knew little, just imagine how much less Darwin knew. The list of things that he didn’t know is practically an encyclopedia of modern biology. He wasn’t just ignorant of how phenotypes were inherited. He also had no knowledge, in those pre-Mendelian days, of genes, to say nothing of DNA and the genetic code. He also knew nothing of population genetics and little of developmental biology—he was oblivious to how molecules build bodies. He had no inkling of life’s true complexity (and many after him thought they could safely neglect it). But to crack the secret of innovation, we need to embrace it. The time-honored way to study life’s complexity is to focus on one or a few genotypes and their phenotype. This is how early geneticists found many genes in the first place—by tracking a phenotypic change back to its origin in a mutated gene. Later in the genome era, the same idea worked well to find out what a stretch of DNA does: Mutate it and see what happens to the phenotype. These strategies led to striking discoveries, mutations in genes that create flies with two pairs of wings instead of one, plants with transformed leaves, microbes able to survive on new foods. They created many examples of mutant genotypes and strangely altered phenotypes. The problem is that examples are not enough. Explorers cannot chart a newly discovered continent by making a single landfall and taking a walk on the beach. They need to circumnavigate it to draw its contours. They have to sail into its interior from its river deltas. And they need to traverse its mountain ranges, deserts, and jungles. We need to do just that to draw the elusive maps of life’s creativity—the genotype-phenotype maps that chart each change in a genotype and how it affects the phenotype. We need genotype-phenotype maps to complete Darwin’s job.55 [Andreas Wagner, Arrival Of The Fittest, CHAPTER ONE “What Darwin Didn’t Know”]Box
March 20, 2015
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// Andreas Wagner on the modern synthesis // A.Wagner: There is, however, a dirty secret behind its success. The architects of the modern synthesis focused on the genotype at the expense of the organism and its phenotype. They neglected the marvelous complexity of organisms with their trillions of cells, each inhabited by billions of molecules whose functions are themselves incredibly complex. And they neglected how all this complexity unfolds from a single fertilized cell, and how genes contribute to this unfolding. By neglecting this complexity, the architects of the modern synthesis effectively ignored its product: the organism itself. They did so knowingly, since they wanted to understand how gene frequencies change over time. In focusing on the genotype, they simplified an organism’s phenotype down to simpler quantities, such as fitness, the average number of genes a typical individual transmits to the next generation. (Fitter organisms contribute more genes to the next generation’s gene pool.) What is more, they also assumed that individual genes play a simple role in determining fitness, for example that fitness is the sum total of many small gene effects. Don’t get me wrong. It is hard to see how the modern synthesis could not have ignored the organism. The price of understanding is always abstraction, neglecting most of a staggeringly complex world to understand one tiny fragment of it. Take it from another theorist, Albert Einstein, who knew what he was talking about when he said that “everything should be made as simple as possible, but no simpler.”32 The modern synthesis was just as simple as it needed to be to answer thousands of questions about the evolution of genes and genotypes. Its very success in understanding natural selection in action was built on getting rid of organismal complexity. But whenever a theory is successful, it is also easy to forget its limitations, and this is exactly what happened in the heyday of the modern synthesis, when the grandeur of life’s evolution became redefined and demoted to a “change in allele frequency within a gene pool.”33 The principal limitation—a high price to pay—was the inability to answer the second great question the Origin had left open: Where do innovative phenotypes come from? The modern synthesis could explain how innovations spread, but not how they originate. [Andreas Wagner, Arrival Of The Fittest, CHAPTER ONE “What Darwin Didn’t Know”]Box
March 20, 2015
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Box: And if we do not know what explains its arrival, then we do not understand the very origins of life’s diversity. Think of a very complicated vacuum container with many nooks and crannies. Now we add a gas. The gas molecules only move by random motion, yet they will fill every available nook and cranny. This is just an analogy, and it certainly doesn't constitute evidence that biological evolution can explore the nooks and crannies of the available fitness landscape, yet it does show the weakness of your own position that random variation is incapable of filling such a space. gpuccio: if what Wagner says were even distantly true, how is it that in the famous ragged landscape esperiment the wildtype form of the sequence could not be found, and required probably a starting random library of 10^70? Without recombination, so you will usually end up on a local fitness peak. gpuccio: 12 letter words are, it seems, about 11400 in English (I confess that I am using Word Finder :) ). The combinations are 26^12, that is 9.542896e+16. The target space/search space ratio is 1.194606e-13. When you have a population and recombination, then finding one in 10^13 can be accomplished in about 10^6 trials or so.Zachriel
March 20, 2015
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//Andreas Wagner on the Darwinian incapability to explain the origin of species // A. Wagner: Only once we have distinguished between genotype and phenotype can we ask a question crucial to understand life’s innovability: How do mutations cause changes in phenotypes and bring forth innovations? Because that was the other great mystery left unanswered at the time of Darwin’s death: Where do innovations come from? Where do the new variants come from that selection needs? And especially those variants that improve an organism, help it survive a little longer, appear sexier to a mate, or have more babies? One could answer this question with a vacuous platitude: New variants arise randomly, by chance. This platitude is still used today, but Darwin was already familiar with it. And he knew that it explains exactly nothing. He opened the chapter on laws of variation in the Origin like this:
I have hitherto sometimes spoken as if the variations . . . had been due to chance. This, of course, is a wholly incorrect expression, but it serves to acknowledge plainly our ignorance of the cause of each particular variation.
This is not a small problem, because natural selection is not a creative force. It does not innovate, but merely selects what is already there. Darwin realized that natural selection allows innovations to spread, but he did not know where they came from in the first place. To appreciate the magnitude of this problem, consider that every one of the differences between humans and the first life forms on earth was once an innovation: an adaptive solution to some unique challenge faced by a living being. It might have been the challenge of converting the light energy from the sun into living matter. Or the challenge of converting another living thing into food. Or simply of moving from one place to another. Every square meter of the earth’s surface, every cubic meter of the oceans, every meadow, forest, and desert, every city and suburb is packed to the limits with organisms, and each organism exhibits countless such innovations. Fundamental ones like photosynthesis and respiration. Protective ones like reptilian scales and insulating feathers. Supportive ones like connective tissue and skeletons. Some are complex, with hundreds of moving parts, others are not. But no matter how large or small, from the ten feet of a blue whale’s tail fluke to the ten microns of a bacterium’s flagellum, every single one exists because, at some point since life’s origin, the right variation occurred. Selection did not—cannot—create all this variation. A few decades after Darwin, Hugo de Vries expressed it best when he said that “natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest” (emphasis added).22 And if we do not know what explains its arrival, then we do not understand the very origins of life’s diversity. [Andreas Wagner, Arrival Of The Fittest, CHAPTER ONE “What Darwin Didn’t Know”]Box
March 20, 2015
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Nice to see you back, G! Our old discussion got buried deep in the archive, so how about restarting it here?
This clearly shows that even the “synonimous” (in the sense of having the same function) forms of a sequence are not connected in the functional space. So much for nature’s “sprawling networks”!
Can you explain what you mean? We normally use "synonymous" to refer to coding DNA sequences producing the same AA sequence. What would "synonymous" proteins be? Having an identical set of biochemical functions? Sharing some functions? A different adjective, e.g. "isofunctional", would describe them more accurately. Wagner doesn't claim that proteins capable of playing the same function have to show a lot of sequential similarity or even be detectably related. Far from being a problem, it reduces the selective pressure on retaining both proteins and may help one of them to evolve in a quasi-neutral way. The "old argument" was based on an experiment in which a sizeable of the functional sequence was replaced by random stuff. That isn't what normally happens in nature. Just to refresh your memory, here's my last comment in that thread:
I don’t think their model implements quasi-neutrality (where fitness is allowed to vary minimally within some small threshold). The paper by Kouyos et al. (2012; see above) shows that for a threshold of 10^(-3) a nearly neutral walk in a rugged landscape can reach a distance of about 100 mutations. By the way, there are other reasons why the study is not very realistic in its simplicity. For example, it assumes a fixed, stationary landscape, while real fitness landscapes can and do change, tracing changes in the environment (in this case, the host, Escherichia coli keeps evolving as well), and forcing the phage to re-adapt to any changes that affect its reproductive success. Perhaps more importantly, the authors start with a randomly generated polypeptide. In natural conditions, any starting sequence would in all likelihood already confer a higher-than-random fitness — or, in the spirit of Wagner, would be fine-tuned for some other functions with a potential for exaptation via minimal nearly neutral modifications. The evolution of new functions does not start in a “fitness vacuum”.
Piotr
March 20, 2015
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By the way, it is funny that the examples with words are always done with very short words, like the MOLD - GOLD "slip of the tongue" in Wagner's article. I repeat here part of what I discussed with Piotr in another thread:
a) I believe that, in all functional spaces, the search space grows faster than the functional space, as the “length” of the information unit increases. Much faster. Both KF and Eric have pointed to that simple fact, and I absolutely agree with them. A very simple consequence of that is that the functional complexity of an information unit is bound to increase with the length of the unit, even if with some great residual variance. Another consequence is that any eventual natural network of “connections” between functional values, if present, is bound to be drastically “diluted” as the length of the information unit increases, leading to isolated functional islands even when for short units some connections existed. So, even if you say that it is rather easy to go from FLOUR to BREAD (but please, see next point), is it equally “easy” to go from QUIXOTICALLY to EXTEMPORIZER? I have not tried, but I would say that the task would be much harder. 12 letter words are, it seems, about 11400 in English (I confess that I am using Word Finder :) ). The combinations are 26^12, that is 9.542896e+16. The target space/search space ratio is 1.194606e-13. In your 5 letter example, with your numbers, the ratio is 0.0005. IOWs, going from 5 letters to 12 letters, the target space has approximately doubled (6000 to 11400), while the search space has become more than 8 billion times greater. The ratio is therefore approximately 8 billion times smaller. These are simple numbers. Do you really believe that your network of connections is as strong in a 12 letter space as it is in a 5 letter space? b) Another very important point. You can “easily” go from FLOUR to BREAD (two states which are not connected at sequence level) through the steps you highlighted, but only if each of the intermediate steps is “selectable”. IOWs, if the network of connections you refer to must be of any relevance to connect to sequence unrelated states, it is absolutely necessary that the system operates through some oracle: in this case, an English dictionary. In this way, English words are recognized as “functional”, and fixed (IOWs, they undergo some form of selection, negative or positive or both). I fully agree with you that a system of connections can help a search, but for that to happen we need three different conditions: 1) The network must be there 2) Each intermediate functional step must be selectable by an oracle, and negative/positive/mixed selection of the intermediate must follow. 3) The distance at sequence level between functional selectable intermediates must be in the range of the probabilistic resources of the random variation in the system. Now, all three conditions must be verified. While you go on trying to show that condition 1) exists in the protein space (which I don’t believe to be true), I would like to remind that the only oracle admitted in the neo darwinian algorithm is NS, and that NS can only recognize a reproductive advantage, and nothing else.
And again:
Can you give me a detailed list of words of 12 letters which go from QUIXOTICALLY to EXTEMPORIZER, where each word is a correct English word, and each word differs from the previous one only of one letter? IOWs, is the space of 12 letter words as interconnected as the space of 5 letter words?
And again:
Piotr: “I just wanted to highlight one point: if functionality obeys some external constraints (here, the “Englishness” of words), functional structures are not randomly dispersed in the sequence space. They tend to cluster together and to form an interconnected web, rather than a rugged landscape with towering lonely peaks. That’s also part of Andreas Wagner’s message.” And I disagree. You are completely ignoring the basic importance of the search space size. Which was the essential point in my arguments. As the search space becomes huge, the functional states do become dispersed in it. For proteins, we can check that simple fact by comparing the sequences of basic superfamilies, which are not related.
Of course, Piotr (and Zachriel) gave their interesting arguments too. The discussion can be found in the last part of this thread: https://uncommondescent.com/darwinism/the-elephant-in-the-room/ although, I think, it remained rather incomplete.gpuccio
March 20, 2015
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Just to repeat an old argument, if what Wagner says were even distantly true, how is it that in the famous ragged landscape esperiment the wildtype form of the sequence could not be found, and required probably a starting random library of 10^70? This clearly shows that even the "synonimous" (in the sense of having the same function) forms of a sequence are not connected in the functional space. So much for nature's "sprawling networks"!gpuccio
March 20, 2015
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I remain amazed at the ambiguity of Wagner's ideas. In this same article, he exploits and abuses the concept of neutral variation to support a view of the existence of "platonic" topologies in the protein functional space that do not exist, that nobody has showed, that are against any reasonable data. I remain amazed. And I still wonder how many can believe in his words, and that he has demonstrated something.gpuccio
March 20, 2015
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Thanks for this, This article articulates just what Ive been trying to say here for months. The key to biology's drama exists outside the cave. The problem with Darwinism is that it tries to explain myriads of diverse structure by appealing to the enemy of structure (random variation). Check this out from the article quote: Let me put this point as strongly as I can. Without these pathways of synonymous texts, these sets of genes that express precisely the same function in ever-shifting sequences of letters, it would not be possible to keep finding new innovations via random mutation. Evolution would not work. So nature’s libraries and their sprawling networks go a long way towards explaining life’s capacity to evolve. But where do they come from? You cannot see them in the glass lizard or its anatomy. They are nowhere near life’s visible surface, nor are they underneath this surface, in the structure of its tissues and cells. They are not even in the submicroscopic structure of its DNA. They exist in a world of concepts, the kind of abstract concepts that mathematicians explore. Does that make them any less real? end quote: The answer to that rhetorical question is HELL YES peacefifthmonarchyman
March 18, 2015
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Andreas Wagner knows nothing about evolution... 1, 2, 3...Enezio E. De Almeida Filho
March 17, 2015
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