Evo-Info review: Do not buy the book until…

Introduction to Evolutionary Informatics, by Robert J. Marks II, the “Charles Darwin of Intelligent Design”; William A. Dembski, the “Isaac Newton of Information Theory”; and Winston Ewert, the “Charles Ingram of Active Information.” World Scientific, 332 pages.
Classification: Engineering mathematics. Engineering analysis. (TA347)
Subjects: Evolutionary computation. Information technology–Mathematics.

… the authors establish that their mathematical analysis of search applies to models of evolution.

I have all sorts of fancy stuff to say about the new book by Marks, Dembski, and Ewert. But I wonder whether I should say anything fancy at all. There is a ginormous flaw in evolutionary informatics, quite easy to see when it’s pointed out to you. The authors develop mathematical analysis of apples, and then apply it to oranges. You need not know what apples and oranges are to see that the authors have got some explaining to do. When applying the analysis to an orange, they must identify their assumptions about apples, and show that the assumptions hold also for the orange. Otherwise the results are meaningless.

The authors have proved that there is “conservation of information” in search for a solution to a problem. I have simplified, generalized, and trivialized their results. I have also explained that their measure of “information” is actually a measure of performance. But I see now that the technical points really do not matter. What matters is that the authors have never identified, let alone justified, the assumptions of the math in their studies of evolutionary models.a They have measured “information” in models, and made a big deal of it because “information” is conserved in search for a solution to a problem. What does search for a solution to a problem have to do with modeling of evolution? Search me. In the absence of a demonstration that their “conservation of information” math applies to a model of evolution, their measurement of “information” means nothing. It especially does not mean that the evolutionary process in the model is intelligently designed by the modeler.1

I was going to post an explanation of why the analysis of search does not apply to modeling of evolution. But I realized that it would give the impression that the burden is on me to show that the authors have misapplied the analysis.2 As soon as I raise objections, the “Charles Ingram of active information” will try to turn the issue into what I have said. The issue is what he and his coauthors have never bothered to say, from 2009 to the present. As I indicated above, they must start by stating the assumptions of the math. Then they must establish that the assumptions hold for a particular model that they address. Every one of you recognizes this as a correct description of how mathematical analysis works. I suspect that the authors recognize that they cannot deliver. In the book, they work hard at fostering the misconception that an evolutionary model is essentially the same as an evolutionary search. As I explained in a sidebar to the Evo-Info series, the two are definitely not the same. Most readers will swallow the false conflation, however, and consequently will be incapable of conceiving that analysis of an evolutionary model as search needs justification.

The premise of evolutionary informatics is that evolution requires information. Until the authors demonstrate that the “conservation of information” results for search apply to models of evolution, Introduction to Evolutionary Informatics will be worthless.


1 Joe Felsenstein came up with a striking demonstration that design is not required for “information.” In his GUC Bug model (presented in a post coauthored by me), genotypes are randomly associated with fitnesses. There obviously is no design in the fitness landscape, and yet we measured a substantial quantity of “information” in the model. The “Charles Ingram of active information” twice feigned a response, first ignoring our model entirely, and then silently changing both our model and his measure of active information.

2 Actually, I have already explained why the “conservation of information” math does not apply to models of evolution, including Joe’s GUC Bug. I recently wrote a much shorter and much sweeter explanation, to be posted in my own sweet time.

a ETA: Marks et al. measure the “information” of models developed by others. Basically, they claim to show that evolutionary processes succeed in solving problems only because the modelers supply the processes with information. In Chapter 1, freely available online, they write, “Our work was initially motivated by attempts of others to describe Darwinian evolution by computer simulation or mathematical models. The authors of these papers purport that their work relates to biological evolution. We show repeatedly that the proposed models all require inclusion of significant knowledge about the problem being solved. If a goal of a model is specified in advance, that’s not Darwinian evolution: it’s intelligent design. So ironically, these models of evolution purported to demonstrate Darwinian evolution necessitate an intelligent designer. The programmer’s contribution to success, dubbed active information, is measured in bits.” If you wonder Success at what? then you are on the right track.

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588 thoughts on “Evo-Info review: Do not buy the book until…

  1. Robin: Ok. Except of course that newer research (like the research I linked to) shows actual mutation moving through populations. As shown, there’s no way to get new features without it.

    And I don’t see anyone in biology running with the idea that there’s no such thing as mutation.

    But do let me know when you find some evidence this “ahead of it’s time” perspective starts becoming popular.

    Of course no one is saying that mutations do not occur. What Margulis was getting at was that accidental mutations are not the driving force behind speciation.

    There are many purposeful changes to genomes and cellular processes that produce variations in the sex cells or daughter cells in the case of asexual reproduction.

    Look at it this way. We develop normally by the means of internal forces within the zygote and subsequent growing unit. There are many external factors which cause cancer to occur and when this happens there is runaway formless growth which is detrimental to the organism as a unit. Compare this with the evolution of life as a whole. The process of changes that come about due to accidental external forces being acted upon by natural selection are real enough, but if that were the only factors in evolution there would be a cancer-like runaway of relatively simple living forms spreading over the globe. We are here and we survive, not because we are more fit than single celled bacteria, because in any Darwinian sense I can think of, we are less fit than bacteria. We survive because of the check put in place to prevent the blind proliferation of living matter.

    An organism as complex as a human develops in spite of Darwinian evolution, not because of it.

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  2. Tom English,

    Right, I wish we could get all evolutionary literature to fix that. Instead of talk of animals getting adaptations in order to accomplish something, they should be described as just occurring. Instead of saying why something exists, it should be explained that it just so happens to exist. But I don’t think you will get many biologists or materialists takers, for obvious reasons.

    I believe most evolutionists want to intentionally use language that is deceptively inaccurate. Or at the very least, they often forget when they are speaking what it is they actually mean to say occurred. It hard to say a rattlesnake got venom because it just so happened to have occurred for no reason, but it lasted.

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  3. keiths:
    phoodoo:

    God says, “Let there be echolocating lizards,” and lo, instantly there are echolocating lizards.

    How would we know if that was unnatural, if a God didn’t tell us?

    Is that the only thing that is unnatural? I am not sure why you are even calling that unnatural, what is unnatural about it, but are there other things?

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  4. Robin: How do you know there are changes to the genome that are not accidental?

    Would you call chromosomal crossover an accidental mutation?

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  5. phoodoo:
    Tom English,

    Right, I wish we could get all evolutionary literature to fix that.Instead of talk of animals getting adaptations in order to accomplish something, they should be described as just occurring.Instead of saying why something exists, it should be explained that it just so happens to exist.But I don’t think you will get many biologists or materialists takers, for obvious reasons.

    I believe most evolutionists want to intentionally use language that is deceptively inaccurate.Or at the very least, they often forget when they are speaking what it is they actually mean to say occurred.It hard to say a rattlesnake got venom because it just so happened to have occurred for no reason, but it lasted.

    Yeah, because that’s totally what John meant, right? LMAO phoodoo, you’re so much fun

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  6. In the days when Sussman was a novice, Minsky once came to him as he sat hacking at the PDP-6.

    “What are you doing?”, asked Minsky.

    “I am training a randomly wired neural net to play Tic-Tac-Toe” Sussman replied.

    “Why is the net wired randomly?”, asked Minsky.

    “I do not want it to have any preconceptions of how to play”, Sussman said.

    Minsky then shut his eyes.

    “Why do you close your eyes?”, Sussman asked his teacher.

    “So that the room will be empty.”

    At that moment, Sussman was enlightened.

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  7. I apologize for having disappeared from the thread. I’m finding it extremely difficult to write even a few words now. So I’m afraid I won’t be catching up.

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  8. Tom English: Here’s a nontechnical post on the Scientific American blog. The author is a science journalist with degrees in biology and zoology.

    Biting the hand that feeds: The evolution of snake venom

    Interestingly, it tells absolutely NOTHING about how the trait evolved, but nonetheless, it is good reading for anyone who needs even more ammunition for doubting the likelihood of random mutations accounting for such a system. Basically it just says the chemical compounds needed are very complex and varied, so….

    The authors also struggles with using statements like, “it just so happened to have occurred and then…” In fact they never say it like that, and instead say, “it happened because”…Which we all know is never actually true in evolutionary theory.

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  9. DNA_Jock:

    CharlieM: No one has responded to my earlier point of how the great orange tip butterfly, has a toxin in its wing tips that is identical to a toxin used by a predatory sea snail to kill prey.

    Anyone have any ideas?

    Well, I will note that the identity is not quite as significant as you seem to think…

    I’m not sure why you think that the article you linked to has any bearing on the question of how the exact same 63 amino acid sequence came to be present in both the great orange tip butterfly and the marbled cone snail.

    From this article

    GT (glacontryphan-M) was unambiguously identified in the wings of HG (Hebomoia glaucippe), and its sequence was determined to share 100% identity with the GT from the sea snail C. marmoreus [UniProtKB: P62903.1; National Center for Biotechnology Information (NCBI): GI:51701274]…

    GT is a protein of 63 amino acids with a known conformation and a series of PTMs, including a specific γ-carboxyglutamic acid modification.

    This site tells us that convergent evolution is the best answer for the identity.

    Scientists were surprised to find a chemically identical toxin in two animals that are not closely related in evolutionary terms. Convergent evolution (independent evolution of similar features in distantly related species) has been proposed as the most logical solution to this riddle. It is assumed that the Great Orange Tip butterfly evolved the toxin as a defensive mechanism to ward off predators, while the Marble Cone snail evolved the toxin to effectively kill prey.

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  10. CharlieM,

    I love when supposed scientists use convergent evolution to explain away the ridiculous odds of something evolving exactly the same twice-from random mutations!

    Its more ridiculous than a rabbit in the Cambrian.

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  11. CharlieM,

    The article you cited notes that lepidoptera harbor a number of ADP-ribosylating toxins (with at least two in Hebomoia glaucippe) , and the article that I cited notes that

    Each one of the ~750 species of the genus Conus is venomous

    and

    Their venoms are complex mixtures typically containing more than 100 bioactive peptides (known as conotoxins). Furthermore, each species of Conus is thought to harbour an almost unique repertoire of conotoxins.

    So there are somewhere between 850 and 75,000 different conotoxins. Obviously, this reduces the significance of the match.

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  12. DNA_Jock: So there are somewhere between 850 and 75,000 different conotoxins. Obviously, this reduces the significance of the match.

    Why? Glacontryphan-M has only been found in 2 species, C. marmoreus and H. glaucippe. What are the odds of this identical sequence appearing in an unrelated animal such as a butterfly but not in any of the closely related cone snails?

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  13. Why does this reduce the significance of the match?
    Well, we are doing ID-math™ here, so we are deliberately ignoring the effects of selection.

    What are the chances that H. glaucippe‘s toxin matches THIS particular toxin in genus Conus?
    Let’s say it is 1 / N, where N is a big™ number.

    What are the chances that H. glaucippe‘s toxin matches one of the (say) eight thousand toxins in genus Conus?
    8,000 / N, where N is the same big™ number.

    If you really don’t understand why adding an extra thousand targets degrades the significance of the match, I’m not sure I can help you out.

    I notice in passing that you have increased the specification to include “but not in any of the closely related cone snails”.
    Why do I have a sneaking suspicion that your addition will be quietly dropped if the same sequence is found in another cone snail…

    It’s Texas-Sharp-Shooter all the way.

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  14. People who wield arguments from improbability are usually as ignorant of probabilistic modeling as they are of evolutionary biology.

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  15. DNA_Jock: If you really don’t understand why adding an extra thousand targets degrades the significance of the match, I’m not sure I can help you out.

    Yum. Targets. Tasty.

    Where would evo theory be without them.

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  16. Tom English:
    People who wield arguments from improbability are usually as ignorant of probabilistic modeling as they are of evolutionary biology.

    Right. Like the improbability that a car can come about through spontaneous shifts in natural elements. If we have enough time, and enough universes how do we know anything is too improbable to occur?

    I guess we don’t.

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  17. CharlieM:
    Robin,

    From your link:

    I would like to ask how random mutations and natural selection achieve the feat of allowing snakes to have this capability in the first place?

    What was the sequence of events between producing the venom, producing glands capable of containing the venom, producing the form of teeth that are capable of delivering the venom into the prey, producing self-immunity to the venom? These are complex processes.

    There’s fairly exhaustive research on the subject of snake venom/gland evolution. Why not actually do some research. Here’s a few starting points:

    http://scienceblogs.com/pharyngula/2008/07/31/evolving-snake-fangs/
    http://www.nature.com/nature/journal/v454/n7204/abs/nature07178.html
    https://prezi.com/ndanrdyvm4pd/evolution-of-venomous-snakes/
    http://news.nationalgeographic.com/news/2008/07/080730-snake-fang.html
    http://www.sciencedirect.com/science/article/pii/S0925477308000853
    https://en.wikipedia.org/wiki/Evolution_of_snake_venom

    And speaking of nasty substances. No one has responded to my earlier point of how the great orange tip butterfly, has a toxin in its wing tips that is identical to a toxin used by a predatory sea snail to kill prey.

    Anyone have any ideas?

    Freely admit that I have no answer for that. Mostly because I have not studied the history and biology of either one of those two animals. But I’d bet there are folks who have. Have you looked?

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  18. Mung: Selection is not a craftsman. Not even a blind one. It does not “work on” anything.

    What does this even mean, Mung? Are you suggesting that if a force changes the concentration and/or arrangement of material, that reorganization can’t be considered “building”? If not, why not?

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  19. CharlieM: Of course no one is saying that mutations do not occur. What Margulis was getting at was that accidental mutations are not the driving force behind speciation.

    Yes, I’m aware of her claims on that. By all accounts, particularly more recent research, she was wrong.

    There are many purposeful changes to genomes and cellular processes that produce variations in the sex cellsor daughter cells in the case of asexual reproduction.

    I have no idea what this is supposed to mean. Can you elaborate?

    Look at it this way. We develop normally by the means of internal forces within the zygote and subsequent growing unit. There are many external factors which cause cancer to occur and when this happens there is runaway formless growth which is detrimental to the organism as a unit. Compare this with the evolution of life as a whole. The process of changes that come about due to accidental external forces being acted upon by natural selection are real enough, but if that were the only factors in evolution there would be a cancer-like runaway of relatively simple living forms spreading over the globe.

    I have no clue why you think there should be an analogy between body growth and development and species genetic change. There are no parallels as far as I can tell.

    We are here and we survive, not becausewe are more fit than single celled bacteria, because in any Darwinian sense I can think of, we are less fit than bacteria. We survive because of the check put in place to prevent the blind proliferation of living matter.

    But we aren’t directly competing with bacteria for anything, so our relative fitness is moot. All you’ve done is demonstrate that you really don’t understand the Theory of Evolution at all and that you’re just criticizing a strawman. I mean…have at it, but that’s hardly a concern for actual science.

    An organism as complex as a human develops in spite of Darwinian evolution, not because of it.

    Except you haven’t demonstrated this at all.

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  20. CharlieM: Would you call chromosomal crossover an accidental mutation?

    Well in homologous regions of matching chromosomes, I would not call it a mutation at all. Be that as it may, your question is the result of a false dichotomy. Processes have effects and entailments. Chromosomal crossover is thus a constant entailment of synapsis. So it is neither random nor purposeful, but rather a processes occurrence.

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  21. Robin,

    Oh my goodness, you have a serious misunderstanding of what an explanation is.

    If someone like PZ Myers writes, “Well, its simple really, teeth from the back moved to the front, and they have separate tooth generating zones in their jaws..The cool observation is that even in front-fanged snakes, it is the posterior zone that generates the fangs. It is also this same primordium that buds off a tube and a sac that will make the post-orbital venom gland — even in the front-fanged snakes, they have a gland located way back behind the eye to produce venom…so you see…”

    It is so far removed from being an explanation that it is comical.

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  22. phoodoo: It is so far removed from being an explanation that it is comical.

    Too much detail for your liking? LOL

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  23. phoodoo: It is so far removed from being an explanation that it is comical.

    Yeah. “God made it” has vastly superior explanatory power.

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  24. phoodoo: It certainly doesn’t have less!

    It does, because it introduces a new entity require more explanation than the
    original problem.

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  25. phoodoo: It certainly doesn’t have less!

    You really need to go and learn what explanatory power means. I mean, really

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  26. phoodoo:
    Robin,

    Oh my goodness, you have a serious misunderstanding of what an explanation is.

    LOL! I’m really not the one having problems with the concept of “explanation” here, Phoodoo. As if the terms “God” and “supernatural” are valid explanations…

    If someone like PZ Myers writes, “Well, its simple really, teeth from the back moved to the front, and they have separate tooth generating zones in their jaws..The cool observation is that even in front-fanged snakes, it is the posterior zone that generates the fangs. It is also this same primordium that buds off a tube and a sac that will make the post-orbital venom gland — even in the front-fanged snakes, they have a gland located way back behind the eye to produce venom…so you see…”

    It is so far removed from being an explanation that it is comical.

    You may not like it; you may not agree with it; you may find wholly incomplete even, but none of that in anyway changes the fact that it is, by definition, an explanation. Whether it’s accurate is certainly debatable, but then every explanation in science is debatable. That’s the whole point of science!

    So really, what’s your actual point Phoodoo?

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  27. The mystery of how a butterfly contains the exact same toxin as a cone snail is worth pursuing, but while I was looking into this I realised how intriguing the cone snail by itself was. I would say that the venom system of these animals are full of examples of irreducible complexity and I’d recommend the following video to anyone who is in the least bit interested (even if they only watch from the 25 minute mark).

    Baldomero “Toto” Olivera (U. Utah, HHMI) 1: Cone Snail Venom Peptides: Venom complexity

    The venom apparatus which is the same in all snails is an amazing assembly. There is a quiver-like sac which houses up to 100 disposable, hyperdermic harpoons in various stages of assembly. When hunting a harpoon is moved into the proboscis ready to use. A pipete-like, muscular bulb forces the venom out. The venom is a concoction of toxic peptides. The venom gland contains multiple toxins which are selected and then assembled in the venom duct. And out of the toxins which are chosen, different venoms are produced for different purposes. The snails discovered the process of combination drug therapy many millions of years ago. They call the groups of toxins that the snails use in a synergistic way a cabal. On its own the venom that the snails use to paralyse their prey will take about 20 minutes to come into effect. But there is a second cabal which has an effect similar to a taser but achieved pharmacologically. This is called the lightning strike cabal.

    Olivera says that “in the real world, effective chemical interactions between organisms need to be much more sophisticated than might be predicted.

    Each species of cone snail have over 500 different components to their venom

    Evolution has led the cone snail down a very specialised path with little chance of any further changes to its lifestyle, form and appearance.

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  28. CharlieM: The mystery of how a butterfly contains the exact same toxin as a cone snail is worth pursuing

    Sure is. I have questions. First, I’m presuming the toxins are peptides. True? (I’m assuming they are for all later questions.) Second, does the butterfly’s peptide sequence exactly match that of one of the cones’? Third, how long is this peptide? Fourth, are the pathways from transcribed mRNA to finished toxin identical? Fifth, how similar are the DNA sequences, including positions of introns if any?

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  29. Robin,

    Because you don’t understand the problem being posed. People like Charlie are asking the question about how and why a system like snakes with venom came to be, and saying, well, they got teeth, and also sacks full of venom, and something to squirt that venom, and a gland to produce that venom! So see, it can happen!

    Such a so called explanation clearly does not understand the question. Its the same as saying, well, we don’t really have a fucking idea, but look, its all here, so it happened!

    And what’s worse Robin, when you make the bullshit excuse that, “Hey, just look on the internet, there are all kinds of explanations that explain how venom in snakes came to be, that’s when it truly takes on its comedic value, because there are people who claim to have a skeptic mind who will say, “Look, there, he just showed it, so now we solved that little problem…whoosh, I am done thinking!”

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  30. John Harshman: Sure is. I have questions. First, I’m presuming the toxins are peptides. True? (I’m assuming they are for all later questions.) Second, does the butterfly’s peptide sequence exactly match that of one of the cones’? Third, how long is this peptide? Fourth, are the pathways from transcribed mRNA to finished toxin identical? Fifth, how similar are the DNA sequences, including positions of introns if any?

    Can’t you just relax, and appreciate a miracle mystery for what it is?

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  31. Tom English: Can’t you just relax, and appreciate a miracle mystery for what it is?

    Is that the holistic, centripetal (or is it centrifugal? I forget.), etheric forces way to do science? I’m always ready to learn.

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  32. Robin,

    I’ve had a look at your links.

    Here and here we are told that snakes fangs are specialised teeth. I would agree with this. The evolutionary trajectory of these snakes is towards an increasingly narrow expression of the archetypal form confirmed by the loss of limbs and the extremely specialised fangs.

    Here we have further talk of specialisation and a comment that fangs evolved in close association with venom glands. Were the accidental mutations working on both of these areas simultaneously?

    Here they say:

    …a study of the embryos of eight front- and rear-fanged species has found that fangs always first appear at the back of the upper jaw before migrating forward in vipers and cobras.

    I have been criticised for linking individual development with evolution. Is this not what is being done here?

    Here is an interesting finding on how a pit viper’s fangs form:

    In an attempt to cast further light on this subject the early development of the fangs was followed in a pit viper, Trimeresurus albolabris, using the expression of Sonic hedgehog (Shh). We demonstrate that the canal is indeed formed by an early folding event, resulting from an invagination of epithelial cells into the dental mesenchyme. The epithelial cells proliferate to enlarge the canal and then the cells die by apoptosis, forming an empty tube through which the poison runs.

    The fangs are sculpted in the same way that bone formation is achieved through osteoblasts and osteoclasts.

    Here the Wikepedia entry on snake venom refers to research which “suggested that venom had evolved independently in a number of snake lineages”. More information coming to light which makes evolution without direction that much more difficult to believe.

    The entry continues:

    Snake venoms attack biological pathways and processes that are also targeted by venoms of other taxa; for instance, calcium channel blockers have been found in snakes, spiders, and cone snails, thus suggesting that venom exhibits convergent evolution.

    They go on to say:

    The various recruitment events had resulted in snake venom evolving into a very complex mixture of proteins. The venom of rattlesnakes, for example, include nearly 40 different proteins from different protein families,[30] whereas other snake venoms have been found to contain more than 100 distinct proteins.

    They assume that snake venom evolved from simple to complex mixtures. How can they be so sure of this?

    And looking at other links I found this

    The researchers also found an answer to the question of how snakes manage to ferry the venom well under the skin of their prey. After all, only there can it unfold its deadly effect. Here too, snakes developed a trick in the course of evolution: When a snake attacks, the fang grooves and the surrounding tissue form a canal. Just like blotting paper, the tissue sucks the venom through this canal. And snake venom has a very special property to facilitate this effect: Just like ketchup, which becomes significantly more fluid upon shaking, the sheer forces that arise from the suction cause the venom to become less viscous, allowing it to flow through the canal quickly as a result of the surface tension.

    And this:

    Venom from an eastern diamondback rattlesnake in the Everglades is distinct from the cocktail of toxins delivered by the same species in the Florida panhandle area, some 500 miles away. But no matter where you go in the Southeastern United States, the venom of the eastern coral snake is always the same. The results challenge common assumptions in venom evolution research, provide crucial information for rattlesnake conservation, and will help coral snake antivenom development…

    “The received wisdom was that venoms are rapidly-evolving, but now we know that’s not necessarily the case.” said Mark Johnston, Editor-in-Chief of GENETICS. “Clearly, venom evolution in these two snake species has been shaped by different forces. The next challenge is to understand why.”

    All interesting stuff which may prompt anyone with an open mind to ponder that “maybe there is more going on in evolution than I assumed”.

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  33. John Harshman:

    CharlieM: The mystery of how a butterfly contains the exact same toxin as a cone snail is worth pursuing

    Sure is. I have questions. First, I’m presuming the toxins are peptides. True? (I’m assuming they are for all later questions.)

    Yes.

    Second, does the butterfly’s peptide sequence exactly match that of one of the cones’?

    Yes, according to an article in PNAS:

    GT was unambiguously identified in the wings of HG, and its sequence was determined to share 100% identity with the GT from the sea snail C. marmoreus [UniProtKB: P62903.1; National Center for Biotechnology Information (NCBI): GI:51701274]

    The article – “Peptide toxin glacontryphan-M is present in the wings of the butterfly Hebomoia glaucippe”

    Third, how long is this peptide?

    Here is the sequence from the cone snail:

    MGKLTILVLV AAVLLSTQVM VQGDRDQPAD RNAVPRDDNP GRARRKRMKV LNESECPWHP WCG

    Here it shows that glacontryphan-M consists of a signal peptide of 23 amino acids, a propeptide of 28 amino acids, and an active peptide of 11 amino acids. So far I haven’t been able to find out if all 63 amino acids are the same in the butterfly or just the 11 amino acids. I don’t know enough about these processes to be able to say either way if the signal and propeptides need to be the same.

    Fourth, are the pathways from transcribed mRNA to finished toxin identical?

    Again, I don’t know.

    Fifth, how similar are the DNA sequences, including positions of introns if any?

    I’ve only seen the amino acid sequence, not the DNA sequence.

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  34. CharlieM,

    Thanks, but your link “an article in PNAS” is bad. So is the second “here”, though the first “here” seems OK.

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  35. John Harshman: Turns out that the match is 63 residues. There may be different post-translational modifications, though.

    IMO a match of 63 amino acids virtually rules out convergence.

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  36. The more I find out about cone snails, the more I am amazed.

    In the following Youtube video Baldomero “Toto” Olivera says at around 7 minutes in:

    So, within a particular superfamily, this shows you the O superfamily, the cysteines are arranged as shown in the diagram, where the first cysteine is disulfide bonded to the fourth, the second to the fifth, etc…and so, that crosslinking gives all the peptides in this superfamily more or less the same shape. However, hypermutation occurs in the mature toxin region in the hatched areas, and so what’s essentially the net result is a story that’s very similar to antibodies. You have conserved structure, you have very rapidly evolving function, or binding specificity because of these conserved and highly variable regions. And so the conserved regions lead to the conservation in structure. The hypervariable regions lead to the rapid evolution of new functions. And so, by having these gene superfamilies that are organized in this way in the venom, what happens is the venom can rapidly evolve new binding specificity, new physiological function. There is a problem: if you have small peptides and they’re disufide bonded, let’s say you have 6, then you have 15 possible ways to arrange the disufide bonds. Only one of these is the correct biologically active form. And what’s remarkable is the snails, in their venom, have essentially the correct isomer every time. We don’t yet understand how they do this, because some of these peptides are as small as 15 amino acids, and if you try to fold them in vitro you’ll always get a mixture. So, this shows you one correct isomer and five examples of wrongly folded forms. And in vitro, if you try this, to fold them, you’ll always get a mixture, but the snails always get it right.

    (Baldomero “Toto” Olivera (U. Utah, HHMI) 2: Conus Venom Peptides: Generation of peptide diversity)
    .

    Every way you look at it the venom system of these cone snails are a wonder. In the same delivery of venom they even have a factor which blocks sodium channels and another which prevents them from closing. They can do this because one acts on muscle synapses and the other on all other synapses. Each species has its own design of harpoon, an example of which I have attached below. To me, that is a beautiful design. Human whalers have been doing only recently what cone snails have been doing for millions of years.

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  37. CharlieM: IMO a match of 63 amino acids virtually rules out convergence.

    Are you kidding, to a confirmed evolutionist, nothing is impossible. You have no idea how strong their faith is.

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  38. phoodoo: Are you kidding, to a confirmed evolutionist, nothing is impossible. You have no idea how strong their faith is.

    Verily I say unto you, no one with faith the size of a mustard seed has any need for ID.

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  39. Mung: Evolution evolved evolution! It just happened. *POOF!*

    Crash and burn. I’d offer to delete that for you, were it not against the rules.

    You can redeem yourself by explaining Section 5.8, “The Search for the Search.”

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  40. phoodoo:
    Robin,

    Because you don’t understand the problem being posed.People like Charlie are asking the question about how and why a system like snakes with venom came to be, and saying, well, they got teeth, and also sacks full of venom, and something to squirt that venom, and a gland to produce that venom!So see, it can happen!

    But that’s not what the links show, so I don’t know what you’re complaining about.

    Such a so called explanation clearly does not understand the question.Its the same as saying, well, we don’t really have a fucking idea, but look, its all here, so it happened!

    Well, if your question is asking for the explanation of a strawman, then no, the explanation is not going to satisfy you. But I and science hardly care about that.

    And what’s worse Robin, when you make the bullshit excuse that, “Hey, just look on the internet, there are all kinds of explanations that explain how venom in snakes came to be, that’s when it truly takes on its comedic value, because there are people who claim to have a skeptic mind who will say, “Look, there, he just showed it, so now we solved that little problem…whoosh, I am done thinking!”

    Again Phoodoo, it’s not my problem or job to force you to read the research on the subject. If you don’t actually want your questions answered, there’s not much I can do to change your mind. All I really care about is that those who actually are curious about such topics and questions understand that there are actual, credible explanations based on research out there.

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  41. CharlieM:
    Robin,

    I’ve had a look at your links.

    Here and here we are told that snakes fangs are specialised teeth. I would agree with this. The evolutionary trajectory of these snakes is towards an increasingly narrow expression of the archetypal form confirmed by the loss of limbs and the extremely specialised fangs.

    Here we have further talk of specialisation and a comment that fangs evolved in close association with venom glands. Were the accidental mutations working on both of these areas simultaneously?

    All sorts of mutations happen simultaneously, so it’s quite likely. However, I think you are either unaware of or simply dismissing the fact that lots of simultaneous mutations are also being discarded. The successful line of venomous snakes are not the only snake lines that evolution “tried” (as it were). Many ended in either non-competitive groups and/or outright failures. So I personally would not use the world “accidental” as it isn’t actually accurate.

    Here they say:

    I have been criticised for linking individual development with evolution. Is this not what is being done here?

    It doesn’t seem so to me, but feel free to elaborate on why you think it is.

    Here is an interesting finding on how a pit viper’s fangs form:

    The fangs are sculpted in the same way that bone formation is achieved through osteoblasts and osteoclasts.

    Ok. I’d hardly call that “sculpting” (since when is “folding” analogous to “sculpting”?), but whatever…

    Here the Wikepedia entry on snake venom refers to research which “suggested that venom had evolved independently in a number of snake lineages”. More information coming to light which makes evolution without direction that much more difficult to believe.

    The entry continues:

    They go on to say:

    They assume that snake venom evolved from simple to complex mixtures. How can they be so sure of this?

    Um…research? You know…actual science?

    C’mon…if you’re going to criticize evolutionary theory and science in general, the least you could do is do some homework on the actual work being done in evolution and science in general.

    Try this for starters:

    http://www.nature.com/nature/journal/v439/n7076/abs/nature04328.html

    https://www.sciencedaily.com/releases/2014/12/141208152658.htm

    http://genome.cshlp.org/content/15/3/403.long

    And looking at other links I found this

    And this:

    All interesting stuff which may prompt anyone with an open mind to ponder that “maybe there is more going on in evolution than I assumed”.

    Why? All of that is in line with what the Theory explains. So, I don’t see a reason to think there is “more going on in evolution than I assumed”. This is like saying that given the behavior of gravity waves, anyone with an open mind might be prompted to ponder that “maybe there is more going on in general relativity”. Um…no. Gravitational waves are in line with General Relativity, in fact they are a prediction of the Theory. You seem to be confusing hypotheses and assumptions with the predictions of a theory itself.

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