Beating a dead horse (Darwin’s Doubt)

First off I must apologize for doing another post on a subject that’s been done to death around here, but I’ve been meaning to make a post about this for a while but other stuff kept coming up. Anyway, things have quietened down at work where I now only have to maintain some cell cultures, so I have a bit of time duing the christmas holiday.

My post, which is a repost of something I also brought up in a thread on Larry Moran’s sandwalk blog, is about a chapter in Stephen Meyer’s book Darwin’s Doubt and what I can, if I’m being generous, only attribute to extremely shoddy scholarship.

Having read the book, a recurring phenomenon is that Meyer time and again makes claims without providing any references for them. Take for instance the claim that the Cambrian explosion requires lots of new protein folds, from Chapter 10 The Origin of Genes and Proteins:

“Axe had a key insight that animated the development of his experimental program. He wanted to focus on the problem of the origin of new protein folds and the genetic information necessary to produce them as a critical test of the neo-Darwinian mechanism. Proteins comprise at least three distinct levels of structure:4 primary, secondary, and tertiary, the latter corresponding to a protein fold. The specific sequence of amino acids in a protein or polypeptide chain make up its primary structure. The recurring structural motifs such as alpha helices and beta strands that arise from specific sequences of amino acids constitute its secondary structure. The larger folds or “domains” that form from these secondary structures are called tertiary structures (see Fig. 10.2).
Axe knew that as new life-forms arose during the history of life—in events such as the Cambrian explosion—many new proteins must also have arisen. New animals typically have new organs and cell types, and new cell types often call for new proteins to service them. In some cases new proteins, while functionally new, would perform their different functions with essentially the same fold or tertiary structure as earlier proteins. But more often, proteins capable of performing new functions require new folds to perform these functions. That means that explosions of new life-forms must have involved bursts of new protein folds as well.”

In the whole section Meyer dedicates to the origin of novel folds, he makes zero references that actually substantiates that the cambrian diversification, or indeed any kind of speciation, or the that new cells types or organs, requires new protein folds. ZERO. Not one single reference that supports these claims. At first It reads like what I quote above, lots of claims, no references. Later on he eventually cites the work of Douglas Axe that attepts to address how hard it is to evolve new folds(and that work has it’s own set of problems, but never mind that). Axe makes the same claim in his ID-journal Bio-complexity papers (which eventually Meyers cites), but in Axe’s papers, that claim is not supported by any reference either. It’s simply asserted as fact. In other words, Meyer makes a claim, then cites Axe making the same claim. Neither of them give a reference.

Meyer mentions Ohno:

“The late geneticist and evolutionary biologist Susumu Ohno noted that Cambrian animals required complex new proteins such as, for example, lysyl oxidase in order to support their stout body structures. When these molecules originated in Cambrian animals, they also likely represented a completely novel folded structure unlike anything present in Precambrian forms of life such as sponges or one-celled organisms. Thus, Axe was convinced that explaining the kind of innovation that occurred during the Cambrian explosion and many other events in the history of life required a mechanism that could produce, at least, distinctly new protein folds.”

No reference is given here either. The claim is simply made initially, so it’s hard to check. Is Meyer and Axe willing to bet that a preceding evolutionary history of, for example, Lysyl oxidase cannot be found in structure and sequence of related molecules? That there ARE no related molecules? Is that his claim? That the Cambrian explosion required tonnes of bona fide Orphan proteins with no preceding history? Where are the references that support this? Did Meyer or Axe look for homologues of Lysyl Oxidase and found none?

It gets much worse, turns out Meyer is making assertions diametrically opposite to what his very very few references say. Remember what Meyer wrote above?

“The late geneticist and evolutionary biologist Susumu Ohno noted that Cambrian animals required complex new proteins such as, for example, lysyl oxidase in order to support their stout body structures.”

Well, much later in the same chapter, Meyer finally references Ohno:

“Third, building new animal forms requires generating far more than just one protein of modest length. New Cambrian animals would have required proteins much longer than 150 amino acids to perform necessary, specialized functions.21”

What is reference 21? It’s “21. Ohno, “The Notion of the Cambrian Pananimalia Genome.”
What does that reference say? Let’s look:

Reasons for Invoking the Presence of the Cambrian Pananimalia Genome.
Assuming the spontaneous mutation rate to be generous 10^-9 per base pair per year and also assuming no negative interference by natural selection, it still takes 10 million years to undergo 1% change in DNA base sequences. It follows that 6-10 million years in the evolutionary time scale is but a blink of an eye. The Cambrian explosion denoting the almost simultaneous emergence of nearly all the extant phyla of the kingdom Animalia within the time span of 6-10 million years can’t possibly be explained by mutational divergence of individual gene functions. Rather, it is more likely that all the animals involved in the Cambrian explosion were endowed with nearly the identical genome, with enormous morphological diversities displayed by multitudes of animal phyla being due to differential usages of the identical set of genes. This is the very reason for my proposal of the Cambrian pananimalia genome. This genome must have necessarily been related to those of Ediacarian predecessors, representing the phyla Porifera and Coelenterata, and possibly Annelida. Being related to the genome – possessed by the first set of multicellular organisms to emerge on this earth, it had to be rather modest in size. It should be recalled that the genome of modern day tunicates, representing subphylum Urochordata, is made of 1.8 x 10^8 DNA base pairs, which amounts to only 6% of the
mammalian genome (9). The following are the more pertinent of the genes that were certain to have been included in the Cambrian pananimalia genome.”

The bold is my emphasis. I trust you can see the problem here. So, Meyer makes a single goddamn reference to support the claim that the Cambrian explosion required a lot of innovation of new proteins, folds, cell-types and so on. What do we find in that references? That Ohno is suggesting the direct opposite, that he is in fact supporting the standard evo-devo view that few regulatory changes were what happened, that the genes and proteins were already present and had long preceding evolutionary histories.

Later Meyer gets a ID-complexitygasm when he asserts, again without any support, that:

“The Cambrian animals exhibit structures that would have required many new types of cells, each requiring many novel proteins to perform their specialized functions. But new cell types require not just one or two new proteins, but coordinated systems of proteins to perform their distinctive cellular functions.”

 

Where does he get this? His ass, that’s where.

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447 thoughts on “Beating a dead horse (Darwin’s Doubt)

  1. stcordova,

    The problem with using BLAST isn’t that it was introduced in 1989. It’s that simple pairwise comparisons are not the best way to determine evolutionary relationships when distances are large. That’s what people have mostly been telling you. Comparing one species of yeast to one species of primate, for all but the most conserved sequences, is a bad idea.

    Again, I have no idea whether yeast lysyl oxidase is homologous to human lysyl oxidase. But you haven’t addressed that question.

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  2. stcordova,

    Contrast that to the supposed phylogeny of the lysyl oxidase and one will see that even under the assumption of organismal UCA the lysyl oxidase looks like functionally convergent TRGs, not UCA products.

    They don’t ‘look like’ that at all. The authors of the Nature paper will have done due diligence in establishing the distinction between homoplasy and divergence, and LGT, not least by extending their dataset. You have not.

    They also break the protein down into domains. Each domain can have a separate evolutionary origin. For example the transmembrane component. Yeast don’t need one. So including the transmembrane sequence in your analysis is bogus, and inflates the difference arbitrarily. I’m betting the transmembrane sequence has homologues too, though. Just not necessarily in a lysyl oxidase gene.

    Hence Meyer’s mention of lysyl oxidases being novel for animals stands.

    No it doesn’t. It”s still wrong. It is not a valid conclusion from your BLAST of just two sequences, removed by a long chalk from the Cambrian boundary. Meyer wasn’t basing his conclusion on any such analysis, but by a misreading of Ohno. It was bogus, and so is your defence of him on that particular ground.

    As suggested by two papers above (one on TRGs the other on enzymatic convergence), the idea of evolutionary convergence and TRGs is a mainstream idea. I don’t know why my opponents in this discussion want to insist on “UCA explains all patterns” even when there are no patterns to speak of.

    I have made absolutely no comment on ‘all patterns’. The Nature paper is about Lysyl oxidase phylogeny. To say that this is based on ‘no patterns’ would be disingenuous. If there were no patterns, there would be no paper.

    The complaint of BLAST being 1989 is like complaining about calculus being old math.

    It wasn’t a complaint, but an observation. Phylogenetic computation and understanding of protein evolution and architecture have moved on since 1989, is all I meant, and it is but one of a vast array of possible comparisons. It is not equally valid at all depths of taxonomic relationship.

    The failure isn’t the BLAST comparison, the failure is this “UCA explains all” mentality even when clearly UCA is a lousy explanation for the divergent lysyl oxidases.

    If you have a valid rebuttal of the Nature paper, publish it. But if you base it on a BLAST of the entire length of just two genes separated by 1.5-2 billion years, I suspect you will be laughed off the park.

    I don’t know how often I have to say “two sequences aren’t enough”, but, well, two sequences aren’t enough. Unless that’s all you have. Like I say above, I mentioned yeast as a joke, and now you’re obsessed with it.

    Cytochrome c is neither here nor there.

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  3. I posted the amino acid sequences and links to the nucleotide sequences, the lack of similarity in lysyl oxidases is blatantly obvious compared to the obvious similarity demonstrated by the Cytocrhome Cs between human and yeast and the 16S Ribsomal RNA between human and yeast.

    The imaginary fit being argued by the OP for lysyl oxidase is even worse than the fit of Ray Comfort’s hand around a banana in his infamous “atheist nightmare” video:

    https://www.youtube.com/watch?v=2z-OLG0KyR4&feature=player_embedded

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  4. stcordova,

    I posted the amino acid sequences and links to the nucleotide sequences, the lack of similarity in lysyl oxidases is blatantly obvious compared to the obvious similarity demonstrated by the Cytocrhome Cs between human and yeast and the 16S Ribsomal RNA between human and yeast.

    Ribosomal sequence and cytochromes are deeply embedded within cellular functioning. Lysyl oxidase is not. You can’t compare every gene on the same basis. Conservational pressure varies.

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  5. stcordova,

    Why are you obsessing over yeast? What do you think would be an appropriate sister group to metazoa for investigating LOX at the boundary of the Cambrian? It certainly ain’t yeast.

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  6. By the way, the Nature (well, actually Scientific Reports) paper that’s been cited several times here is the first hit you get when you google “lysyl oxidase choanoflagellate”; that’s how I found it before going back to see if it had been mentioned before. That should show Sal how you really go about determining if two proteins are homologous and demonstrate to him how useless his pairwise comparison is. And it may be that his irrelevant objections indicate that deep down he realizes this.

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  7. The point is not whether one can build a phylogenetic case for organisms. I’ve even provided two molecules that one can start building the phylogenies with:

    Cytochrome-C
    16S Ribosomal RNA

    One can even visualize without the assistance of computers the “phylogeny” of Cytochrome -C.

    I’m not focusing on phylogeny of organisms and proteins in general, I’m focusing on whether the lysyl oxidase in mammals is novel relative to something like lysyl oxidase yeast (presumed more ancient). If the genes today aren’t different than above random, then everything is speculation except that it is clear human LOX has substantial novel relative to yeast LOX (AOC1).

    If Ray Comfort’s hand fits a banana better than yeast lysyl oxidase residues fit around human lysyl oxidase residues, that bodes badly for the OP.

    I showed what a good phylogenetic fit looks like with Cytochrome C and 16S Ribosomal RNA. That’s what I mean by similarity!

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  8. Ray Comfort has not given a lot of thought to the design implications of things that perfectly fit his mouth.

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  9. stcordova: If Ray Comfort’s hand fits a banana better than yeast lysyl oxidase residues fit around human lysyl oxidase residues, that bodes badly for the OP.

    Having once been a teenager, I can understand how that might have come to pass.

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  10. Rumraket: That may be what ID proponents generally believe. I’m sure it is.

    What ID proponents generally believe or do not believe is irrelevant. What is relevant is what is argued by Meyer in the chapter under discussion. Agreed?

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  11. Allan Miller: Ohno does not say they needed a new lysyl oxidase. This is how Meyer (and you?) are interpreting this.

    Well, when Salvador took up the LOX issue I decided to focus on the other issues raised by the OP, so I’ve only been following along and haven’t really become involved. It seems like a side issue to the larger issues. Meyer only mentions it twice and then only by way of example. At most it would be a bad example.

    I am frankly not sure how we’ll settle this debate without knowing far more than we do. [Or perhaps until I know far more than I do.]

    This seems to be a lively and interesting discussion for many parties, so maybe we have time to take things bit by bit, and Sal seems to be faltering a bit on the lysyl oxidase, so perhaps I’ll take a break from the other things and have a look at that specifically.

    You are probably aware that I am not a young earth creationist [but then, neither is Meyer, afiak] and that I don’t need things to magically appear out of thin air, as it were. So if there are precursors it’s no skin off my nose to admit it. Honestly I’d love to know how Meyer would react to the critique of his use of Ohno. My sense is that he would correct himself if he’s wrong. Unlike Elizabeth, I don’t think I have any reason to believe he’s fundamentally dishonest or otherwise less than a professional.

    It did catch my eye that you mentioned it’s role in animals as a membrane protein, and that is a particular are of interest for me.

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  12. Having read the book, a recurring phenomenon is that Meyer time and again makes claims without providing any references for them.

    Oddly enough, the same can be said of this book on the Cambrian Explosion.

    Perhaps there is a conspiracy of shoddy scholarship afoot when it comes to the Cambrian explosion.

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  13. One could use Ohno to argue for Meyer’s position. 🙂

    …nearly every extant phylum of the kingdom Animalia emerged within the time span of 6-10 million years. Thus, the term Cambrian explosion became more real than originally intended.

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  14. Ohno again, sounding oddly Meyer-esque:

    Assuming the spontaneous mutation rate to be generous 10^-9 per base pair per year and also assuming no negative interference by natural selection, it still takes 10 million years to undergo 1% change in DNA base sequences. It follows that 6-10 million years in the evolutionary time scale is but a blink of an eye. The Cambrian explosion denoting the almost simultaneous emergence of nearly all the extant phyla of the kingdom Animalia within the time span of 6-10 million years can’t possibly be explained by mutational divergence of individual gene functions.

    ETA: Ohno doesn’t cite any source for this claim.

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  15. Mung:
    One could use Ohno to argue for Meyer’s position.

    One could, but one would be quote-mining. And by the way, Ohno is wrong in that claim. Over half the phyla have no fossil record and several have fossil records that either precede or post-date the Cambrian explosion. It appears that the explosion was to some extent a taphonomic artifact, and in fact we mostly don’t see it until it’s over.

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  16. stcordova: I’m not focusing on phylogeny of organisms and proteins in general, I’m focusing on whether the lysyl oxidase in mammals is novel relative to something like lysyl oxidase yeast (presumed more ancient). If the genes today aren’t different than above random, then everything is speculation except that it is clear human LOX has substantial novel relative to yeast LOX (AOC1).

    It seems to me that you are changing the subject. Your previous claim was that the yeast and human proteins are not homologous, unless I misunderstood you. Now your claim is that they may be homologous but that the human protein has changed enough from the ancestral to be “novel”. Not sure what you mean by that, but it’s a different claim, at least.

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  17. Ohno:

    Compared with their Ediacarian predecessors, Cambrian animals in general were characterized by their much stouter bodies. The stoutness of the body is likely due to the formation of ligaments and tendons, which in turn requires the crosslinking of collagen triple helices.

    A ligament is a kind of tissue, as is a tendon.

    As noted in the previous chapter and as reviewed extensively elsewhere (Frank 1985, 1988; Akeson 1984), both tendons and ligaments are highly complex structures with a number of unique functional characteristics. While similar in many ways, tendons and ligaments have some important differences in both structure and function which should be appreciated.

    The Biology of Tendons and Ligaments

    If the structure and function of ligaments and tendons arose in the Cambrian animals then this would support Meyer’s claims of the need for new cell types and organs.

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  18. Ohno:

    …in all vertebrates, from fish to mammals, hemoglobins are encased in a very specialized cell type, erethrocytes.

    When did this cell type appear and how is this type of cell produced?

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  19. Mung:
    When did this cell type appear and how is this type of cell produced?

    Hard to tell when, as erythrocytes tend not to be preserved in fossils. As for how, in the ordinary way, by mitosis of stem cells.

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  20. Multicellularity has arisen perhaps twenty times or more in different eukaryotic lineages, but only three of those lineages – metazoans, fungi, and embryophytes – have gone on to produce bodies with differentiated cell types, which raises the question of whether some clades possessed more of the features required for multicellularity than others, and of this subset of lineages, whether cellular differentiation was favored in only a few of them. Because choanoflagellates are the best living candidates for the metazoan sister group, it is not surprising that their genome contains some genes otherwise unknown outside of Metazoa. … In all, more than seventy protein domains known to be shared by choanoflagellates and metazoans are unknown elsewhere. … Thus it appears that many of these genes had not yet been assembled into the form they take in metazoans at the point that choanoflagellates diverged.

    The Cambrian Explosion: The Construction of Animal Biodiversity
    Douglas H. Erwin
    James W. Valentine
    p. 296 – 297

    The section goes on to provide some specific examples unique to metazoans.

    This provides direct support for Meyer’s claims.

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  21. Their genome [writing of the Placozoa], however, has many genes that are important in eumetazoan development but that are unknown in sponges, including at least thirty-five different transcription factors representing at least four different families.

    The Cambrian Explosion: The Construction of Animal Biodiversity. p. 299

    More direct support for Meyer’s claims.

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  22. From the OP:

    Where does he get this? His ass, that’s where.

    That hypothesis is becoming increasingly untenable.

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  23. The evolutionary path from sponge to placozoan remains entirely speculative …The pathway between sponge and eumetazoan is the most puzzling of all.

    More support for Meyer.

    If we define eumetazoans as having epithelial tissues, placozoans would branch later than, or represent a branch of, that stem ancestor. If, however, we require the stem ancestor to have nerves and muscles as well, placozoans branch at an earlier position along the ancestral path, assuming tht they have not lost nerve and muscle cells along the way (which is certainly a possibility).

    More support for Meyer.

    Like placozoans, these ediacarans do not appear to have organs, which raises the question as to whether they may be related to placozoans.

    More support for Meyer.

    All quotes from Erwin and Valentine p. 300.

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  24. Mung: This provides direct support for Meyer’s claims.

    How do you figure that? It seems to me that it directly contradicts Meyer’s claims, which is that metazoans suddenly appear in the Cambrian with no precursors and possessing a wealth of genes unknown elsewhere. Yet you have quoted a statement that metazoans share many of these genes with choanoflagellates.

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  25. Hi John,

    Meyer claims that metazoan evolution involved the introduction of new cell types. The Erwin/Valentine quote supports that claim.

    Multicellularity has arisen perhaps twenty times or more in different eukaryotic lineages, but only three of those lineages – metazoans, fungi, and embryophytes – have gone on to produce bodies with differentiated cell types

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  26. John Harshman: It seems to me that it directly contradicts Meyer’s claims, which is that metazoans suddenly appear in the Cambrian with no precursors and possessing a wealth of genes unknown elsewhere.

    It might seem that way to you if you’ve not read Meyer and if you’ve not read Erwin/Valentine.

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  27. John Harshman: Yet you have quoted a statement that metazoans share many of these genes with choanoflagellates.

    Because there are many shared genes, the choanoflagellates are considered to be the closest sister group to the metazaons. Yet the choanoflagellates are not metazoans. It follows that there must be differences between the two that are unique to metazoans not shared by a common ancestor.

    At some point after the apparent split, these must have evolved. This includes such things as new cell types and organs, which is precisely what Meyer claims.

    The question I’d ask of all those following the LOX discussion is, what is the homologue in choanoflagellates?

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  28. Mung: Next I’ll support my claim that the main argument of the chapter encompasses the entire history of life, and not just the Cambrian.

    Thus, Axe was convinced that explaining the kind of innovation that occurred during the Cambrian explosion and many other events in the history of life required a mechanism that could produce, at least, distinctly new protein folds. (p. 191)

    Darwin’s Doubt (p. 191)

    As an engineer, Axe understood that building a new animal required innovation in form and structure. As a protein scientist, he understood that new protein folds could be viewed as the smallest unit of structural innovation in the history of life.

    Darwin’s Doubt (p. 191)

    Could random mutation generate such novel protein folds? Axe realized that answering this question depended upon measuring the rarity of functional genes and proteins in sequence space and determining whether random genetic mutations would have enough opportunities to search the relevant sequence spaces within evolutionary time.

    Darwin’s Doubt (p. 191-192)

    These quotes are from the exact same section quoted in the OP. One of them is even quoted in the OP.

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  29. “Having developed a method that eliminated the main sources of estimation error in earlier mutagenesis experiments, Axe was now in a position to answer that question with unprecedented rigor. Once he did, he could determine whether random genetic changes would have enough opportunities – even on the scale of evolutionary time – to search the relevant sequence spaces for functional genes and proteins.”

    Darwin’s Doubt (p. 194)

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  30. What is the conditional probability that such a folded protein could arise as the result of random mutations in duplicated non-functional sections of a genome? Axe realized that in order to answer that question he needed a way to estimate the number of opportunities that random mutations had for producing a new protein fold with a selectable function during the whole history of life on earth.

    – Darwin’s Doubt (p. 202)

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  31. Since Axe wanted to know how many novel sequences capable of generating a selectable function might have arisen in the history of life

    …if he could estimate the total number of organisms that had lived during the history of life on earth

    – Darwin’s Doubt (p. 202)

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  32. Mung:
    Did bacteriorhodopsin somehow become rhodopsin in the Cambrian?

    http://pdb101.rcsb.org/motm/27

    An empirical test of convergent evolution in rhodopsins
    Kristine A. Mackin, Richard A. Roy and Douglas L. Theobald*

    Abstract

    Rhodopsins are photochemically reactive membrane proteins that covalently bind retinal chromophores. Type I rhodopsins are found in both prokaryotes and eukaryotic microbes, while type II rhodopsins function as photoactivated G-protein coupled receptors (GPCRs) in animal vision. Both rhodopsin families share the seven transmembrane α-helix GPCR fold and a Schiff base linkage from a conserved lysine to retinal in helix G. Nevertheless, rhodopsins are widely cited as a striking example of evolutionary convergence, largely because the two families lack detectable sequence similarity and differ in many structural and mechanistic details. Convergence entails that the shared rhodopsin fold is so especially suited to photosensitive function that proteins from separate origins were selected for this architecture twice. Here we show, however, that the rhodopsin fold is not required for photosensitive activity. We engineered functional bacteriorhodopsin variants with novel folds, including radical non-circular permutations of the α-helices, circular permutations of an eight-helix construct, and retinal linkages relocated to other helices. These results contradict a key prediction of convergence and thereby provide an experimental attack on one of the most intractable problems in molecular evolution: how to establish structural homology for proteins devoid of discernible sequence similarity.

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  33. Mung: You are conflating new cell types with new proteins with new protein folds, all of which are different things. And you are conflating the time between the common ancestor of metazoans and choanoflagellates and the end of the Cambrian explosion with the explosion itself. Of course that isn’t your fault; it’s Meyer’s.

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  34. Mung: What ID proponents generally believe or do not believe is irrelevant. What is relevant is what is argued by Meyer in the chapter under discussion. Agreed?

    I agree, he argues in his own words, that:

    When these molecules originated in Cambrian animals, they also likely represented a completely novel folded structure unlike anything present in Precambrian forms of life.

    And that:

    New animals typically have new organs and cell types, and new cell types often call for new proteins to service them. In some cases new proteins, while functionally new, would perform their different functions with essentially the same fold or tertiary structure as earlier proteins. But more often, proteins capable of performing new functions require new folds to perform these functions. That means that explosions of new life-forms must have involved bursts of new protein folds as well.

    In the first quote, the implication is that “these molecules” (such as lysyl oxidase and others) originated in cambrian animals, and that they had novel protein folds that did not exist in precambrian life.

    In the seconds quote, the implication is that the cambrian explosion would have required “bursts of new protein folds as well”. That this would be “typical” of “new life forms”.

    You yourself agreed with Meyer, when you said

    Moreover, I would think it obvious that new proteins would be required given all the new animals that appeared in the Cambrian, and that it is the claim that all the proteins already pre-existed in some hypothetical ancestor that is the extra-ordinary claim that requires evidence.

    Both are wrong. His one and only reference argues the opposite. We now know even better than Ohno did, that it is wrong. As I have explained now multiple times and you have completely ignored, Meyer SHOULD have written:
    “New animals typically have new organs and cell types, but new cell types rarely call for new protein folds to service them. In most cases new proteins, while functionally new, would perform their different functions with essentially the same fold or tertiary structure as earlier proteins.”

    Writing THAT would have been correct. He wrote the opposite.

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  35. Mung: Oddly enough, the same can be said of this book on the Cambrian Explosion.

    Perhaps there is a conspiracy of shoddy scholarship afoot when it comes to the Cambrian explosion.

    Cute. I don’t own that book so I can’t check. If the book is full of claims without references, that’s crap too. If the book makes claims, then later references them with a reference that argues the opposite, then that’s an egregious mistake and the authors should be made aware of it.

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  36. Mung:
    Ohno again, sounding oddly Meyer-esque:
    “Assuming the spontaneous mutation rate to be generous 10^-9 per base pair per year and also assuming no negative interference by natural selection, it still takes 10 million years to undergo 1% change in DNA base sequences. It follows that 6-10 million years in the evolutionary time scale is but a blink of an eye. The Cambrian explosion denoting the almost simultaneous emergence of nearly all the extant phyla of the kingdom Animalia within the time span of 6-10 million years can’t possibly be explained by mutational divergence of individual gene functions.

    ETA: Ohno doesn’t cite any source for this claim.

    No, that’s because he supplies the calculation that show this. Ohno is claiming it on the basis of a calculation he makes.

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  37. Mung:
    Ohno:

    A ligament is a kind of tissue, as is a tendon.

    If the structure and function of ligaments and tendons arose in the Cambrian animals then this would support Meyer’s claims of the need for new cell types and organs.

    Yes, but that point is not in dispute. The whole deal here is about protein folds. Clearly new “cell types” are new, because they have “new functions”. But the point is what those functions are due to. Meyer argues it has much to do with new protein folds, then cites Ohno, who argues it mostly doesn’t (in fact that it can’t), and is rather due to changes in regulatory elements in stead. Which is now known to be pretty much spot on.

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  38. Mung:
    Ohno:

    When did this cell type appear and how is this type of cell produced?

    Not particularly relevant, because the globin fold can be traced to the last universal common ancestor of all cellular life. So while cells that utilize globin-fold proteins we call hemoglobins (because they carry heme, which is also truly ancient) have specialized functions, the individual molecules discussed (heme, globins and hemoglobin) all predate the cambrian diversification by literally billions of years.

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  39. Mung: The Cambrian Explosion: The Construction of Animal Biodiversity
    Douglas H. Erwin
    James W. Valentine
    p. 296 – 297
    The section goes on to provide some specific examples unique to metazoans.

    “Because choanoflagellates are the best living candidates for the metazoan sister group, it is not surprising that their genome contains some genes otherwise unknown outside of Metazoa. … In all, more than seventy protein domains known to be shared by choanoflagellates and metazoans are unknown elsewhere. Thus it appears that many of these genes had not yet been assembled into the form they take in metazoans at the point that choanoflagellates diverged.”

    This provides direct support for Meyer’s claims.

    Your quote argues they’re shared among choanoflaggelates and metazoa, thus signficiantly predating the cambrian explosion. So if “direct support” means “off by at least 60 million years”, then yeah I guess.

    Also, I’d like to know what’s hiding inside the ellipsis I’ve bolded. And what, exactly, is meant by the statement “assembled into the form they take in..” ? The last sentence is talking about genes, the previous one before the bolded ellipsis is talking about protein domains. There’s a hell of a difference between the two.

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  40. Mung: It might seem that way to you if you’ve not read Meyer and if you’ve not read Erwin/Valentine.

    You’ve yet to supply a quote rfom Erwin/Valentine that shows this. The one you brought talked about protein domains going back at least 60 million years before the cambrian, then another sentence was talking about genes, which is not synonymous with protein domains. You had those two sentences separated by an ellipsis, so there’s no reason to think E/W is using the terms interchangeably.

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  41. Mung: The question I’d ask of all those following the LOX discussion is, what is the homologue in choanoflagellates?

    The post you make immediately after the one where you ask this question shows this in the phylogeny (it’s in the Holozoa). Or, what do you mean by “what is the homologue” ? Are you asking if there is one in them?

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  42. Mung: Because there are many shared genes, the choanoflagellates are considered to be the closest sister group to the metazaons. Yet the choanoflagellates are not metazoans. It follows that there must be differences between the two that are unique to metazoans not shared by a common ancestor.

    They’re unicellular, for one. Metazoa are not. There’s also something about their plasma membrane and clustering of genes in phylogenetic relationships here:
    https://en.wikipedia.org/wiki/Choanoflagellate#Classification

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