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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
Nick:
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.
If true, so what?. Why is this evidence for Darwinian evolution and not for Design evolution? Besides, 10 million years is not nearly enough to go from preCambrian to Cambrian via random incremental evolutionary steps. No amount of time is ever enough. Why? Simply because the combinatorial explosion kills ANY stochastic search mechanism dead. Read and weep, troll.Mapou
December 26, 2015
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gpuccio:
But again, Meyer’s statements about new protein folds in metazoa are simply true and obvious.
Meyer claims that new cell type and organs appeared and that new genes and proteins appeared do, to me at least, not seem to require that he cite his sources. They seem to me obvious. But if you're going to be an anti-ID skeptic you may as well go whole hog and blame Meyer for poor scholarship because he doesn't provide a source for everything he says. Whether new protein folds were required though, seems less obvious. And even if we could show that new protein folds also appeared, wouldn't phylogenetic analysis push them way back in time so that a committed anti-Meyer skeptic could claim they were already there, in advance? The last refuge of the anti-ID skeptic, it was already there, in the beginning. The irony. :) Thanks gpuccio!Mung
December 26, 2015
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Nick comes stops by and tries to smear Meyer and VJT. Is he reduced to trolling these days? And for what it's worth, Nick, if you're still watching, I think this piece at ENV was in very poor taste and I hope West will issue an apology.Mung
December 26, 2015
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I heard that the Bilateria appeared before the Porifera. Is that true Nick?Mung
December 26, 2015
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Nick,
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
It appears that you are admitting there are no actual bilaterian fossils in the precambrian layers; instead, you are inferring they nevertheless existed based on certain "trackways and burrows." Is that what you are saying Nick? If not, you need to clear it up, because it certainly appears that is what you are saying. If yes, *palm-forehead* you people are getting desperate. I will give you some time to clear this up before I make an OP of it.Barry Arrington
December 26, 2015
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Nick Matzke -- biology's Baghdad Bob.Florabama
December 26, 2015
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Actually 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, it is not as if Darwinists have ever demonstrated the origin of a new protein by unguided Darwinian processes and that they therefore have a plausible mechanism in place for explaining the origin of new proteins. The last four decades worth of lab work are surveyed here, and no evidence for Darwinian evolution creating new proteins surfaces. In fact it is found that unguided material processes excel at breaking things rather than creating anything new:
“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/
More from Behe
Michael Behe - Observed (1 in 10^20) Edge of Evolution - video - Lecture delivered in April 2015 at Colorado School of Mines 25:56 minute quote - "This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not." https://www.youtube.com/watch?v=9svV8wNUqvA Kenneth Miller Steps on Darwin's Achilles Heel - Michael Behe - January 17, 2015 Excerpt: Enter Achilles and his heel. It turns out that the odds are much better for atovaquone resistance because only one particular malaria mutation is required for resistance. The odds are astronomical for chloroquine because a minimum of two particular malaria mutations are required for resistance. Just one mutation won't do it. For Darwinism, that is the troublesome significance of Summers et al.: "The findings presented here reveal that the minimum requirement for (low) CQ transport activity ... is two mutations." Darwinism is hounded relentlessly by an unshakeable limitation: if it has to skip even a single tiny step -- that is, if an evolutionary pathway includes a deleterious or even neutral mutation -- then the probability of finding the pathway by random mutation decreases exponentially. If even a few more unselected mutations are needed, the likelihood rapidly fades away.,,, So what should we conclude from all this? Miller grants for purposes of discussion that the likelihood of developing a new protein binding site is 1 in 10^20. Now, suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. In that case the odds would be the multiple of the two separate events -- about 1 in 10^40, which is somewhat more than the number of cells that have existed on earth in the history of life. That seems like a reasonable place to set the likely limit to Darwinism, to draw the edge of evolution. http://www.evolutionnews.org/2015/01/kenneth_miller_1092771.html
As Behe touched upon, the numbers coming out for the evolution of novel proteins by unguided processes are prohibitive:
The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway - Ann K. Gauger and Douglas D. Axe - April 2011 Excerpt: We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions. But evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2011.1/BIO-C.2011.1 "Biologist Douglas Axe on Evolution's (non) Ability to Produce New (Protein) Functions " - video Quote: It turns out once you get above the number six [changes] -- and even at lower numbers actually -- but once you get above the number six you can pretty decisively rule out an evolutionary transition because it would take far more time than there is on planet Earth and larger populations than there are on planet Earth. https://www.youtube.com/watch?v=8ZiLsXO-dYo "Enzyme Families -- Shared Evolutionary History or Shared Design?" - Ann Gauger - December 4, 2014 Excerpt: If enzymes can't be recruited to genuinely new functions by unguided means, no matter how similar they are, the evolutionary story is false.,,, Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. We have now addressed two objections raised by our critics: that we didn't test the right mutation(s), and that we didn't use the right starting point. We tested all possible single base changes in nine different enzymes, Those nine enzymes are the most structurally similar of BioF's entire family We also tested 70 percent of double mutations in the two closest enzymes of those nine. Finally, some have said we should have used the ancestral enzyme as our starting point, because they believe modern enzymes are somehow different from ancient ones. Why do they think that? It's because modern enzymes can't be coopted to anything except trivial changes in function. In other words, they don't evolve! That is precisely the point we are making. http://www.evolutionnews.org/2014/12/a_new_paper_fro091701.html "Shared Evolutionary History or Shared Design?" - Ann Gauger - January 1, 2015 Excerpt: The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. per ENV
bornagain77
December 26, 2015
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All great stuff. Keep in mind, though, that in these times, fact and evidence matter very little compared to narrative and spin. Matzke can say anything he likes, as long as the narrative an spn put off the day of reckoning for those he speaks for. In fact, if science were simply to devolve into finding support for naturalism, that day would never come. Science would decline but not everyone would be wore off for that.News
December 26, 2015
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Thank you for the link, Barry. A truly fascinating look into the mind of a committed Darwinist with a zero-concession policy. Matzke snivels
...are exactly why biologists are so dismissive of Meyer, ID, and UD
Right. And yet here you are Nick, continuing to haunt the pages of UD year after year. Do you spend as much time at websites advocating geocentrism? Remember this?
It's over for the Discovery Institute. Turn out the lights. The fat lady has sung. The emperor of ID has no clothes. The bluff is over. Oh sure, they'll continue to pump out the blather. They'll find more funding, at least for a while, from some committed ideologue or another. But no one with any objectivity will take them seriously any longer as scientists.
RexTugwell
December 26, 2015
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Of course new folds, superfamilies and families of proteins appear in metazoa. Just look at this paper: http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0008378&representation=PDF Table 1 attributes 58 new domains and 557 new domain combinations at the root of metazoa. OK, it's not exactly as much as the 1984 domains and 4631 domain combinations at the root of cellular organisms, but we certainly know that OOL is a much bigger problem for darwinists than the origin of metazoa in terms of origin of protein coding sequences. That's probably why Meyer dedicated his previous book to OOL, and dealed with the Cambrian explosion after that. But the important points are: a) Metazoa certainly require new protein folds, protein superfamilies and proteins families, and new combinations too, in a rather abundant neasure. It is really silly to try to deny that. b) The origin of metazoa certainly requires a lot more of new epigenetic information. Unless darwinists still want to believe that cell differentiation is just a lucky way of using what already is there, in spite of all that epigenetics is discovering, then certainly the evolution from metazoa on is mainly an evolution of epigenetic procedures. It is true that the bulk of protein sequences and folds appears at OOL. Many of the most important acquisitions in that realm are already present in LUCA. The second main jump is certainly the appearance of eukaryotes (492 new domains, 6056 new domain combinations, according to that paper). And the third big jump is the appearance of metazoa. In terms of protein sequences. On the contrary, there are very good reasons to believe, even with our still rudimentary understanding of epigenetics, that the acquisition of new epigenetic information follows an opposite trend: some of it is already in prokaryotes, but a lot of it appears in eukaryotes, and the biggest jump of all takes place with the appearance of metazoa. IOWs, the desing of life works at the beginning prevalently on the gross structure of the final effectors (proteins), while gradually it shifts to much more complex control networks (epigenetics). But again, Meyer's statements about new protein folds in metazoa are simply true and obvious.gpuccio
December 26, 2015
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In contrast to Matzke's "there's nothing new here folks, move along." Creatures of Accident: The Rise of the Animal Kingdom Yes, there really are differences between a sponge and a jellyfish. Maybe Nick believes in front-loading. :)Mung
December 25, 2015
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Rex @ 9:
Did Nick really make such a ridiculous claim?
Indeed he did Rex. See comment 13 (and the comments leading up to it for context) of this post. Barry Arrington
December 25, 2015
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Matzke: New “genes” and “new proteins” are not the same thing as “new protein folds”. Until you can empirically demonstrate through multiple scientific test results, repeatedly, and with independent verification that the alleged mechanisms of evolution can produce the molecular machinery required to produce any old functioning protein with contextual relevance of what a so called primitive alleged precursor organism has need of, your argument regarding "New “genes” and “new proteins” are not the same thing as “new protein folds”.... is MEANINGLESS within this context. It is UNBELIEVABLE someone with this perspective can actually get some sort of academic degree under the guise of "science". And actually be employed by a publicly funded institution to represent some sort of "scientific" endeavor. And not understand the lack of true SCIENCE in their public proclamations that are mere philosophical conjecture.bpragmatic
December 25, 2015
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CLAVDIVS @13, Anytime one must create a new useful protein, one is faced with a combinatorial explosion that kills any stochastic search. The search space is so huge, it might as well be called "infinite". PS. It's all extremely simple math, the kind that Darwinists seem to have a lot of trouble grasping.Mapou
December 25, 2015
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Mapou - What do you mean by 'combinatorial explosion' in this context?CLAVDIVS
December 25, 2015
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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.
Whatever you say Nick. There's a very nice figure in the Erwin/Valentine book. Figure 9.2 on page 299.Mung
December 25, 2015
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Mung: Meyer clearly understands the difference and VJT doesn’t even address protein folds. Nick Matzke: It’s true VJT doesn’t really address folds LoL. Dood. I know. That's what I said.
...but that’s just more evidence that VJT’s “rebuttal” is totally incomprehending of Rasmussen’s critique of Meyer.
Move the goalposts. Fine, Nick.Mung
December 25, 2015
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Nick:
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.
And yet, one does not need to be a biologist to understand that the combinatorial explosion kills ANY stochastic search mechanism dead. This means RM+NS and the whole abiogenesis nonsense. So they give PhDs in biology for flipping burgers, now? You people are both mentally and morally challenged.Mapou
December 25, 2015
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it is not as silly as when you said that 500 coins on a table all heads would “not really” warrant a design inference. Nick, you still hold the record for the single stupidest thing ever said on UD.
Did Nick really make such a ridiculous claim? That explains everything. Hey Nick, how's your review of Denton's book coming along?RexTugwell
December 25, 2015
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Oh please. This is just silly. Actually, it’s just false. Meyer clearly understands the difference and VJT doesn’t even address protein folds.
Dood! Read the opening post. Search on the word "fold". VJ Torley quotes Rasmussen. Rasmussun is talking about folds. In the part that Torley quotes. It's true VJT doesn't really address folds, but that's just more evidence that VJT's "rebuttal" is totally incomprehending of Rasmussen's critique of Meyer. VJT couldn't find anything in Meyer addressing the hole that Rasmussen points out, so he ignorantly quoted a bunch of irrelevant stuff, because I guess Quoting Big Words N Stuff constitutes a rebuttal in his book. All the other irrelevanices in this thread are even more supporting evidence that ID guys just don't know what they are talking about.NickMatzke_UD
December 25, 2015
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Starting at this link people can read quotes from the Erwin and Valentine book The Cambrian Explosion: The Construction of Animal Biodiversity. Nick's probably not read it. Starting at this link people can read quotes from the T. Ryan Gregory edited book The Evolution of the Genome Nick's probably not read that one either.Mung
December 25, 2015
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Nick Matzke:
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.
All these things Ohno misses and fails to mention, somehow ID advocates take this stuff that was never written and turn it into gospel truth. That's hilarious. Really.Mung
December 25, 2015
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NickMatzke
VJ Torley, your post is silly in several ways.
But you will have to admit it is not as silly as when you said that 500 coins on a table all heads would "not really" warrant a design inference. Nick, you still hold the record for the single stupidest thing ever said on UD. I suspect your record is like DiMaggio's consecutive games with a hit record -- theoretically breakable but not practically.Barry Arrington
December 25, 2015
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The notion of the Cambrian pananimalia genome. People can see for themselves whether what Nick says can be found in the paper.Mung
December 25, 2015
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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.
Oh please. This is just silly. Actually, it's just false. Meyer clearly understands the difference and VJT doesn't even address protein folds.Mung
December 25, 2015
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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." So if someone chips rocks to make a spearhead, and then someone else uses the minerals in the rock to build a skyscraper or a computer, there has been no information explosion. You're kidding, right?anthropic
December 25, 2015
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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. 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. (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. 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? 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. 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.NickMatzke_UD
December 25, 2015
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