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This is embarrassing: “Darwin’s Doubt” debunker is 14 years behind the times

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Over at The Skeptical Zone, Mikkel “Rumraket” Rasmussen has written a post critical of Dr. Stephen Meyer, titled, Beating a dead horse (Darwin’s Doubt), which is basically a rehash of comments he made on a thread on Larry Moran’s Sandwalk blog last year. The author’s aim is to expose Dr. Stephen Meyer’s “extremely shoddy scholarship,” but as we’ll see, Rasmussen’s own research skills leave a lot to be desired.

Did Dr. Meyer fail to document his sources?

Rasmussen focuses his attack on chapter 10 of Dr. Meyer’s book, “Darwin’s Doubt.” He writes:

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:

(Rasmussen proceeds to quote from Meyer’s book, on which he comments below – VJT.)

In the whole section Meyer dedicates to the origin of novel folds, he makes zero references that actually substantiate [his assertion] that the [C]ambrian diversification, or indeed any kind of speciation, or the [appearance of] new cells types or organs, require[d] new protein folds. ZERO. Not one single reference that supports these claims. At first it reads like what I quote[d] above, lots of claims, no references. Later on he eventually cites the work of Douglas Axe that atte[m]pts to address how hard it is to evolve new folds (and that work has its 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.

(N.B. For ease of readability, I have used square brackets to correct Rasmussen’s spelling and punctuation errors, and I have also inserted four extra words, without which his meaning would have been obscure to readers, in the preceding paragraph – VJT.)

Rasmussen repeats his accusation that Dr. Meyer frequently makes claims in his book without providing any references for them, at the very end of his post:

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.

Do new cell types require new kinds of proteins?

I find it quite astonishing that Rasmussen would require documentation for Dr. Meyer’s claim that new cell types would require new types of proteins, for three reasons. First, it’s a well-known fact that each different cell type has different cluster of differentiation proteins. Bojidar Kojouharov, a Ph.D. Student in Cancer Immunology, describes these proteins as follows:

Clusters of Differentiation (CD) are cell surface proteins used to differentiate one cell type from another. Each CD marker is a different surface protein from the others. As such, it will likely have different functions and may be expressed on different cells. Technically, different CD markers don’t really have to have anything in common, other than the fact that they are on the cell’s surface. Usually, it’s safe to assume any Clusters of Differentiation is a protein.

Second, it is widely admitted by authors in the field that the complex organisms which appeared in the Cambrian would have required a host of new cell types. Here, for instance, is what P. V. Sukumaran, of the Geological Society of India, says in his paper, Cambrian Explosion of Life: the Big Bang in Metazoan Evolution (RESONANCE, September 2004, pp. 38-50):

Yet another feature of the Cambrian explosion is the quantum jump in biological complexity. The early Cambrian animals had roughly 50 cell types while the sponges that appeared a little earlier had only 5… (p. 44, sidebar)

Unicellular life is relatively simple; there is little division of labour and the single cell performs all functions of life. Obviously the genetic information content of unicellular organisms is relatively meagre. Multicellular life, on the other hand, requires more genetic information to carry out myriads of cellular functions as their cells are differentiated into different cell types, tissues and organs. But new cell types themselves require specialised proteins, and novel proteins arise from novel gene sequences, that is new genetic information. As the organisms that appeared in the Cambrian explosion had many more novel and specialised cell types than their prokaryotic ancestors, the amount of new genetic information that arose in the Cambrian explosion represents a large increase in biological information. (p. 47)

Third, it turns out that Dr. Meyer provided the very references that Rasmussen chides him for failing to supply, over 14 years ago, in his 2001 paper, The Cambrian Explosion: Biology’s Big Bang, which he co-authored with Paul Nelson and Paul Chien, which is listed on page 471 of the bibliography of Dr. Meyer’s book, Darwin’s Doubt. (Actually, the bibliography cites a later and slightly more polished 2003 version of the same paper.) Allow me to quote from pages 32-33 of the 2001 paper (emphases mine – VJT):

As noted, the new animals of the Cambrian explosion would have required many new cell types and, with them, many new types of proteins acting in close coordination. It follows, therefore, that if the neo-Darwinian mechanism cannot explain the origin of new cell types (and the systems of proteins they require), it cannot explain the origin of the Cambrian animals. Yet given the number of novel proteins required by even the most basic evolutionary transformations, this now seems to be precisely the case.

Consider, for example, the transition from a prokaryotic cell to a eukaryotic cell. This transition would have produced the first appearance of a novel cell type in the history of life. Compared to prokaryotes, eukaryotes have a more complex structure including a nucleus, a nuclear membrane, organelles (such as mitocondria, the endoplasmic recticulum, and the golgi apparatus), a complex cytoskeloton (with microtubulues, actin microfilaments117 and intermediate filaments) and motor molecules.118 Each of these features requires new proteins to build or service, and thus, as a consequence, more genetic information. (For example, the spooled chromosome in a modern eukaryotic yeast [Saccharomyces] cell has about 12.5 million base pairs, compared to about 580,000 base pairs in the prokaryote Mycoplasma.)119 The need for more genetic information in eukaryotic cells in turn requires a more efficient means of storing genetic information. Thus, unlike prokaryotic cells which store their genetic information on relatively simple circular chromosomes, the much more complex eukaryotic cells store information via a sophisticated spooling mechanism.120 Yet this single requirement — the need for a more efficient means of storing information — necessitates a host of other functional changes each of which requires new specialized proteins (and yet more genetic information) to maintain the integrity of the eukaryotic cellular system.

For example, nucleosome spooling requires a complex of specialized histones proteins (with multiple recognition and initiation factors) to form the spool around which the double stranded DNA can wind.121 Spooled eukaryotic DNA in turn uses “intron spacers,” (dedicated sections of non-coding DNA), in part to ensure a tight electrostatic fit between the nucleosome spool and the cords of DNA.122 This different means of storing DNA in turn requires a new type of DNA polymerase to help access, “read,” and copy genetic information during DNA replication. (Indeed, recent sequence comparisons show that prokaryotic and eukaryotic polymerases exhibit stark differences).123 Further, eukaryotes also require a different type of RNA polymerase to facilitate transcription. They also require a massive complex of five jointly necessary enzymes to facilitate recognition of the promoter sequence on the spooled DNA molecule.124 The presence of intron spacers in turn requires editing enzymes (including endonucleases, exonucleases and splicesomes) to remove the non-coding sections of the genetic text and to reconnect coding regions during gene expression.125 Spooling also requires a special method of capping or extending the end of the DNA text in order to prevent degradation of the text on linear (non-circular) eukaryotic chromosomes.126 The system used by eukaryotes to accomplish this end also requires a complex and uniquely specialized enzyme called a telomerase.127

Thus, one of the “simplest” evolutionary transitions, that from one type of single-celled organism to another, requires the origin of many tens of specialized novel proteins, many of which (such as the polymerases) alone represent massively complex, and improbably specified molecules.128 Moreover, many, if not most, of these novel proteins play functionally necessary roles in the eukaryotic system as a whole. Without specialized polymerases cell division and protein synthesis will shut down. Yet polymerases have many protein subunits containing many thousands of precisely sequenced amino acids. Without editing enzymes, the cell would produce many nonfunctional polypeptides, wasting vital ATP energy and clogging the tight spaces within the cytoplasm with many large useless molecules. Without tubulin and actin the eukaryotic cytoskeloton would collapse (or would never have formed). Indeed, without the cytoskeleton the eukaryotic cell can not maintain its shape, divide, or transport vital materials (such as enzymes, nutrients, signal molecules, or structural proteins).129 Without telomerases the genetic text on a linear spooled chromosome would degrade, again, preventing accurate DNA replication and eventually causing the parent cell to die.130

Even a rudimentary analysis of eukaryotic cells suggests the need for, not just one, but many novel proteins acting in close coordination to maintain (or establish) the functional integrity of the eukaryotic system. Indeed, the most basic structural changes necessary to a eukaryotic cell produce a kind of cascade of functional necessity entailing many other innovations of design, each of which necessitates specialized proteins. Yet the functional integration of the proteins parts in the eukaryotic cell poses a severe set of probabilistic obstacles to the neo-Darwinian mechanism, since the suite of proteins necessary to eukaryotic function must, by definition, arise before natural selection can act to select them.

References:
117 Russell F. Doolittle, “The Origins and Evolution of Eukaryotic Proteins,” Philosophical Transactions of the Royal Society of London B 349 (1995): 235-40.
118 Stephen L. Wolfe, Molecular and Cellular Biology (Belmont, CA: Wadsworth, 1993), pp. 3, 6-19.
119 Rebecca A. Clayton, Owen White, Karen A. Ketchum, and J. Craig Ventner, “The First Genome from the Third Domain of Life,” Nature 387 (1997): 4459-62.
120 Stephen L. Wolfe, Molecular and Cellular Biology, pp. 546-50.
121 Ibid.
122 H. Lodish, D. Baltimore, et. al., Molecular Cell Biology (New York: W.H. Freeman, 1994), pp. 347-48. Stephen L. Wolfe, Molecular and Cellular Biology, pp. 546-47.
123 Edgell and Russell Doolittle, “Archaebacterial genomics: the complete genome sequence of Methanococcus jannaschii,” BioEssays 19 (no. 1, 1997): 1-4. Michael Y. Galperin, D. Roland Walker, and Eugene V. Coonin, “Analogous Enzymes: Independent Inventions in Enzyme Evolution,” Genome Research 8 (1998): 779-90.
124 Stephen L. Wolfe, Molecular and Cellular Biology, pp. 580-81, 597.
125 Ibid., pp. 581-82, 598-600, 894-96.
126 Ibid., p. 975.
127 Ibid., pp. 955-975.
128 Ibid., p. 580.
129 Ibid., pp. 17-19.
130 Ibid., pp. 955-975.

And here’s a highly pertinent quote from pages 5-6 of the paper:

Each new cell type requires many new and specialized proteins. New proteins in turn require new genetic information encoded in DNA. Thus, an increase in the number of cell types implies (at a minimum) a considerable increase in the amount of specified genetic information. For example, molecular biologists have recently estimated that a minimally complex cell would require between 318 to 562 kilobase pairs of DNA to produce the proteins necessary to maintain life.20 Yet to build the proteins necessary to sustain a complex arthropod such as a trilobite would require an amount of DNA greater by several orders of magnitude (e.g., the genome size of the worm Caenorhabditis elegans is approximately 97 million base pairs21 while that of the fly Drosophila melanogaster (an arthropod), is approximately 120 million base pairs.22 For this reason, transitions from a single cell to colonies of cells to complex animals represent significant (and in principle measurable) increases in complexity and information content. Even C. elegans, a tiny worm about one millimeter long, comprises several highly specialized cells organized into unique tissues and organs with functions as diverse as gathering, processing and digesting food, eliminating waste, external protection, internal absorption and integration, circulation of fluids, perception, locomotion and reproduction. The functions corresponding to these specialized cells in turn require many specialized proteins, genes and cellular regulatory systems, representing an enormous increase in specified biological complexity. Figure 5 shows the complexity increase involved as one moves upward from cellular grade to tissue grade to organ grade life forms. Note the jump in complexity required to build complex Cambrian animals starting from, say, sponges in the late Precambrian. As Figure 5 shows Cambrian animals required 50 or more different cell types to function, whereas sponges required only 5 cell types.

(Note: Figure 5 can be viewed in this later version of the paper, where it is labeled as Figure 10 – VJT.)

References:
20 Mitsuhiro Itaya, “An estimation of the minimal genome size required for life,” FEBS Letters 362
(1995): 257-60. Claire Fraser, Jeannine D. Gocayne, Owen White, et. al., “The Minimal Gene Complement of Mycoplasma genitalium,” Science 270 (1995): 397-403. Arcady R. Mushegian and Eugene V. Koonin, “A minimal gene set for cellular life derived by comparison of complete bacterial genomes,” Proceedings of the National Academy of Sciences USA 93 (1996): 10268-73.
21 The C. elegans Sequencing Consortium, “Genome Sequence of the Nematode C. elegans: A Platform for Investigating Biology,” Science 282 (1998): 2012-18.
22 John Gerhart and Marc Kirschner, Cells, Embryos, and Evolution (London: Blackwell Science, 1997), p.
121

Did Dr. Meyer distort the words of geneticist Susumu Ohno?

Rasmussen also accuses Dr. Meyer of distorting the words of Susumu Ohno, a geneticist and evolutionary biologist whose work he discussed in chapter 10 of his book, Darwin’s Doubt:

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.

Once again, Rasmussen hasn’t done his homework. A little digging on my part revealed that Dr. Meyer had previously discussed the Dr. Ohno’s claims at considerable length and responded to those claims, in his 2001 paper, The Cambrian Explosion: Biology’s Big Bang, which he co-authored with Paul Nelson and Paul Chien (bolding mine – VJT):

Ironically, even attempts to avoid the difficulty posed by the Cambrian explosion often presuppose the need for such foresight. As noted, Susumo Uno, the originator of the hypothesis of macroevolution by gene duplication, has argued that mutation rates of extant genes are not sufficiently rapid to account for the amount of genetic information that arose suddenly in the Cambrian.114 Hence he posits the existence of a prior “pananimalian genome” that would have contained all the genetic information necessary to build every protein needed to build the Cambrian animals. His hypothesis envisions this genome arising in a hypothetical common ancestor well before the Cambrian explosion began. On this hypothesis, the differing expression of separate genes on the same master genome would explain the great variety of new animal forms found in the Cambrian strata.

While Ohno’s hypothesis does preserve the core evolutionary commitment to common descent (or monophyly), it nevertheless has a curious feature from the standpoint of neo-Darwinism. In particular, it envisions the pananimalian genome arising well before its expression in individual animals.115 Specific genes would have arisen well before they were used, needed or functionally advantageous. Hence, the individual genes within the pananimalian genome would have arisen in a way that, again, would have made them imperceptible to natural selection. This not only creates a problem for the neo-Darwinian mechanism, but it also seems to suggest, as Simon Conway Morris has recently intimated,116 the need for foresight or teleology to explain the Cambrian explosion. Indeed, the origin of a massive, unexpressed pre-Cambrian genome containing all the information necessary to build the proteins required by not-yet-existent Cambrian animals, would strongly suggest intelligent foresight or design at work in whatever process gave rise to the pananimalian genome. (pp. 31-32)

In short: Dr. Meyer was not only aware that Dr. Ohno had proposed the existence of a pananimalian genome; he also explicitly referred to it in his 2001 paper, in order to demonstrate that Intelligent Design would be the best explanation of such a genome.

I’ll leave it to my readers to decide whether it is Dr. Meyer or Rasmussen who is guilty of “extremely shoddy scholarship.” Let me conclude by recalling an old saying: “People who live in glass houses shouldn’t throw stones.”

Comments
Proteins are easy to evolve, except in the Cambrian. there's no evidence of any evolution at all during the Cambrian. Just a bunch of shuffling. It's like coming up with a whole bunch of new card games just by shuffling a deck of cards.Mung
December 29, 2015
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vjtorley, I see that you mentioned Axe’s alleged response to my discussion of Axe’s 2004 article. What you fail to point out that Axe almost completely ignored my criticisms and conclusions, and he continues, to this day, to pretend that these valid arguments do not exist. To briefly summarize: in the purported response you linked to, Axe said (among other things – the other alleged responses to my essay miss the points entirely): According to Hunt, I “molded a variant that would be exquisitely sensitive to mutation.” [2] Venema expressed the same concern, that the starting sequence I used was “intentionally ‘hamstrung’ with multiple mutations to render it far less functional than its natural counterpart.” [7] Both Hunt and Venema seem to think the outcome would have been more favorable (i.e., functional sequences would have been more prevalent) had I used the highly proficient natural enzyme as a starting point rather than the handicapped version. Actually, as a demonstration will show, the opposite is true. Axe’s demonstration does no such thing. Furthermore, he completely ignores the crux of my criticism. Referring to Figures 1 and 3 from my essay: The point of Axe’s study was to enumerate the totality of sequences that could give rise to a particular functionality. This totality of sequences is represented by the base of the hill shown in Fig. 1. To do this, Axe crafted, by extensive mutagenesis and deliberate selection, a feeble enzyme that would be exceedingly sensitive to mutation. Importantly, the variant he created was temperature-sensitive. This means that he deliberately molded an enzyme that would have very steep sides (that is the necessary outcome of a ts mutant – even tiny straying from the ts sequence necessarily will destroy function) and a very small base, as I show in Fig. 3. What Axe claims is that the base of the hill in Fig. 3 is, not just representative to that of the natural enzyme shown in Fig. 1, but identical to the base of the hill shown in Fig. 1. He not only provides zero evidence, or even theoretical argument, for this claim, he ignores the fact that the hill that defines the ts variant will undoubtedly have a very different shape, including at its base. In other words, he completely ignores the fundamental flaw in his study, and he continues to this day to pretend that the flaw does not exist. At the end of my discussion of Axe’s 2004 article my essay, I state: 10^-10 -> 10^-63 (or thereabout): this is the range of estimates of the density of functional sequences in sequence space that can be found in the scientific literature. The caveats given in Section 2 notwithstanding, Axe’s work does not extend or narrow the range. This statement was true in 2004, it was true in 2007, and it is true today. As long as this is the case, any arguments that rely on Axe’s work to “prove” the unevolvability of proteins are wrong.Arthur Hunt
December 29, 2015
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More evidence for the mystical front-loading hypothesis: https://en.wikipedia.org/wiki/Meiosis https://en.wikipedia.org/wiki/Sexual_reproduction There simply must have been a single-cell, asexually reproducing, front-loaded organism.Mung
December 29, 2015
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The group believed to be closest to the animals is the Choanoflagellates. Single-cell with asexual reproduction. So on the road to all the Cambrian animals we need multi-cellularity and sexual reproduction, at a minimum.Mung
December 29, 2015
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Nick Matzke: I'm just coming onto the scene, but a few reactions nonetheless: NM says:
VJ Torley, your post is silly in several ways: 1. “New genes” and “new proteins” are not the same thing as “new protein folds”. You can have many different kinds of proteins that all draw from the same folds. You can’t quote sources talking about new genes/new proteins/new information and just blithely assume this automatically means new folds. Rasmussen gets this, Meyer misses this, you miss this.
Nick, this is pure silliness. The 'critical' need of specificity has to do with "new proteins," not "new folds." I think it's fairly obvious that the combinatorial space for DNA is much, much more specified, and hence, improbable, than the 'physical space' that proteins require as they fold. Can you not see that there are infinitely less configurations of 'folds' as compared to configurations of 'new proteins'? Then why this silly attempt to 'impeach' the scientific credentials of Meyer?
2. The pan-animalian genome idea means that all of these animals are built with not only the same basic folds, but the same basic gene set. This is dramatically less of an “information explosion” than would be required if they all needed different genes.
And where is the 'evidence' for this "pan-animalian genome"? It's no more than a theoretical construct built out of necessity.
(All that said, Ohno isn’t even particularly an expert on the Cambrian Explosion. The pan-animalian genome idea is a good one nevertheless. But he misses things, which the ID advocates then naively take as gospel truth, since they have such a blind and un-nuanced idea of “authority” in science. E.g., because he’s not a paleontologist, one thing Ohno misses, IIRC, is that there is clear evidence of bilaterians in the Precambrian — trackways and burrows indicating billaterial symmetry, a coelom, etc., and these continually increase in complexity through the small shelly fossils, only reaching the “classic” Cambrian Explosion tens of millions of years later. This is all true regardless of one’s interpretation of the Edicarans etc. Thus, it’s idiotic to say, as Meyer does, that Ohno’s hypothesis means “the pananimalian genome ar[ose] well before its expression in individual animals.” Fossil traces of bilaterians are there before the Explosion, they had worm-level complexity, all of those common genes between all the phyla basically are what is required to specify a bilaterian body plan, which is what worms have.
But, Nick, you've succeeded here in missing Meyer's devastating critcism of Ohno's hypothesis: viz., as pointed out in bold type by vjt:
While Ohno’s hypothesis does preserve the core evolutionary commitment to common descent (or monophyly), it nevertheless has a curious feature from the standpoint of neo-Darwinism. In particular, it envisions the pananimalian genome arising well before its expression in individual animals.115 Specific genes would have arisen well before they were used, needed or functionally advantageous. Hence, the individual genes within the pananimalian genome would have arisen in a way that, again, would have made them imperceptible to natural selection. This not only creates a problem for the neo-Darwinian mechanism, but it also seems to suggest, as Simon Conway Morris has recently intimated,116 the need for foresight or teleology to explain the Cambrian explosion. [My italics]
Again, Nick, you miss Meyer's point. The whole notion of a "pan-animalian" genome is hypothetical, and, worse, contradictory to Darwinian expectations.
3. Bringing in the origin of eukaryotes is also silly, since eukaryotes arose probably a billion years before the Cambrian. Whether or not new protein folds originated with eukaryotes (probably, although many many folds are shared between eukaryotes and prokaryotes), this is in no possible way an argument that new folds originated in the Cambrian. This is totally obvious! How can you not get this is, in a post allegedly taking on Rasmussen head-on?
Nick, this is blather. Where did you pull up the "billion years" from? Is it your 'guess'? And, again, who cares about protein folds when we're talking about new proteins. Where does the information for these new proteins come from? (And, this says nothing of the new "co-chaperone" proteins that would be necessary for folding)
Even the intended argument is hazy, but seems to be something like: the origin of the first eukaryotic cell, a “simple” transition, required lots of new proteins and protein folds, therefore the origin of new cell types must also. But that’s just crazy. Different cell types in a multicellular eukaryote will have much more in common than a eukaryote cell and a prokaryote cell. The origin of eukaryotes is probably the biggest and most fundamental evolutionary event apart from the origin of life itself. The origin of multicellularity, the Cambrian Explosion (not the same thing as the origin of multicellularity, another thing ID/creationists often miss), etc. are all minor by comparison.
Nick, you've moved from blather to bluster here. What was the 'first' eukaryotic cell? Was it yeast? Now compare a yeast cell to an axion. Is this "minor by comparison"? All of this is speculation, yet you act as if all of this is perfectly known.
These kinds of catastrophic, fundamental mistakes and lack of knowledge of absolute basics — which are totally obvious to anyone who has a basic grasp of the field — are exactly why biologists are so dismissive of Meyer, ID, and UD. Imagine if someone went around claiming that the U.S. Constitution was fatally flawed, and then claimed that the First Amendment was about gun control. Most people would just shake their heads and walk away, concluding that kooks who can’t get these basics right aren’t worth listening to.
Wow. Here's what you said just above: "The origin of eukaryotes is probably the biggest and most fundamental evolutionary event apart from the origin of life itself." Did you notice you used the word "probably"? I did. You want to compare contentious, poorly known areas of knowledge to clearly known areas of knowledge? We KNOW what the U.S. Constitution says. We know what the First Amendment says. But we don't know if: (i) eukaryotes developed a "billion years ago," or (ii) what the "evolutionary" transition between prokaryotes and eukaryotes looked like. Bluster is still not a substitute for rational argument.PaV
December 29, 2015
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@florabama #22 'Nick Matzke — biology’s Baghdad Bob.' How about : Nick Matzke - biology's Donald Rumsfeld : "That's not the way the world really works anymore." He continued "We're an empire now, and when we act, we create our own reality. And while you're studying that reality—judiciously, as you will — we'll act again, creating other new realities, which you can study too, and that's how things will sort out. We're history's actors … and you, all of you, will be left to just study what we do." Unfortunately, in means modern man is doomed thereby to hear the endlessly repeated refrain : "Gee! Isn't Evolution wonderful. It never ceases to surprise us ? And there were we thinking bla bla bla."Axel
December 29, 2015
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Only artificial selection can optimize. Natural selection is a process of elimination. It is not an optimizing process.Virgil Cain
December 29, 2015
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Mung: If it’s such a simple thing to evolve new protein folds, why are there not more of them? Is the choice of extant folds contingent or necessary? A frozen accident, or optimized through selection? To what degree? The geometry of the vast Protein Universe is still largely unknown. Mung: If it’s such a simple thing to evolve new protein folds, why not believe that new ones arose during the Cambrian explosion? Some did, but they are small in number. Most folds were inherited. Think of it as an erector set. Once you have the basic components, you can build most anything you want. In the case of proteins, the components can even be extensively modified.Zachriel
December 29, 2015
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I have a couple questions for people to consider. If it's such a simple thing to evolve new protein folds, why are there not more of them? If it's such a simple thing to evolve new protein folds, why not believe that new ones arose during the Cambrian explosion?Mung
December 29, 2015
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The vertebrate homeotic complex comprises four distinct Hox gene clusters (Hox A, B, C, D) that are organized into thirteen homology (or paralogue) groups. http://people.ucalgary.ca/~browder/virtualembryo/hox.html
Mung
December 29, 2015
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Nick Matzke:
The differences that they have are basically due to differential duplication of genes and subsequent modification of genes, and sometimes rearrangement/recombination of pre-existing gene chunks.
So, new genes and new proteins, and by your own references to Grishin this could easily result in new folds. That's what you're saying? Help me out here Nick.Mung
December 29, 2015
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Nick Matzke:
This is protein homology 101, if you don’t understand stuff like this, what basis do you have for even having an opinion on these topics, or on the correctness of Meyer?
That's an easy one, Nick. We look at other things Meyer said in the same argument, the things you keep wanting to ignore, the things we know are true. New genes New proteins New cell types New organs These things are simpler to validate and their origins in the Cambrian animals is far less controversial. Which of those did Meyer get wrong, Nick? From the above, Meyer makes an inference about new protein folds. It's an inference. The problem you have, and other critics like Rumraket, is that you fail to properly grasp the argument and instead of addressing the argument you try to focus on details that are of little to no relevance.Mung
December 29, 2015
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Nick Matzke:
Ohno’s paper on the pan-animalian genome points out that these bilaterians all share their basic gene/protein set...
This is simply false, Nick. Ohno's paper shows no such thing. (Yes, I've read the paper.)
...and if this is true, then anyone who knows that folds are even more conserved than proteins on average knows that the folds must be mostly shared also.
I also think it's reasonable to assume that you know it is false considering your further qualification "if this is true." Have you even read the paper Nick?Mung
December 29, 2015
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Hi Nick, I'd like to address a brief remark of yours in #101 above:
The whole friggin’ point of Ohno’s article on the pan-animalian genome was that the gene and protein complements are basically shared across bilaterians as well! There was, in fact, not a huge amount of origination of genes and proteins required to produce the Cambrian phyla, and we know this because they all have the same basic complement of genes and proteins. The differences that they have are basically due to differential duplication of genes and subsequent modification of genes, and sometimes rearrangement/recombination of pre-existing gene chunks. All of this is totally obvious from actually reading Ohno with any care — but you and Meyer just can’t seem to get it through your skulls, I think because have such a strong, unquestioned prior belief that the origin of morphological diversity just has to involve lots of new genes and new proteins. Ohno’s point was that the main thing going on was just redeployment (different regulation) of preexisting genomes.
Might I remind you that Ohno's hypothesis of a pan-animalian genome is just that: a hypothesis. Might I also remind you that even if all animal phyla turn out to have the same basic complement of genes and proteins, there is also abundant evidence of genes and proteins which are unique to each phylum. The origin of these genes and proteins needs to be accounted for. As I have repeatedly stated in my comments above, the question of when these genes and proteins originated does not concern me greatly. Meyer maintains in his book, Darwin's Doubt (p. 189), that many of them must have originated in (or very shortly before) the Cambrian. On this point, he is probably wrong, as you've pointed out. However, in his 2001 article, Biology's Big Bang, which I cited above, Meyer briefly considers the possibility that Ohno's "pan-animalian genome" theory may be correct after all, but points out that even if it were true, it would raise a problem for Darwinism: "Specific genes would have arisen well before they were used, needed or functionally advantageous." But even if Meyer were wrong here as well, and the genes in the ancestral pan-animalian genome turned out to have functions that were later co-opted or ex-apted by their Cambrian descendants, the much larger point which Meyer makes on pages 192 to 207 of his book, in which he discusses the work of Dr. Douglas Axe, is that the likelihood of even one functional protein fold originating on the primordial Earth is vanishingly low - especially when we're talking about the kinds of long-chain proteins required for the appearance of animal life. This is the argument on which Meyer's whole case stands or falls. In your reviews of Darwin's Doubt, you've failed to address this central argument, instead focusing your fire on peripheral issues like the duration of the Cambrian explosion (frankly, who cares if it was 10 million years or 30 million?) and whether Anomalocaris was an arthropod or not. You ask why I haven't discussed the article by Yang and Bourne. My take on the article is that while its phylogeny is plausible enough, it fails to establish that the mechanisms which it mentions could have actually generated new protein domains, as proposed by the authors. In particular, the authors nowhere reference Dr. Axe's work or his arguments. You also mention Grishin's work, which, you say, "shows examples where minor mutational changes cause proteins to shift fold — even while maintaining function!" For a rebuttal of Grishin's claims, I suggest you have a look at this article by Casey Luskin. Luskin argues that Grishin "assumes from the outset that there are Darwinian pathways, but it does not demonstrate that those pathways exist... Rather than showing how natural selection and random mutation might have increased the information in these genes, what the paper primarily finds is mere sequence homology... No step-by-step Darwinian pathway for the evolution of ... proteins is given." The article quotes Professor Michael Behe, who writes: "Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?" If you think that Luskin has done Meyer a grave injustice and that Meyer's central argument is badly flawed, then by all means, make your case. But before you do, please read Dr. Axe's article, Correcting Four Misconceptions about my 2004 Article in JMB, in which he responds to common criticisms of his work by Venema, Matheson, Hunt and others. And finally, if you think Dr. Axe's claims are wrong, then I suggest you devote a full-length post on Panda's Thumb to that very issue. I think it's fair to say that if you could successfully refute the arguments in Axe's 2010 paper, The Case Against a Darwinian Origin of Protein Folds, then the scientific case for biological (as opposed to cosmological) Intelligent Design would come crashing to the ground. So get to work, Nick. What's holding you back?vjtorley
December 29, 2015
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Nick Since when is computer simulations facts? Your litrature bluff are not real world examples, they are intellegent designed software that are working towards a goal to achieve a specific result. This to you are facts? Then it stands to reason that you are a very religious person taking assumptions by faith and converting them with your weak intentional states to facts. Shameful. You are what we call a religious zealot.Andre
December 28, 2015
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Nick:
Note that in real science, it is better to just fess up to mistakes, issue a correction, and move on.
Then why haven't you fessed up to your mistake that I pointed out in comment 5, issued a correction, and moved on? BTW, when you are going to answer the question that has been on the table for two and a half years? (See here) It is a simple question Nick.Barry Arrington
December 28, 2015
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83 vjtorleyDecember 28, 2015 at 8:38 am Hi Nick Matzke, You write:
I’ve known about Grishin’s work for a long time. Whether or not I ever had occasion to reference it is a different question – I don’t think I’ve ever written an extended discussion of the origin of protein folds. But, as it happens, I used to save potentially useful references on CiteUlike, and lo and behold: http://www.citeulike.org/user/matzke/tag/evolution . That’s 2 Grishin articles and several others on the same topic. In April 2005.
You did indeed save two articles by Grishin in 2005 (under the name “matzke” rather than “Nick Matzke,” which is why my Google search never picked it up), but you didn’t use them for a long time afterwards. I might add that the articles by Grishin which you saved were written in 2001 and 2002 – i.e. at least two years before the publication of Dr. Douglas Axe’s paper, “Estimating the prevalence of protein sequences adopting functional enzyme folds” (Journal of Molecular Biology, 2004 Aug; 341(5):1295-315). Neither of the papers you saved even attempts to estimate the antiquity of the various protein folds found in animals – in fact, neither paper even mentions animals as such (Metazoa). So the relevance of these articles to Intelligent Design or to Dr. Meyer’s book, Darwin’s Doubt, is highly debatable.
Aggggh. There are two claims Meyer makes: 1. The natural evolution of new protein folds is wildly improbable. 2. The Cambrian Explosion required lots of new protein folds. Grishin's work (and related work) addresses #1. He shows examples where minor mutational changes cause proteins to shift fold -- even while maintaining function! Point #2 is addressed by looking at the distribution of folds amongst organisms, and observing that there are few folds unique to bilaterian animals. This has been obvious for years -- Ohno's paper on the pan-animalian genome points out that these bilaterians all share their basic gene/protein set, and if this is true, then anyone who knows that folds are even more conserved than proteins on average knows that the folds must be mostly shared also. But point #2 is also addressed, more explicitly, also in this very thread, in this article: Song Yang, Philip E. Bourne (2009). The Evolutionary History of Protein Domains Viewed by Species Phylogeny. PLoS ONE 4(12): e8378. doi:10.1371/ journal.pone.0008378 http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0008378&representation=PDF How can you have possibly missed this?? It's like you have short-term memory loss or something...
From what I can tell (h/t Bob O’H), you never mentioned Grishin’s work in your posts until June 2014 – and that was in a very brief Twitter post.
Who cares? I even mentioned in my Panda's Thumb review of Meyer that I was doing it quickly and wouldn't have time to introduce everything in a for-beginners way, or put in all relevant citations. I think you are just grasping at straws, trying to find any possible way of saving Meyer's reputation, and by implication yours. Note that in real science, it is better to just fess up to mistakes, issue a correction, and move on. That's how you build a reputation in science.
You also write: Meyer asserted the Cambrian explosion required many new protein folds. This is clearly false and has been disproven, and Meyer definitely should have known this, and his defenders should have also (Most of the folds are indeed shared with fungi — but also closer outgroups — choanoflagellates, sponges, etc.) Until you admit Meyer made a mistake there, there is little point in continuing. I really think you’re being a bit rude to Dr. Meyer here. Take a look at his Acknowledgments page (p. 414), where he states: “I’d also like to acknowledge the two anonymous biologists and two paleontologists who gave such careful attention to improving the scientific rigor and accuracy of the manuscript during the peer-review process.” If there are any scientific mistakes in Meyer’s book, it’s these guys who should take the fall for it, not Meyer.
What? The author isn't responsible for what he writes? This is, though, evidence that whatever reviewers Meyer got were not serious people. Probably they were either creationists or off-the-deep-end people like Mark McMenamin.
He did, after all, do his level best to ensure that his book from free from mistakes. He is, as he states, “not a biologist, but a philosopher of biology.”
There were so many mistakes in the book, I doubt this is true. He did his level best to make a pro-ID case from the Cambrian Explosion, based on what he thought he learned about the topic in the 1980s, and doing his best to ignore everything that has happened since then indicating that the "lawn of phyla" view, popular in the 1980s, is incorrect. Then he stuck in a bunch of basically irrelevant material, like assertions about how lots of protein folds had to originate in the Cambrian, basically because he thought it helped his argument to cite Axe.
You write that most of the protein folds found in animals are indeed shared with fungi. Since you’re a biologist working in the field, I’ll take your word for it, although I still have a question as to how scientists determine that fold A and fold B are in fact the same fold: is “sameness” a clear-cut term, in this context, or does “the same” just mean highly similar?
It is a safe generalization that if two protein sequences have statistical similarity indicating homology, then they have the same structure. Note that this generalization is not absolute -- Nick Grishin and colleagues have collected cases where similar sequences produce different structures. But this is rare. This is protein homology 101, if you don't understand stuff like this, what basis do you have for even having an opinion on these topics, or on the correctness of Meyer?
Granting that the protein folds found in animals are more ancient than animals themselves, it would appear that the protein folds shared by animals and fungi go back about 1,300 million years, since that’s the time when timetree.org estimates that animals and fungi diverged. (Animals and plants diverged about 200 million years earlier, but you do not claim that plants possess these protein folds too.) However, the actual proteins that are used by the various phyla of animals are likely to be far more recent, and may well go back no further than the Ediacaran period (ca. 635-542 Mya) in most cases, which is much closer to Dr. Meyer’s timetable.
100 million years wrong would still quite a lot of wrong, actually. And once it's conceded that the protein folds came long before the Cambrian Explosion, then you've conceded that Meyer was wrong to raise Douglas Axe in the context of the Cambrian Explosion! Game over!
Dr. Meyer may have gotten his facts somewhat wrong on the antiquity of protein folds, but he was basically right on proteins – which is what my OP discussed.
Heh! You've argued in a circle! The whole friggin' point of Ohno's article on the pan-animalian genome was that the gene and protein complements are basically shared across bilaterians as well! There was, in fact, not a huge amount of origination of genes and proteins required to produce the Cambrian phyla, and we know this because they all have the same basic complement of genes and proteins. The differences that they have are basically due to differential duplication of genes and subsequent modification of genes, and sometimes rearrangement/recombination of pre-existing gene chunks. All of this is totally obvious from actually reading Ohno with any care -- but you and Meyer just can't seem to get it through your skulls, I think because have such a strong, unquestioned prior belief that the origin of morphological diversity just has to involve lots of new genes and new proteins. Ohno's point was that the main thing going on was just redeployment (different regulation) of preexisting genomes. This was Rasmussen's original point also! It's just stunning that you are still trying to resuscitate Meyer's dead horse on this point.NickMatzke_UD
December 28, 2015
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And more pap from Arthur Hunt:
Since CMS is known to occur in plants in nature, quite apart from any sort of breeding, this statement implies that, according to Virgil Cain, there was no recombination in the mitochondria of the wild relatives of maize.
Wrong again, Art. Recombination is a design feature of living organisms. Meaning organisms were designed to do so.
I would note that, by equating “random” with “non-scientific”,
Except I didn't do that. What are you, 5 years old? Even Dawkins said that science can only allow so much luck. Saying that generations of recombinations- ie random shuffling- produces new genes, is saying nothing more than sheer dumb luck produced the genes. What I said was: The fact is we have no idea if recombination is random or part of the design of organisms. And the fact is all you have to explain it is sheer dumb luck and the fact is positions that rely on sheer dumb luck are not scientific. As far as anyone knows this new gene was a result of human intervention and the reaction the organism had towards that. The organism engineered the new gene, Art.Virgil Cain
December 28, 2015
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Arthur Hunt:
Mung, do you mean this in a book-learning sense (we’ve known about gated ion channels for a long time) or an evolutionary sense (gated ion channels are ancient proteins)?
Both. They are essential for life as we know it.Mung
December 28, 2015
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Mung, do you mean this in a book-learning sense (we've known about gated ion channels for a long time) or an evolutionary sense (gated ion channels are ancient proteins)?Arthur Hunt
December 28, 2015
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Art, there's nothing new about gated ion channels.Mung
December 28, 2015
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I would note that, by equating "random" with "non-scientific", Virgil Cain is essentially tossing out many (most, all?) uses of formal statistical testing as tools in science (and engineering, for that matter).Arthur Hunt
December 28, 2015
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The fact is that trait would never have appeared if we had never messed with corn. Since CMS is known to occur in plants in nature, quite apart from any sort of breeding, this statement implies that, according to Virgil Cain, there was no recombination in the mitochondria of the wild relatives of maize. And that this capacity was restored by ancient Americans some thousands of years ago. Of course we know this is not correct.Arthur Hunt
December 28, 2015
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Arthur Hunt:
So, Virgil Cain, you continue to insist that plant breeders in the 50’s and 60’s knew, from first principles, that a gated ion channel would lead to the CMS trait.
Nonsense. The fact is that trait would never have appeared if we had never messed with corn.
That is, after all, the only alternative to the mechanism that was (and is) actually in play.
More nonsense. You think it was all sheer dumb luck. How, exactly, is that science?
The fact is, we know enough about the enzymes that catalyze homologous and non-homologous recombination to state in no uncertain terms that, as far as the CMS-T trait is concerned, the rearrangements involved were random, not guided towards the production of this specific gated ion channel.
The fact is we have no idea if recombination is random or part of the design of organisms. And the fact is all you have to explain it is sheer dumb luck and the fact is positions that rely on sheer dumb luck are not scientific. As far as anyone knows this new gene was a result of human intervention and the reaction the organism had towards that.Virgil Cain
December 28, 2015
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Mung, if Axe et al. are correct, then the chances that a breeder could hit this jackpot via random shuffling are so low as to completely preclude the generation of the trait. History says otherwise. Axe et al. may have nothing against shuffling as a biochemical occurrence, but they most definitely rule out this process as a way to new protein-coding genes. History tells us that they are wrong.Arthur Hunt
December 28, 2015
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So, Virgil Cain, you continue to insist that plant breeders in the 50's and 60's knew, from first principles, that a gated ion channel would lead to the CMS trait. That is, after all, the only alternative to the mechanism that was (and is) actually in play. How, pray tell, did breeders manage this impressive feat of logic, given that the relevant theory (the chemisomotic hypothesis) had yet to be formulated in the 50's and wasn't widely accepted until the late 70's? The fact is, we know enough about the enzymes that catalyze homologous and non-homologous recombination to state in no uncertain terms that, as far as the CMS-T trait is concerned, the rearrangements involved were random, not guided towards the production of this specific gated ion channel.Arthur Hunt
December 28, 2015
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Art, neither Axe nor Meyer have anything against random shuffling. If you shuffle a poker deck you get a card belong to one of 13 ranks and one of 4 suits. You don't get a community chest card from Monopoly.Mung
December 28, 2015
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Arthur Hunt- You have no idea if the shuffling is random or by design
You seem to be claiming that some plant breeders somewhere in the 1950s deliberately, using recombinant DNA methods, crafted the mitochondrial genome seen in CMS-T corn.
Nope. Try again.
The fact is that the trait was the result of random genome shuffling that created a gated ion channel from scratch.
That is your opinion and not a fact. The fact is corn is the result of many generations of human tinkering, including the cytoplasm. And because of that fact alone weird things happened.Virgil Cain
December 28, 2015
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Virgil Cain, the sorts of random shufflings and rearrangements that underlie the SCLB epidemic happen in nature all the time. And they yield similar phenotypic outcomes. You seem to be claiming that some plant breeders somewhere in the 1950s deliberately, using recombinant DNA methods, crafted the mitochondrial genome seen in CMS-T corn. That's just preposterous. The fact is that the trait was the result of random genome shuffling that created a gated ion channel from scratch. That's random shuffling, and Axe et al. claim that such processes cannot, regardless of the context in which the trait originated, produce something as complex as a multi subunit gated ion channel.Arthur Hunt
December 28, 2015
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vjtorley:
Dr. Meyer may have gotten his facts somewhat wrong on the antiquity of protein folds, but he was basically right on proteins...
I don't recall Meyer making any claim about the antiquity of proteins folds. I think he should at least be credited with understanding they are as old as the oldest prokaryote. The debate is over whether any new protein folds were needed for the Cambrian animals. The alternative is front-loading. :)Mung
December 28, 2015
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