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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
Arthur Hunt- Corn is the result of artificial selection. That means variations occurred that normally would not have. This has been pointed out to you before and you ignored it then too. Willful ignorance is not an argument.
T-cytoplasm was a man-made change in corn plants used to foster the quick and profitable production of high-yielding, hybrid corn seed.
from blight in the corn beltVirgil Cain
December 28, 2015
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Nick Matzke then: It’s true VJT doesn’t really address folds. Nick Matzke now: Wow, that’s a really long way of avoiding admitting error in your Opening Post, VJ Torley. The OP doesn't even deal with protein folds and Nick knows it.Mung
December 28, 2015
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vjtorley, you continue to rely on arguments made by Axe and Meyer that concern the supposed rarity of function in protein sequence space. If Axe and Meyer were correct, then the Southern corn leaf blight epidemic of 1969-1970 cannot have possibly occurred - the "math" of Axe and Meyer (and Behe) is pretty clear on this, SCLB is an impossibility if they are correct. Are you of the opinion that this epidemic is a fiction? If not, then why to you cling to an incorrect view of protein structure, function, and evolution, one that demands that you deny obvious historical facts such as this? Has the Agriculture Dept. of the Discovery Institute come up with a way to revise history when it comes to this series of events? I am curious as to your thought processes when it comes to this subject.Arthur Hunt
December 28, 2015
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Do IDer's know know about ancient genes?
These signaling pathways pre-date the animals that use them now. Based on genomic analyses, these signaling molecules have been around well before the first bilaterian animals ever existed. They are expressed in organisms that lack these body axes completely. Even more surprising, many of the molecules used to make complex structures such as muscles, eyes, and brains also predate their use for those purposes.
http://www.evolutionnews.org/2015/12/5_of_our_top_st101891.htmlMung
December 28, 2015
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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. 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. 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. 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." 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? 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. 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. And you still haven't refuted the arguments in Dr. Axe's paper, The Case Against a Darwinian Origin of Protein Folds, which Meyer cites repeatedly in Darwin's Doubt and Signature in the Cell.vjtorley
December 28, 2015
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Nick Matzke:
Meyer asserted the Cambrian explosion required many new protein folds. This is clearly false and has been disproven,
Except it hasn't been disproven as no one knows what is required to account for the diversity observed.Virgil Cain
December 28, 2015
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I would not be too quick to presuppose that no new protein folds were required for the Cambrian explosion: It has recently been found that unique ORFan proteins are a far bigger problem than Darwinists would have preferred to believe:
Unexpected features of the dark proteome – Oct. 2015 Excerpt: Nearly half of the dark proteome comprised dark proteins, in which the entire sequence lacked similarity to any known structure. Dark proteins fulfill a wide variety of functions,,, We deliberately chose this stringent definition of “darkness,” so we can be confident that the dark proteome has completely unknown structure.,,, ,,,in eukaryotes and viruses, about half (44–54%) of the proteome was dark (Fig. 1B). Of the total dark proteome, nearly half (34–52%) comprised dark proteins. We repeated the above analysis using an even more stringent definition for darkness—combining PMP (2) and Aquaria (SI Methods) — but this had little effect (Fig. S1).,,, Lower Evolutionary Reuse. For each protein, we calculated how frequently any part of its sequence has been reused across all other known proteins (SI Methods). Dark proteins were reused much less frequently than nondark proteins (Fig. 4 C and Fig. S8), suggesting that dark proteins may be newly evolved proteins or rare proteins adapted to specific functional niches. This result was partly expected, given how darkness was defined and given the progress of structural genomics in targeting large protein families with unknown structure (8). Low evolutionary reuse also partly explains why dark proteins have few known interactions (Fig. 4 B and Fig. S8), because many interactions are inferred by homology (33). http://www.pnas.org/content/early/2015/11/16/1508380112.full.pdf The Dark Proteome and Dark Evolution – Evolution Did It – Cornelius Hunter – Nov. 23, 2015 Excerpt: “Thus, our results suggest that many of the uncharacterized orphan sequences … are indeed real proteins.” http://darwins-god.blogspot.com/2015/11/the-dark-proteome-and-dark-evolution.html
Moreover, 'context dependency', where quantum information is shown to physically reside along the entire protein chain, greatly exasperates the search problem for unguided Darwinian processes.
Quantum criticality in a wide range of important biomolecules Excerpt: “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” they say. That’s a discovery that is as important as it is unexpected. “These findings suggest an entirely new and universal mechanism of conductance in biology very different from the one used in electrical circuits.” The permutations of possible energy levels of biomolecules is huge so the possibility of finding even one that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,, “what exactly is the advantage that criticality confers?” https://medium.com/the-physics-arxiv-blog/the-origin-of-life-and-the-hidden-role-of-quantum-criticality-ca4707924552 Proteins ‘ring like bells’ - June 2014 As far back as 1948, Erwin Schrödinger—the inventor of modern quantum mechanics—published the book “What is life?” In it, he suggested that quantum mechanics and coherent ringing might be at the basis of all biochemical reactions. At the time, this idea never found wide acceptance because it was generally assumed that vibrations in protein molecules would be too rapidly damped. Now, scientists at the University of Glasgow have proven he was on the right track after all. Using modern laser spectroscopy, the scientists have been able to measure the vibrational spectrum of the enzyme lysozyme, a protein that fights off bacteria. They discovered that this enzyme rings like a bell with a frequency of a few terahertz or a million-million hertz. Most remarkably, the ringing involves the entire protein, meaning the ringing motion could be responsible for the transfer of energy across proteins. The experiments show that the ringing motion lasts for only a picosecond or one millionth of a millionth of a second. Biochemical reactions take place on a picosecond timescale and,,, (are) optimised enzymes to ring for just the right amount of time. Any shorter, and biochemical reactions would become inefficient as energy is drained from the system too quickly. Any longer and the enzyme would simple oscillate forever: react, unreact, react, unreact, etc. The picosecond ringing time is just perfect for the most efficient reaction. These tiny motions enable proteins to morph quickly so they can readily bind with other molecules, a process that is necessary for life to perform critical biological functions like absorbing oxygen and repairing cells.,,, Klaas Wynne, Chair in Chemical Physics at the University of Glasgow said: “This research shows us that proteins have mechanical properties that are highly unexpected and geared towards maximising efficiency.” http://www.gla.ac.uk/news/headline_334344_en.html Proteins with cruise control provide new perspective: Excerpt: “A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order.” http://www.princeton.edu/main/news/archive/S22/60/95O56/ (A Reply To PZ Myers) Estimating the Probability of Functional Biological Proteins? Kirk Durston , Ph.D. Biophysics - 2012 Excerpt (Page 4): The Probabilities Get Worse This measure of functional information (for the RecA protein) is good as a first pass estimate, but the situation is actually far worse for an evolutionary search. In the method described above and as noted in our paper, each site in an amino acid protein sequence is assumed to be independent of all other sites in the sequence. In reality, we know that this is not the case. There are numerous sites in the sequence that are mutually interdependent, (i.e. context dependent), with other sites somewhere else in the sequence. A more recent paper shows how these interdependencies can be located within multiple sequence alignments.[6] These interdependencies greatly reduce the number of possible functional protein sequences by many orders of magnitude which, in turn, reduce the probabilities by many orders of magnitude as well. In other words, the numbers we obtained for RecA above are exceedingly generous; the actual situation is far worse for an evolutionary search. http://powertochange.com/wp-content/uploads/2012/11/Devious-Distortions-Durston-or-Myers_.pdf "Why Proteins Aren't Easily Recombined, Part 2" - Ann Gauger - May 2012 Excerpt: "So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required." http://www.biologicinstitute.org/post/23170843182/why-proteins-arent-easily-recombined-part-2 Explaining Innovation - Ann Gauger - January 20, 2015 Excerpt: Even though the two enzymes (Kbl2 and BioF2) we worked with look alike, the way they are put together is distinct. The particular amino acids that cause them each to fold into the same structure are unique in sequence and holistic in their interactions. Each requires high-level, top-down design. As we discuss in our recent paper: "It may be that our prior attempts to convert Kbl2 to perform the function of BioF2 failed not because we made the wrong alterations but rather because it is misguided even to think of this as an exercise in alteration. ... They use similar structures not because they are both adjusted versions of some older enzyme, but instead because the purposes they serve happen to call for similar structures. As we found in this work, it is not that Kbl has amino acid residues that are incompatible with the function of BioF2, but rather that Kbl2 is comprehensively suited to one function, while BioF2 is comprehensively suited to another." ,,, Kbl2 and BioF2 represent two distinct ideas or concepts requiring holistic design. http://www.evolutionnews.org/2015/01/the_goalposts_o092861.html
bornagain77
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Wow, that's a really long way of avoiding admitting error in your Opening Post, VJ Torley. 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. Start a new thread if you want to talk about new topics, and everyone can make up their own minds about whether to discuss those. PS: Your Google skills need work. 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.NickMatzke_UD
December 28, 2015
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vjtorley - There's evidence that Nick M. knew of Nick G. in June 2014.Bob O'H
December 28, 2015
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Hi Nick Matzke, I'm afraid I don't buy your excuse for mentioning protein folds just once in your review of Darwin's Doubt. You state that you were pressed for time. OK, but eight days later, when you responded to Casey Luskin's rebuttal of your review, you had much more time at your disposal. Why, then, does the word "protein" not appear even once in your reply to Luskin? And why doesn't the word "fold" appear either? Strange. I can only conclude that at the time when you penned your reviews, you didn't know enough about proteins or protein folds to rebut Dr. Meyer's argument concerning the rarity of functional proteins in protein space, and about the need for thousands of different kinds of protein folds in order to account for the diversity of animal life. However, you've done a bit of reading since then, and now you're trying to pretend that you've known all along that Meyer was wrong on this point. Am I right? "Oh yeah? Where's your evidence?" I hear you ask. Happy to oblige. I did a quick Google search on the terms "Nick Matzke" and "Grishin", and the earliest document I could find where your names were associated was comment of yours in an article you wrote on Panda's Thumb, titled, "Game over for antievolutionary No Free Lunch argument." The date of the comment: December 5, 2015. The article itself was written on December 4, 2015 - just a little over three weeks ago. As far as I can tell, that's your earliest mention of Grishin's work on proteins. I also searched on Google Scholar for anything containing both your names, but came up blank. Here's what you said in your comment on December 5, 2015:
Protein folds are the emergency backup-backup-backup argument after claims about specified complexity, “evolution can’t produce new information”, “evolution can’t produce new genes”, etc., have been debunked and tacitly abandoned. Most protein folds are very widespread (shared not just among animals but across eukaryotes and often prokaryotes also) so their origins must be very ancient – the argument that Meyer, Luskin etc. have been making lately, which is that a whole bunch of new protein folds had to originate in the Cambrian Explosion, is just ignorant crazypants. So the origin of protein folds will typically be rarer and more ancient than almost anything short of the origin of life itself, and thus harder to study. But all that said, there is nevertheless a lot that can be said. In fact, there are known cases where tiny amounts of mutation can convert one protein fold into another one. Look up: Nick Grishin. https://scholar.google.com.au/scholar?q=Nick+Grishin%2C+protein+folds&btnG=&hl=en&as_sdt=0%2C5 Michael Buratovich (2015). Leaving the Fold. “Darwin’s Doubt and the Evolution of Protein Folds.” Reports of the National Center for Science Education Vol 35, No 5 (2015) http://reports.ncse.com/index.php/rncse/article/view/379/751
I note that your first link takes us to a Google page with the search parameters "Nick Grishin, protein folds". That's rather sloppy, Nick. Your second link is much more substantive: it takes the reader to an article that actually addresses Dr. Axe's and Dr. Meyer's arguments. However, I was totally unimpressed with Buratovich's response to Axe's arguments on the rarity of functional proteins in protein space. First, he takes issue with Meyer's use of Axe's lower estimate of 1 in 10^77, saying that he neglected to mention an upper bound of 1 in 10^53. In fact, Meyer's book, Signature in the Cell, cites both upper and lower estimates, and argues that since the simplest living cells require about 250 different proteins, it doesn't make much practical difference we use: we still obtain a vanishingly low probability. I might add that Taylor et al. have acknowledged that "Even a library with the mass of the Earth itself — 5.98 × 10^27 g — would comprise at most 3.3 × 10^47 different sequences, or a miniscule (sic) fraction of such diversity." Second, Buratovich says that the numbers aren't that bad for proteins shorter than 150 amino acids, and there are plenty of those in Nature. True, but what he omits to mention is that all living things require at least some proteins which are 150 amino acids long. What's more, as Dr. Cornelius Hunter has previously pointed out, there are no good scientific grounds for thinking that life-forms based on shorter, simpler proteins could have existed in the beginning, giving rise to more advanced life-forms requiring larger, more complex ones later on. As he puts it: “The larger ones appear to be needed, and there are not obvious gradual pathways to forming them.” Third, Buratovich argues that the estimate refers only to the proportion of amino acids that will perform a specified function, and that it is not (his italics) the estimation of the (probability of the) evolution of a protein fold. That's just flat out false. He's mis-read Axe's argument: basically, he's accusing Axe (or Meyer) of committing Hoyle's fallacy. If it were that simple, Meyer and Axe would have been utterly discredited long ago. Fourth, Buratovich states that the proportion of amino acid sequences that are functional depends on the way you define functionality, and that if you define it in a more relaxed way, the true proportion is about 1 in 5x10^23. But the protein they used was a short one (95 amino acids). And as Dr. Cornelius Hunter wrote to me in a personal communication back in 2014:
Taylor, et. al. deals with a simple, helix only, protein (homodimeric AroQ), biased the sequence toward helix forming amino acids and sequence patterns, did not fully randomize the sequence but only randomized regions, and is vague about how they arrive at their 10^24 tries required. Even if their calculation of 10^24 is reasonable, you’re dealing with a pretty simple protein... AroQ is toward the simple end of the spectrum… And finally there are several studies on slightly more complex, challenging proteins, all of which come in at around 10^60 – 10^80 attempts required.”
I refuted most of Buratovich's silly arguments in section 11 of my June 2014 post, The dirty dozen: Twelve fallacies evolutionists make when arguing about the origin of life. I note that some of them reference articles dating back to 2001. That's ancient history. As for protein folds: I can't really comment here, except to say that: (i) even if all animals share the same set of protein folds, the question we need to answer in order to ascertain how old they are is whether closely related organisms (e.g. fungi) share them as well; (ii) even if it should turn out that these folds go back to the dawn of life, the point is that there are still thousands of them, and the question we need to answer is: how did unguided processes manage to locate these "needles in a haystack"? Until you can address those questions, Nick, you can't expect to be taken seriously.vjtorley
December 28, 2015
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The interesting thing about Darwinists claiming that genes/proteins can randomly 'poof' into existence is that no one can seem to catch this random 'poofing' in action. First off, it is hard to find anything that is truly 'random' in its action in the cell as is presupposed in Darwinian thought:
"It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns” James Shapiro - Evolution: A View From The 21st Century - (Page 82)
In fact, the genome is best viewed as a read/write memory instead of a read only memory as is viewed in Darwinian thought:
How life changes itself: the Read-Write (RW) genome. - 2013 Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences. http://www.ncbi.nlm.nih.gov/pubmed/23876611
Secondly, unguided material processes are far more likely to break something in the cell to gain a short term fitness advantage that they are ever likely to build up functional complexity/information for future use:
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
Moreover, in the four decades worth of lab work that Dr. Behe surveyed, there was not even any evidence of just one novel gene being created. Instead, all gain of function mutations, as far as I could tell, involved 'compensatory mutations' that compensated for a gene that was deleted. Thirdly, humans trying to intelligently design proteins that outperform what is already found in life fall far short of what is already found in life. To believe unguided material processes can out engineer our best molecular engineers of today is logically absurd to a very high degree.
Creating Life in the Lab: How New Discoveries in Synthetic Biology Make a Case for the Creator - Fazale Rana Excerpt of Review: ‘Another interesting section of Creating Life in the Lab is one on artificial enzymes. Biological enzymes catalyze chemical reactions, often increasing the spontaneous reaction rate by a billion times or more. Scientists have set out to produce artificial enzymes that catalyze chemical reactions not used in biological organisms. Comparing the structure of biological enzymes, scientists used super-computers to calculate the sequences of amino acids in their enzymes that might catalyze the reaction they were interested in. After testing dozens of candidates,, the best ones were chosen and subjected to “in vitro evolution,” which increased the reaction rate up to 200-fold. Despite all this “intelligent design,” the artificial enzymes were 10,000 to 1,000,000,000 times less efficient than their biological counterparts. Dr. Rana asks the question, “is it reasonable to think that undirected evolutionary processes routinely accomplished this task?” http://www.amazon.com/gp/product/0801072093
Dr. Fuz Rana, at the 41:30 minute mark of the following video, speaks on the tremendous effort that went into building the preceding protein:
Science - Fuz Rana - Unbelievable? Conference 2013 - video http://www.youtube.com/watch?v=-u34VJ8J5_c&list=PLS5E_VeVNzAstcmbIlygiEFir3tQtlWxx&index=8 Computer-designed proteins programmed to disarm variety of flu viruses - June 1, 2012 Excerpt: The research efforts, akin to docking a space station but on a molecular level, are made possible by computers that can describe the landscapes of forces involved on the submicroscopic scale.,, These maps were used to reprogram the design to achieve a more precise interaction between the inhibitor protein and the virus molecule. It also enabled the scientists, they said, "to leapfrog over bottlenecks" to improve the activity of the binder. http://phys.org/news/2012-06-computer-designed-proteins-variety-flu-viruses.html
Exactly how is it possible for unguided material processes, without intelligent foresight, to 'leapfrog over bottlenecks' to improve the activity of a binder?
“I build molecules for a living, I can’t begin to tell you how difficult that job is. I stand in awe of God because of what he has done through his creation. Only a rookie who knows nothing about science would say science takes away from faith. If you really study science, it will bring you closer to God." James Tour – one of the leading nano-tech engineers in the world - Strobel, Lee (2000), The Case For Faith, p. 111
Dr. James Tour, who, in my honest opinion, currently builds the most sophisticated man-made molecular machines in the world, will buy lunch for anyone who can explain to him exactly how Darwinian evolution works:
Does Science Make Faith Obsolete? James Tour - video - March 9, 2015 (talk given February 18, 2015 - 30:20 minute mark - he publicly asks Darwinists to explain macro-evolution to him) https://www.youtube.com/watch?feature=player_detailpage&v=CB3ZmLatcUI#t=1827
After commenting on the failure of ANY atheist to ever respond to his request for lunch for 8 or 10 years in order to explain macro-evolution to him, Dr Tour comments:
“One graduate student from Berkeley, (i.e. Matzke), said that he would come if he had a ticket so somebody said “I’ll buy you the ticket”, but then he said, “Well, I’m not going to go because Tour doesn’t want it recorded.” The reason I didn’t want it recorded is because I did not want one-ups-man-ship. I said ‘I’ll buy you lunch, just explain it to me’. And then the guy said he would send me some articles on evolution of a complex system from a molecular perspective and I am still waiting. That’s over one year ago he was suppose to send them to me. They don’t exist.” – James Tour – 35:22 minute mark of the video https://youtu.be/CB3ZmLatcUI?t=2122
I guess that Dr. Matzke thought it wise not to try his usual literature bluff on a leading nano-tech engineer in the world. Given Dr. Tour's prestige and expertise, it is one literature bluff that certainly could have backfired on Matzke big time
A short history of Matzke's literature bluffing – Nov. 2015 https://uncommondescent.com/intelligent-design/darwins-view-of-the-fossil-record/#comment-589458
bornagain77
December 27, 2015
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Nice litrature bluffing again. As soon as you give us in the lab evidence that new genes just poof into existence be sure to drop by and deliver the news. Until then you may huff and puff all you like. I believe Dembski as much as stated that new protein-coding genes can poof into existence. IIRC, check out pp.218–219 of No Free Lunch. Want to (re)discover one on your own? The route taken to identify the so-called ecf mutant in E. coli in the 1970's is pretty intriguing and suggestive. And the phenotype is quite in line with the gene he talks about in NFL. Maybe some enterprising IDer can see if the Discovery Institute would pay for, say, a couple of months of lab work and sequencing.Arthur Hunt
December 27, 2015
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Nick Matzke:
If you fight through Berlinski’s pointlessly purple prose, you end up realizing that Berlinski concedes that, yes, natural evolutionary processes *can* produce new genes with new functions.
That is your interpretation. However there isn't any evidence for such a thing.Virgil Cain
December 27, 2015
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The earliest animals were extremely simple, with only a handful of different kinds of cells, assembled by relatively few developmental genes. By the end of the Cambrian explosion, their descendants had evolved many different types of cells and used a complicated network of interacting genes to build their bodies. - Carl Zimmer. Evolution p. 128Mung
December 27, 2015
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Without those new Cambrian genes, we might still be like the lancelets, our tiny brainless heads still swaying in the tides. - Carl Zimmer. Evolution p. 126 Don't know why Nick made me think of that.Mung
December 27, 2015
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The living world as we know it would not exist without features that are put in place to allow future events to come to fruition. for example birds build nests to house the eggs which are yet to be laid. The genome of an animal contains the information to build the tissues of the adult form well before differentiation takes place. So if the protein folds necessary to construct the diversity of forms known to have appeared during the Cambrian explosion were in place before that event occurred then that would be consistent with the preparative nature of unfolding life. Growth and expansion precede differentiation and diversity of form. Life had prepared for the sudden appearance of the Cambrian forms just as the organs of an individual animal were prepared in the blastula.CharlieM
December 27, 2015
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Nick Nice litrature bluffing again. As soon as you give us in the lab evidence that new genes just poof into existence be sure to drop by and deliver the news. Until then you may huff and puff all you like. For those wondering what Nick is all excited about his "proof" is good old designed programs doing directed simulations and is in no way an indication that undirected evolution is responsible because Nick, tbe upstanding and honest person that he is, won't tell you that it does not fit in with his agenda of being a book burner.Andre
December 27, 2015
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66 vjtorleyDecember 27, 2015 at 9:35 am Hi everyone, May I note for the record that protein folds are mentioned in only a single sentence of Nick Matzke’s review of Dr. Meyer’s book, Darwin’s Doubt. The relevant sentence reads: “The basic protein domains mostly originated very far back in evolutionary history, where things like ultrahigh population sizes help out, as well as the fact that there are probably a fairly limited number of protein domains, and the fact that point mutations and rearrangements can, on occasion, produce new or modified protein folds, in some cases without having much effect on enzymatic activity.” However, no references are given to support this claim – the very failure that Mikkel “Rumraket” Rasmussen upbraids Dr. Meyer for.
Well, I was writing an off-the-cuff blogpost in a limited amount of time, Meyer and allies were claiming that Meyer's book deserved attention as a revolutionary new scientific work that was overthrowing a good chunk of modern mainstream biology. But, since you asked, I was referring to the work of people like Nick Grishin:
Evolution of protein structures and functions LN Kinch, NV Grishin - Current opinion in structural biology, 2002 Within the ever-expanding repertoire of known protein sequences and structures, many examples of evolving three-dimensional structures are emerging that illustrate the plasticity and robustness of protein folds. The mechanisms by which protein folds change often include the fusion of duplicated domains, followed by divergence through mutation. Such changes reflect both the stability of protein folds and the requirements of protein function.
Fold change in evolution of protein structures NV Grishin - Journal of structural biology, 2001 Typically, protein spatial structures are more conserved in evolution than amino acid sequences. However, the recent explosion of sequence and structure information accompanied by the development of powerful computational methods led to the accumulation of examples of homologous proteins with globally distinct structures. Significant sequence conservation, local structural resemblance, and functional similarity strongly indicate evolutionary relationships between these proteins despite pronounced structural differences at the fold level. Several mechanisms such as insertions/deletions/substitutions, circular permutations, and rearrangements in ?-sheet topologies account for the majority of detected structural irregularities. The existence of evolutionarily related proteins that possess different folds brings new challenges to the homology modeling techniques and the structure classification strategies and offers new opportunities for protein design in experimental studies.
Discrete–continuous duality of protein structure space RI Sadreyev, BH Kim, NV Grishin - Current opinion in structural biology, 2009 Recently, the nature of protein structure space has been widely discussed in the literature. The traditional discrete view of protein universe as a set of separate folds has been criticized in the light of growing evidence that almost any arrangement of secondary structures is possible and the whole protein space can be traversed through a path of similar structures. Here we argue that the discrete and continuous descriptions are not mutually exclusive, but complementary: the space is largely discrete in evolutionary sense, but continuous geometrically when purely structural similarities are quantified. Evolutionary connections are mainly confined to separate structural prototypes corresponding to folds as islands of structural stability, with few remaining traceable links between the islands. However, for a geometric similarity measure, it is usually possible to find a reasonable cutoff that yields paths connecting any two structures through intermediates.
What? Reading Meyer and Axe didn't inform you of any of this? I saw Nick Grishin speak at SMBE 2014: https://twitter.com/NickJMatzke/status/476357446160502784 My main impression from seeing his more recent work is that the evolution of protein fold change is a whole subfield with more people involved than there are active ID authors. Yet you could read the ID literature and never even know this existed.
By the way, David Berlinski and Tyler Hampton have written a devastating reply to Matzke’s review of Dr. Meyer’s book. The reply is titled, Hopeless Matzke.
Heh. That review is ridiculous. If you fight through Berlinski's pointlessly purple prose, you end up realizing that Berlinski concedes that, yes, natural evolutionary processes *can* produce new genes with new functions. This undermines Meyer's fundamental argument that only intelligence can produce new information, as well as shooting down a whole more specific section of Meyer's book where Meyer claims that the extensive evolutionary literature on the origin of new genes is all doubtful.NickMatzke_UD
December 27, 2015
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Note that Meyer himself admits that in some cases, new proteins can perform a new function “with essentially the same fold or tertiary structure as earlier proteins.” What he contends is that it’s more common, however, for proteins capable of performing new functions to require new folds to perform these functions. All you’ve said, in response to Meyer, is that “[y]ou can have many different kinds of proteins that all draw from the same folds.” That in no way invalidates Meyer’s point. If you think Dr. Meyer’s claim is factually mistaken, then where’s your documentation to back it up?
I can't believe you haven't gotten it yet. It's very simple. We have genomes from many bilaterian phyla. We can look at what genes/proteins they have, and what protein folds they have. And as far as we can tell, they all have basically the same collection of protein folds (and, mostly, the same genes/proteins too, although there are many duplications and rearrangements, so it depends what you mean here). Therefore, whatever new functions, new developmental biology, new "information", etc., that originated with the Cambrian Explosion phyla, did not actually require lots of new protein folds. Because they don't actually have lots of new protein folds. This is known to every serious student of the question, but apparently not to Meyer and his followers. That, or it's ignored because they desperately want to somehow make Axe relevant to the Cambrian Explosion.NickMatzke_UD
December 27, 2015
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Nick, Your "review" came out 24 hours after the book was published. When are you going to admit that it is impossible to read a book and write a 9,000 word review of the book in 24 hours? What really happened Nick (he asked as if he did not already know the answer)?Barry Arrington
December 27, 2015
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@vjt, FWIW I had the same thought this morning. Matzke also gave short shrift (one sentence) to developmental biology in his review. Alas, when you're acting like a second grader and jockeying to be first in line (in this case the first to "review" Darwin's Doubt) shortcuts are taken and details are overlooked.RexTugwell
December 27, 2015
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Hi everyone, May I note for the record that protein folds are mentioned in only a single sentence of Nick Matzke's review of Dr. Meyer's book, Darwin's Doubt. The relevant sentence reads: "The basic protein domains mostly originated very far back in evolutionary history, where things like ultrahigh population sizes help out, as well as the fact that there are probably a fairly limited number of protein domains, and the fact that point mutations and rearrangements can, on occasion, produce new or modified protein folds, in some cases without having much effect on enzymatic activity." However, no references are given to support this claim - the very failure that Mikkel "Rumraket" Rasmussen upbraids Dr. Meyer for. By the way, David Berlinski and Tyler Hampton have written a devastating reply to Matzke's review of Dr. Meyer's book. The reply is titled, Hopeless Matzke.vjtorley
December 27, 2015
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Nick Matzke:
Rasmussen/Rumraket says Meyer’s scholarship is shoddy because of Meyer’s uninformed claims about lots of protein folds having to originate in the Cambrian Explosion.
No one knows what was required, Nick. Meyer could be right and no one can show that he is wrong. And there isn't any known mechanism to account for the diversity observed. You lose.Virgil Cain
December 27, 2015
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To all: The following paper, kindly linked by Dionisio in another thread, is probably of some relevance for the discussion here: Regulation of alternative splicing in Drosophila by 56 RNA binding proteins http://genome.cshlp.org/content/25/11/1771.full.pdf
Abstract: Alternative splicing is regulated by RNA binding proteins (RBPs) that recognize pre-mRNA sequence elements and activate or repress adjacent exons. Here, we used RNA interference and RNA-seq to identify splicing events regulated by 56 Drosophila proteins, some previously unknown to regulate splicing. Nearly all proteins affected alternative first exons, suggesting that RBPs play important roles in first exon choice. Half of the splicing events were regulated by multiple proteins, demonstrating extensive combinatorial regulation. We observed that SR and hnRNP proteins tend to act coordinately with each other, not antagonistically. We also identified a cross-regulatory network where splicing regulators affected the splicing of pre-mRNAs encoding other splicing regulators. This large-scale study substantially enhances our understanding of recent models of splicing regulation and provides a resource of thousands of exons that are regulated by 56 diverse RBPs.
gpuccio
December 27, 2015
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Evolution is a fascinating thing indeed. All sorts of things can evolve. For instance, something very fascinating evolved, something involving text, something that eventually showed up within the Bible. I can't explain exactly how this evolved. A crystal clear repetitive and logical pattern appears over and over within the Bible. But, since it is of no immediate financial benefit to anyone, nor any other immediate benefit that I can think of, it therefore is of no interest. If insane, meaning if you are interested in the non-interesting, go to http://goo.gl/38qhp and click on the flashing words "Watch/Listen".YouThinkSo
December 27, 2015
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Meyer's argument regarding protein folds depends on the work of Douglas Axe. There can be no doubt about this upon any fair reading of chapter 10 of Darwins Doubt. Further, it has been extensively documented at TSZ that the time scale involved is the entire history of life. Again, there can be no doubt about this upon any fair reading of chapter 10 of Darwins Doubt. It was also explained over at TSZ that the claim that there wasn't enough time in the Cambrian is merely a corollary of the overall conclusion of the argument. Nick is probably unaware of any of this.Mung
December 26, 2015
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Hi Nick Matzke, Thank you for your posts. It's perfectly consistent for Dr. Meyer to argue that (a) judging from the fossil evidence, the Cambrian explosion appears to have happened very quickly, over a few million years, but that (b) even if the underlying events at the biochemical level and the genetic level occurred more slowly, over a few billion years, there still wouldn't be enough time available. You take issue with Meyer's statement:
“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.”
Note that Meyer himself admits that in some cases, new proteins can perform a new function "with essentially the same fold or tertiary structure as earlier proteins." What he contends is that it's more common, however, for proteins capable of performing new functions to require new folds to perform these functions. All you've said, in response to Meyer, is that "[y]ou can have many different kinds of proteins that all draw from the same folds." That in no way invalidates Meyer's point. If you think Dr. Meyer's claim is factually mistaken, then where's your documentation to back it up?vjtorley
December 26, 2015
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RexT: One thing is for certain: Meyer, ID and UD are being dismissed. Yes true, thanks to the idea that stupid nature could accidentally come up with a spectacular work of art, a stunning symphony, or the invention of mathematics. Cuz see, stupid nature has this principle it must live by called survival, which requires spectacular works of art, stunning symphonies, and the invention and application of say, the Jacobian determinant. Plain as day, can't everybody see it? Except we're left with where did the principle of survival get invented, maybe stupid nature itself did so which would mean that the principle itself would have to be stupid, and therefore not have any way of motivating itself to attain the hegemony required of itself in order to write a beautiful symphony sometime to maintain itself i.e. survive, and then prove it isn't stupid after all. But rather, possibly intelligent.groovamos
December 26, 2015
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Most animals, including us, use a standard tool kit of body-building genes. It contains tools for marking off the coordinates of an animals body - front and back, left and right, head and tail. It also contains a set of genes that control the development of entire organs such as eyes and limbs. The tool kit is remarkably unchanged from one species to another... Judging from the fossil record, this tool kit must have gradually evolved in the millions of years that preceded that Cambrian explosion. – Carl Zimmer. Evolution.
I just love the "toolkit" and "tools for" language. Warms the heart of a designer. Must have evolved in the millions of years before the Cambrian? Why? What are some of the remarkable features of this "toolkit" that existed before the animals in the Cambrian came along? Nick? Anyone?Mung
December 26, 2015
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Of all the differences between ourselves and our amoeba-like ancestors a billion years ago, one is paramount: we have bodies. Instead of a single cell, we are made of trillions. This vast collection isn't just a bag of identical copies, but a menagerie of dozens of types of cells, organized into hundreds of body parts [some are organs] from spleens to eyelashes to skeletons to brains. And most remarkable of all, each of our bodies is built out of a single original cell. As that cell multiplies into an embryo, genes begin producing proteins that control its development. - Carl Zimmer. Evolution. It is absolutely mind-boggling to think that what everyone ought to know is held against Meyer because he failed to cite all his sources for all his claims. Oh, wait. It's not about that!Mung
December 26, 2015
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