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Mike Behe: A Blind Man Carrying a Legless Man Can Safely Cross the Street

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(11 January 2012) Here

The work of Finnegan et al (2012) strikes me as quite thorough and elegant. I have no reason to doubt that events could have unfolded that way. However, the implications of the work for unguided evolution appear very different to me then they’ve been spun in media reports. ( http://tinyurl.com/7lawgpl ) The most glaringly obvious point is that, like the results of Lenski’s work, this is evolution by degradation. All of the functional parts of the system were already in place before random mutation began to degrade them. Thus it is of no help to Darwinists, who require a mechanism that will construct new, functional systems. What’s more, unlike Lenski’s results, the mutated system of Thornton and colleagues is not even advantageous; it is neutral, according to the authors. Perhaps sensing the disappointment for Darwinism in the results, the title of the paper and news reports emphasize that the “complexity” of the system has increased. But increased complexity by itself is no help to life — rather, life requires functional complexity. One can say, if one wishes, that a congenitally blind man teaming up with a congenitally legless man to safely move around the environment is an increase in “complexity” over a sighted, ambulatory person. But it certainly is no improvement, nor does it give the slightest clue how vision and locomotion arose.

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Comments
"All DNA does is code" That is a lot. The problem is there is no adequate naturalistic explanation of code emergence without agency. Physicality is informationally inert, on massive observation.Eugene S
January 14, 2012
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The discussion of whether amino acid sequence similarity can be explained by convergent evolution is interesting but besides the point. Behe was quite willing to accept the Thornton group's (non-convergent) evolutionary explanation for the different variety of V-ATPase. The question is whether this exposes a weakness in Behe's view that the origin of irreducibly complex systems poses a significant challenge to non-intelligently guided evolution. I think Behe is correct in maintaining that it doesn't expose a weakness in his view. What Thornton's group has succeeded in doing is showing how an IC system can become more complex. It does not succeed in showing how an IC system came into existence. Let's suppose that only the fungi variety of the V-ATPase existed, and Thornton's group was able to discover that it arose from a simpler form of V-ATPase. But this simpler form is itself IC. Would they have weakened Behe's case? Certainly not very significantly. For they still haven't shown how the simpler IC system came to be. So I find Thornton group's work to be very interesting, but not very enlightening to the ID debate.Bilbo I
January 14, 2012
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But you don't say why those positions would be better explained by convergence, what is the signature, why isn't copying an inferior explanation?Starbuck
January 13, 2012
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But I bet you don’t actually mean convergence. Convergence of significant sequence similarity like that seen within the rod would be so improbable that it would likely indicate either ancestry or special creation, and it’s the latter that you’re really advocating isn’t it? There is such a thing as adaptive convergence, but what is your evidence for that with regard to the rod?
But I do mean convergence at the molecular level, and more precisely adaptive convergence, whereby this sequence similarity is the result of similar functional constraints on the amino acid sequences of these proteins. Thus, natural selection is in the equation so it's not all that improbable. There are some clues for this view, too. For starters, while the FlgK in Salmonella is closer in sequence identity to Salmonella FlgE than to Buchnera FlgE, FlgK still shares about 37 residues that are identical in Buchnera FlgE, but are not identical in Salmonella FlgE, even though, on the whole, FlgK of Salmonella is closer to Salmonella FlgE. Given that there are 74 identical positions when we align FlgK and Buchnera FlgE, this means that 50% of these positions could possibly be the result of convergent evolution. Admittedly, this could be explained away by rapid sequence divergence on the part of Salmonella FlgE, but this is just a bit ad hoc. I suspect that those "convergent" positions are the result of adaptive evolution, rather than simply being neutral, and this can be tested using some cool techniques.
It seems to me that the only reason why you reject gene duplication as an explanation for the rod is that you want Genesis 1 to be literally true.
O.O Dear me. The topic changes from biology to religion. And guess what? It's not I who is changing the topic to religion. It might interest you to know that I'm not even claiming to be a theist - I may very well be an atheist, an agnostic, or a theist - I'm not saying. But, for the record, no, I don't accept Genesis as true. So, please, please stop assuming things, okay?Genomicus
January 13, 2012
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But I bet you don't actually mean convergence. Convergence of significant sequence similarity like that seen within the rod would be so improbable that it would likely indicate either ancestry or special creation, and it's the latter that you're really advocating isn't it? There is such a thing as adaptive convergence, but what is your evidence for that with regard to the rod? It seems to me that the only reason why you reject gene duplication as an explanation for the rod is that you want Genesis 1 to be literally true.Starbuck
January 13, 2012
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Starbucks: I am well aware that BLASTing these flagellar rod proteins will result in hits with each other. That's why I said that the E-values are in fact significant with these sequences. The point really isn't if good sequence similarity can be established for these proteins; rather, the question is if this sequence similarity is the result of gene duplication of convergent evolution at the molecular level.Genomicus
January 13, 2012
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No problemoStarbuck
January 13, 2012
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Sorry Starbuck, my bad! completely wrong topic,,,,,, should have read more carefully before I posted.bornagain77
January 13, 2012
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"the authors found significant cases of molecular convergence in 13 mitochondrially-encoded proteins of lizards and snakes." The key phrase here is "across 13 proteins". They found about 100 convergent sites across 13 proteins. Which is a handful per protein, which is what I said was typical for reported cases. Proteins are typically 100-500+ amino acids. (And, those proteins are a small subset of the ~20,000 proteins in these reptile genomes.)NickMatzke_UD
January 13, 2012
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I didn't mention the t3ss in my post, and I'm not sure how that paper refutes Nick's hypothesis.Starbuck
January 13, 2012
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Sequence convergence seems rather more common than was first thought, but that might simply be because we have much more gene and genome data to sift though than was previously possible. I would say that any homology at the sequence level could be ancestral, the product of either adaptive convergence or could be the result of homoplasious mutations. It is only by looking at these sequences in a phylogenetic context that we can begin to tease these possibilities apart. Signatures have been found in genes, and it looks like work has begun on whole genomes, to work out the frequency with which sequence convergence occurs. You might also be interested in the following: Liu, Y, Rossiter SJ, Han X, Cotton JA and Zhang S (2010) Cetaceans on a molecular fast track to ultrasonic hearing. Current Biology 20, 1834-1839. Davies KTJ, Cotton JA, Kirwan J, Teeling EC and /Rossiter SJ/ (2012) Parallel signatures of sequence evolution among hearing genes in echolocating mammals: an emerging model of genetic convergence. Heredity, DOI 10.1038/hdy.2011.119 http://www.nature.com/hdy/journal/vaop/ncurrent/abs/hdy2011119a.htmlStarbuck
January 13, 2012
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notes as to Starbuck's post:
"One fact in favour of the flagellum-first view is that bacteria would have needed propulsion before they needed T3SSs, which are used to attack cells that evolved later than bacteria. Also, flagella are found in a more diverse range of bacterial species than T3SSs. ‘The most parsimonious explanation is that the T3SS arose later," Howard Ochman - Biochemist - New Scientist (Feb 16, 2008) Phylogenetic Analyses of the Constituents of Type III Protein Secretion Systems Excerpt: We suggest that the flagellar apparatus was the evolutionary precursor of Type III protein secretion systems. http://www.horizonpress.com/jmmb/v2/v2n2/02.pdf I am convinced that the T3SS is almost certainly younger than the flagellum. If one aligns the amino acid sequences of the flagellar proteins (that have homologous counterparts in the T3SS), and if one also aligns the amino acid sequences of the T3SS proteins, one finds that the T3SS protein amino acid sequences are much more conserved than the amino acid sequences of the flagellar proteins. There are two possible explanations for this: (1) The T3SS is younger than the flagellum, or (2) The T3SS proteins are under more functional constraints than flagellar proteins, and so the sequences in T3SS proteins cannot diverge as much. We may rule out option #2 in the light of both in vitro and in silico mutagenesis. For example, I performed an in silico alanine scan on flagellar proteins and their T3SS homologues using SNAPs and found that flagellar proteins are under more functional constraints than T3SS proteins. (E.g., ~39% of the positions in FliF result in a non-neutral mutation when an in silico alanine scan is performed, ~34% of the positions in YscJ result in a non-neutral mutation — YscJ is FliF’s T3SS homologue, for those of you who do not know). https://uncommondescent.com/intelligent-design/why-were-so-many-darwin-defenders-no-shows-at-the-world%E2%80%99s-premier-evolutionary-conference/comment-page-2/#comment-389250 Indeed? Consider the facts: The flagellar proteins are all longer than the T3SS proteins, with the exception of FliN (YscQ is the only T3SS protein that is longer than its flagellar homologue). Further consider that the flagellar proteins have a higher degree a “functional specificity” than their T3SS counterparts. By this I mean that, in order for the flagellar proteins to carry out their function, very specified amino acid residues need to be in the proteins. This is not true of T3SS proteins: T3SS proteins seem to be capable of tolerating more amino acid substitutions than flagellar proteins. The implication of this? Namely, very specific mutations would not be needed for the T3SS proteins to carry out their function. T3SS proteins are generally less stable than their flagellar counterparts, yet they can still carry out their function. Let’s just take a look at one example of how it is very plausible for a T3SS protein to evolve from its flagellar homologue: FliF is ~550 amino acid residues in length, while its homologous counterpart (YscJ) is ~270 amino acid residues in length. Obviously, FliF has an extra ~200 residues because those residues are required for flagellar function, but those extra residues are NOT required for YscJ to function. A simple deletion event of those ~200 residues would result in the YscJ function. Yet, to get from YscJ to FliF would require very specific mutations, because those ~200 residues are rather specific and need to be specific in order to carry out the flagellar function. “A gene duplication followed by very specific amino acid substitutions would be needed to get from YscJ –> FliF, yet a simple deletion event would be needed to get from FliF –> YscJ.” So, not-very-specific mutations are needed to get from a flagellum to a T3SS. Incidentally, I should like to know what new binding sites would have to evolve in order to get from flagellum to T3SS — I do not deny that new binding sites can evolve, I am just curious about this. And, of course, I accept the idea that new information can arise through mindless processes. In conclusion: while the evolution of a T3SS –> flagellum would require very specific mutations, the evolution of flagellum –> T3SS could be accomplished by just a few, not very specific mutations. https://uncommondescent.com/intelligent-design/why-were-so-many-darwin-defenders-no-shows-at-the-world%E2%80%99s-premier-evolutionary-conference/comment-page-3/#comment-389432 A Darwinian mechanism for the origin of the flagellum is not the only explanation for homology. Just take a look at the sequences designed by Fisher et al. If one aligns those designed, un-evolved sequences, one finds that they are homologous to each other. In short, designed sequences can also result in homology. In light of this, sequence homology can hardly be explained only by Darwinian mechanisms. References: Fisher et al. “De Novo Designed Proteins from a Library of Artificial Sequences Function in Escherichia Coli and Enable Cell Growth.” Firstly, I think I’ve already sufficiently demonstrated exactly why it’s plausible for the T3SS proteins to evolve from their flagellar homologues, but it is less plausible for flagellar proteins to evolve from their T3SS counterparts. While a single truncating mutation would be sufficient for YscJ to evolve from FliF, a fairly large number of very specific mutations would have to occur for FliF to evolve from YscJ. Indeed, it certainly seems like there is no real obstacle to a flagellum à T3SS evolution, and just some truncating mutations would be needed for the T3SS proteins to evolve from their flagellar homologues (and, of course, some mutations would follow that would improve the overall T3SS structure, stabilizing it, etc.). That said, I will now point out where I think your argument is lacking in rigor: Do T3SS have highly conserved functional regions and binding sites? Yes, but here’s why it’s perfectly plausible for those features of T3SS to evolve, while it is not quite so plausible for those features to evolve in the flagellum. If the T3SS evolved from the flagellum, it would evolve with the binding sites that were in the flagellar proteins (unless a function evolved from the flagellum that did not require binding sites). In other words, the T3SS didn’t evolve any new binding sites – it just ‘inherited’ the binding sites that were present in the flagellum. The same argument is true, of course, for highly conserved functional regions et al. The conclusion? To my knowledge, no new binding sites or highly conserved functional regions would have to evolve in order for the T3SS to evolve from the flagellum.,,, Incidentally, given that the modern T3SS is definitely not ancestral to the flagellum, you are left without any evidence as to where FliF, FliP, FliM, etc., might have come from. https://uncommondescent.com/intelligent-design/why-were-so-many-darwin-defenders-no-shows-at-the-world%E2%80%99s-premier-evolutionary-conference/comment-page-4/#comment-389603
further notes:
Bacterial Flagellum - A Sheer Wonder Of Intelligent Design - video http://www.metacafe.com/watch/3994630 Bacterial Flagellum: Visualizing the Complete Machine In Situ Excerpt: Electron tomography of frozen-hydrated bacteria, combined with single particle averaging, has produced stunning images of the intact bacterial flagellum, revealing features of the rotor, stator and export apparatus. http://www.sciencedirect.com/science/article/pii/S096098220602286X Electron Microscope Photograph of Flagellum Hook-Basal Body http://www.skeptic.com/eskeptic/08-08-20images/figure03.jpg Engineering at Its Finest: Bacterial Chemotaxis and Signal Transduction - JonathanM - September 2011 Excerpt: The bacterial flagellum represents not just a problem of irreducible complexity. Rather, the problem extends far deeper than that. What we are now observing is the existence of irreducibly complex systems within irreducibly complex systems. How random mutations, coupled with natural selection, could have assembled such a finely set-up system is a question to which I defy any Darwinist to give a sensible answer. http://www.evolutionnews.org/2011/09/engineering_at_its_finest_bact050911.html Biologist Howard Berg at Harvard calls the Bacterial Flagellum “the most efficient machine in the universe."
The flagellum has steadfastly resisted all attempts to elucidate its plausible origination by Darwinian processes, much less has anyone ever actually evolved a flagellum from scratch in the laboratory;
Genetic Entropy Refutation of Nick Matzke's TTSS (type III secretion system) to Flagellum Evolutionary Narrative: Excerpt: Comparative genomic analysis show that flagellar genes have been differentially lost in endosymbiotic bacteria of insects. Only proteins involved in protein export within the flagella assembly pathway (type III secretion system and the basal-body) have been kept... http://mbe.oxfordjournals.org/cgi/content/abstract/msn153v1
bornagain77
January 13, 2012
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I suggest you do some PSI-BLAST searches with it here: http://blast.ncbi.nlm.nih.gov/Blast.cgi?PAGE=Proteins&PROGRAM=blastp&BLAST_PROGRAMS=blastp&QUERY=P0A1I7.1&LINK_LOC=protein&PAGE_TYPE=BlastSearch I suggest you restrict the search to the Swissprot database to save cluttering up the page. You will find the homology to FlgG and FlgE by the second iteration and to FlgF by the third iteration. Similar considerations apply to flagellins and hook proteins, where the length of the surface-exposed central domain is highly variable.Starbuck
January 13, 2012
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By using gene duplications Nick Matzke is engaging in question-begging. By refusing to understand taht ID is not anti-evolution Nick Matzke is engaging in wilfull ignorance. By thinking that by getting the components you can get the proper assembly configuration Nick matzke is relying on imagination.Joe
January 13, 2012
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petrushka the link is broken or somthing. try "minimal size of flagellin" in google from the article: Various deletions were introduced into the central region of Escherichia coli flagellin (497 residues) without destroying its ability to form flagellar filaments. The smallest flagellin retained only the N-terminal 193 residues and the C-terminal 117 residues, which are suggested to be the domains essential for filament formation. J Bacteriol. 1988 July; 170(7): 3305–3309 if you read the paper you can see that after they cut smoe amino acid the flagellin become invalid elizabeth yes,they fail to do that.if an half of protein is useless,how can you get to a full protein?mk
January 13, 2012
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Nick Matzke:
Um, not really. Known cases of sequence convergence are rare and typically limited to a handful of amino acids, or to very weak/vague sequence similarities. Gene duplication is overwhelmingly the more common and more likely explanation for decent amounts of sequence similarity. Gene duplication produces a copy of a sequence. Copying gives you the similarity.
The key phrase here is "known cases." There have been few extensive investigations on the pervasiveness of convergent evolution at the molecular level. There is,of course, the study by Gareth Jones, "Molecular Evolution: Gene Convergence in Echolocating Mammals." However, a more impressive paper on the subject came out in 2010. In a paper entitled "Adaptive molecular convergence: Molecular evolution versus molecular phylogenetics," by Castoe et al., the authors found significant cases of molecular convergence in 13 mitochondrially-encoded proteins of lizards and snakes. I don't think you can really call this a case of a "handful of amino acids" or "very weak/vague sequence similarities." So, the point here is that significant convergent evolution at the molecular level isn't all that implausible. Unfortunately, as of this date (AFAIK), no real research has been made to investigate the pervasiveness of molecular convergence among bacterial genomes. Anyways, I've been up all night long exploring some sequence stuff with FlgBCEFGK, so I won't make my main case here yet. Suffice it to say that, interestingly, when the Salmonella rod proteins FlgE and FlgK (a cladogram generated by ClustalW suggests that they are more closely related to each other than to the other rod proteins)are aligned using ClustalW, the sequence identity (~15%) isn't all that impressive. Of course, when we BLAST these proteins and find that they share sequence similarity along with significant E-values, the possibility that they are indeed related by gene duplication is quite strong. Nevertheless, we shouldn't dismiss that possibility of convergent evolution since a case may be made for it. By the way, the percentage of identical codons per identical amino acid residues in sequence alignments of these proteins is basically what we would expect under the convergence hypothesis. Just saying. So, basically, the key point of my little essay is: don't rule out molecular convergence since research shows that this can quite plausibly occur. Now I'm off to catch a wink of sleep, and I probably won't respond until my little adventures with FlgBCEFGK sequences are completed.Genomicus
January 13, 2012
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Nick, After years and years of seeing people drag out the “it’s just degradation!” excuse in a multitude of self-contradictory ways, without the slightest bit of reflection on rigorously defining what distinguishes “degradation” from “improvement”, I figured I would point it out. Yeah, Nick - do you realize that you can "improve" something while degrading it in the relevant sense? That these are not exclusive terms? Behe himself, in the very article quoted, alludes to this - he's stated it explicitly before, on multiple occasions. Not to mention that in Thornton's case, he doesn't think that what took place was a case of "improvement" in a selection sense. Don't think you can get out of this one by complaining that you're criticizing some supposed lack of rigor on the part of ID proponents - there was no contradiction here or no Behe's behalf pointed out by you, certainly not from myself. I asked you straight up whether Thornton's case was one of acquiring 'multiple parts' by degradation, as Behe claimed. It seems the answer was "yes", but since "yes" sounds bad, we had to get the usual Matzke bluff and fury which amounted to 'These ID people think that if a cellular machine loses parts due to mutations, it's degradation! But they ALSO think that if a cellular machine is copied and errors accumulate so both copies now can only do 1/2 of the functions they originally did, that that too is degradation! Look how ****ing slippery they are! It's as if they think BOTH cases are examples of degradation - how can that be!?' Behe’s supposed challenge to evolution was about how you get systems with multiple required parts. It was supposed to be hard for evolution to produce systems with multiple required parts, because a system missing the part is “by definition nonfunctional” and couldn’t be preserved by evolution. No, Nick. Behe's supposed challenge was not merely 'How do you get multiple parts?', full stop. It had and has to do with irreducibly complex systems, such that removing those parts meant the system could no longer function as it was. The "If I bust apart a mousetrap, I can make a stupid tie clip!" answer to Behe wasn't a relevant reply to him in the past, and the "If you start with a cellular machine capable of performing multiple discrete functions, duplicate it, then break different parts of the machine, you get two machines that don't do the same thing insofar as they each only do 1/2 of what the original machine already could do" reply isn't accurate now. And what's more, you goddamn know it. Word games like this are just cheap excuses for not dealing with the actual evidence, they are not serious responses to the data.nullasalus
January 12, 2012
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further note: Falk’s fallacy - Feb. 2010 Excerpt: This (the immune system) is one of the most amazing processes ever described.,,, Whatever may be said about it, it is a highly regulated, specified, directed and choreographed process. It is obviously the product of overwhelmingly brilliant design,,, https://uncommondescent.com/intelligent-design/falks-falacy/ Response to Kathryn Applegate - Caroline Crocker PhD.- cell biologist and immunologist - October 2010 Excerpt: Diversity of antibodies generated by B cells is due to deliberate, cell-engineered changes in the DNA sequence, not random mutations. In fact, I have never before heard the process whereby functional antibodies are formed (before they encounter antigen) described as mutation. And it is well-known that the appearance of functionality as a result of a mistake-mutation is extremely rare. Of course, after encountering antigen the hypervariable regions of the antibody DNA do undergo somatic hypermutation, but again this is in particular places and is controlled by enzymes.,,, https://uncommondescent.com/intelligent-design/comments-on-kathryn-applegate%E2%80%99s-may-posts-on-biologos/#more-15176 Generation of Antibody Diversity is Unlike Darwinian Evolution - microbiologist Don Ewert - November 2010 Excerpt: The evidence from decades of research reveals a complex network of highly regulated processes of gene expression that leave very little to chance, but permit the generation of receptor diversity without damaging the function of the immunoglobulin protein or doing damage to other sites in the genome. http://www.evolutionnews.org/2010/11/response_to_edward_max_on_talk040661.htmlbornagain77
January 12, 2012
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Nick to show others how dishonest you, and your cohorts at the NCSE (National Center for Selling Evolution), are I reference this:
"A Masterful Feat of Courtroom Deception": Immunologist Donald Ewert on Dover Trial - audio http://intelligentdesign.podomatic.com/player/web/2010-12-20T15_01_03-08_00
In this following podcast, Casey Luskin interviews microbiologist and immunologist Donald Ewert about his previous work as associate editor for the journal Development and Comparitive Immunology, where he realized that the papers published were comparative studies that had nothing to do with evolution at all.
What Does Evolution Have to Do With Immunology? Not Much - April 2011 http://intelligentdesign.podomatic.com/entry/2011-04-06T11_39_03-07_00
The blatant deception, from neo-Darwinists at Dover, did not stop with immunology;
The NCSE, Judge Jones, and Bluffs About the Origin of New Functional Genetic Information – Casey Luskin – March 2010 http://www.discovery.org/a/14251
Materialists/Atheists like to claim evolution is indispensable to experimental biology and led the way to many breakthroughs in medicine, Yet in a article entitled "Evolutionary theory contributes little to experimental biology", this expert author begs to differ.
"Certainly, my own research with antibiotics during World War II received no guidance from insights provided by Darwinian evolution. Nor did Alexander Fleming's discovery of bacterial inhibition by penicillin. I recently asked more than 70 eminent researchers if they would have done their work differently if they had thought Darwin's theory was wrong. The responses were all the same: No. Philip S. Skell - (the late) Professor at Pennsylvania State University. http://www.discovery.org/a/2816 Podcasts and Article of Dr. Skell http://www.evolutionnews.org/2010/11/giving_thanks_for_dr_philip_sk040981.html Darwinian Medicine and Proximate and Evolutionary Explanations - Michael Egnor - neurosurgeon - June 2011 http://www.evolutionnews.org/2011/06/darwinian_medicine_and_proxima047701.html Intelligent Design and Medical Research - video http://www.metacafe.com/w/7906908
In fact, as to the somewhat minor extent evolutionary reasoning has influenced medical diagnostics, it has actually led to much ‘medical malpractice’ in the past:
Evolution's "vestigial organ" argument debunked Excerpt: "The appendix, like the once 'vestigial' tonsils and adenoids, is a lymphoid organ (part of the body's immune system) which makes antibodies against infections in the digestive system. Believing it to be a useless evolutionary 'left over,' many surgeons once removed even the healthy appendix whenever they were in the abdominal cavity. Today, removal of a healthy appendix under most circumstances would be considered medical malpractice" (David Menton, Ph.D., "The Human Tail, and Other Tales of Evolution," St. Louis MetroVoice , January 1994, Vol. 4, No. 1). "Doctors once thought tonsils were simply useless evolutionary leftovers and took them out thinking that it could do no harm. Today there is considerable evidence that there are more troubles in the upper respiratory tract after tonsil removal than before, and doctors generally agree that simple enlargement of tonsils is hardly an indication for surgery" (J.D. Ratcliff, Your Body and How it Works, 1975, p. 137). The tailbone, properly known as the coccyx, is another supposed example of a vestigial structure that has been found to have a valuable function—especially regarding the ability to sit comfortably. Many people who have had this bone removed have great difficulty sitting. http://www.ucg.org/science/god-science-and-bible-evolutions-vestigial-organ-argument-debunked/
Darwinian evolution is simply useless, indeed a hindrance, to science;
Science Owes Nothing To Darwinian Evolution - Jonathan Wells - video http://www.metacafe.com/watch/4028096
bornagain77
January 12, 2012
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Umm, that the rod proteins in the flagellum can be accounted for by gene duplication doesn’t mean that this is how they arose. Thus, although the rod proteins FlgBCFG share sequence similarity with each other, this doesn’t imply gene duplication per se. There is always the possibility of convergent evolution at the molecular level accounting for this sequence similarity.
Um, not really. Known cases of sequence convergence are rare and typically limited to a handful of amino acids, or to very weak/vague sequence similarities. Gene duplication is overwhelmingly the more common and more likely explanation for decent amounts of sequence similarity. Gene duplication produces a copy of a sequence. Copying gives you the similarity. This is even more true in the case of the flagellum axial rod, where we already have various examples of multiple flagellin proteins in a single genome, etc. (the "classic" Salmonella just has one, but many bacteria don't follow the classic pattern), some of them specialized for different structural functions (e.g. another hook-flagellin linker protein). The gene duplication explanation is obvious, plausible, and simple, and matches everything we already know about molecular mechanisms and their commonality. The "convergence" explanation, in this case, is desperate special pleading with no support except for wishful thinking by ID fans. Let me give you a hint -- you would have a better chance of arguing that the rod/hook family and the flagellin+linker family have independent origins. The homology evidence is much weaker there. But within each family, it's rock solid, you can easily bring it up on any BLAST search.NickMatzke_UD
January 12, 2012
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null, After years and years of seeing people drag out the "it's just degradation!" excuse in a multitude of self-contradictory ways, without the slightest bit of reflection on rigorously defining what distinguishes "degradation" from "improvement", I figured I would point it out. Behe's supposed challenge to evolution was about how you get systems with multiple required parts. It was supposed to be hard for evolution to produce systems with multiple required parts, because a system missing the part is "by definition nonfunctional" and couldn't be preserved by evolution. The Thornton lab's article demonstrates one way you can increase the number of required parts. As I said in my first comment, it doesn't explain everything, but it is clear that the duplication-and-divergence mechanism explains a lot of the required parts in these various systems. This is a huge point against Behe's claim.NickMatzke_UD
January 12, 2012
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Not enough detail, eh? We've heard that before. http://ncse.com/book/export/html/2520 Please give us the equally detailed and well-tested ID explanation for the origin of the vertebrate immune system.NickMatzke_UD
January 12, 2012
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bornagain77, What's with the triple commas?champignon
January 12, 2012
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Which is why Thornton et al is the current enemy. How dare he actually test whether cousin sequences can be linked by a common ancestor sequence. I know, right? Why can't Behe be appreciative of Thornton and company, right? Why can't he say something like this guy: "I never thought it would happen but, in my estimation, Richard Lenski has acquired a challenger for the title of “Best Experimental Evolutionary Scientist.” Lenski, of course, is the well-known fellow who has been growing E. coli in his lab at Michigan State for 50,000 generations in order to follow its evolutionary progress. His rival is Joseph Thornton of the University of Oregon who, by inferring the sequences of ancient proteins and then constructing (he calls it “resurrecting”) their genes in his lab, is able to characterize the properties of the ancestral proteins and discern how they may have evolved into more modern versions with different properties." Or maybe this: "The work of Finnegan et al (2012) strikes me as quite thorough and elegant." Why can't ID proponents talk about people's ideas like this, rather than treating them as the enemy?nullasalus
January 12, 2012
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It’s not a word game, nullasalus. That you think it is is a measure of the communication problem here. It's not a communication problem. It's an actual disagreement - they exist, you know - in this case, borne out of Matzke making it sound as if gaining parts, losing parts, gaining specification and losing specification are all instances of degradation according to ID proponents, when (at least in Behe's case) what's being argued is that how parts are gained, how they are lost, etc, is what matters. I have an extremely low opinion of your intellectual honesty, and I have no interest in wasting my time with you. You said Matzke said what he did better than you could have - I agree. How about leaving this task to your better?nullasalus
January 12, 2012
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Nick Matzke:
Furthermore, cases of what are obviously duplicated-and-modified parts in “molecular machines” are absolutely ubiquitous. Fully half of the core flagellum proteins (those of the rod, hook, and filament) can be accounted for this way.
Umm, that the rod proteins in the flagellum can be accounted for by gene duplication doesn't mean that this is how they arose. Thus, although the rod proteins FlgBCFG share sequence similarity with each other, this doesn't imply gene duplication per se. There is always the possibility of convergent evolution at the molecular level accounting for this sequence similarity.Genomicus
January 12, 2012
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It's not a word game, nullasalus. That you think it is is a measure of the communication problem here.Elizabeth Liddle
January 12, 2012
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Nick, I asked a pretty simple question, and I asked it fairly. That it provoked a whole lot of hand-waving and bluster doesn't encourage me. Behe, and all you ID guys, I'm not an "ID guy", and you know it. I don't think ID is science, though admittedly that position is tied to my not thinking anti-ID is science either. I asked my question because if Behe was wrong about what he said, I wanted to know why. rely on an arbitrary and continuously-changing definition of “degradation”. When parts are lost, that’s “degradation”. When parts are gained (as here), *that’s* degradation. When binding site specificity increases, that’s called degradation, since the generality and versatility of the ancestral binding site has been reduced. But when binding site specificity *decreases*, that’s *also* called degradation, since loss of specificity must be degradation. "Parts are gained here", Behe claims (if I understand him), in the sense that a cellular machine capable of performing tasks A, B and C was started with. This machine was duplicated, and eventually you ended up with three machines that only did A, only did B, and only did C. This really does not seem to challenge anything Behe has discussed. Furthermore, your understanding of Behe seems flawed here. It's not that gaining parts must mean degradation, and losing parts must mean degradation, and more specificity must mean degradation, and less specificity must mean degradation. If you "gain a part" by copying the machine such that drift and selection causes it to lose functionality (Likewise for "become more specified") because mutations made it incapable of doing anything else, that's degradation. If you "lose a part" because mutations have rendered some parts incapable of functioning or lost altogether, that's degradation. If your machine "becomes less specified" because its ability to limit what it applies to relies on a part that becomes broken by mutation, that's degradation. (Example: 'I can only get through this door if I have the right keycard. But if I smash the lock, anyone can get through.' I think it's fair to call this an example of degradation.) Word games like this are just cheap excuses for not dealing with the actual evidence, they are not serious responses to the data. Sorry for stealing that from you, but holy hell, it applies to you a hell of a lot more than it seems to apply to Behe here. I gave you a chance - I asked you a fair question, utterly bereft of culture-warriorisms, Behe-cheerleading, or otherwise. Your response was to rant, blow smoke and - frankly - try to BS people. Not good.nullasalus
January 12, 2012
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Nick states:
It’s all just a word game used to avoid the evidence for evolution.
How deeply twisted and Ironic of you to state that Nick, because neo-Darwinists, of which you yourself are a prime example, are engaged full force in deceptive word games (obfuscation) to make it appear as if evolution (atheistic/materialistic neo-Darwinian evolution that is) has any substantiating evidence at all. Moreover If you want to falsify ID, Michael Behe (that would be Doctor Michael Behe to you!) lays out a very simple criteria right here:
Michael Behe on Falsifying Intelligent Design - video http://www.youtube.com/watch?v=N8jXXJN4o_A
Myself, instead of the pathetically low hurdle that Dr. Behe required, I would demand that neo-Darwinists 'randomly evolve' a molecular machines, or novel functional protein folds, from scratch, repeatedly, so as to establish Darwinian grand claims 'scientifically': i.e. In spite of the fact of finding molecular motors permeating the simplest of bacterial life, there are no detailed Darwinian accounts for the evolution of even one such motor or system.
"There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject." James Shapiro - Molecular Biologist
The following expert doesn't even hide his very unscientific preconceived philosophical bias against intelligent design,,,
‘We should reject, as a matter of principle, the substitution of intelligent design for the dialogue of chance and necessity,,,
Yet at the same time the same expert readily admits that neo-Darwinism has ZERO evidence for the chance and necessity of material processes producing any cellular system whatsoever,,,
,,,we must concede that there are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations.’ Franklin M. Harold,* 2001. The way of the cell: molecules, organisms and the order of life, Oxford University Press, New York, p. 205. *Professor Emeritus of Biochemistry, Colorado State University, USA Michael Behe - No Scientific Literature For Evolution of Any Irreducibly Complex Molecular Machines http://www.metacafe.com/watch/5302950/ “The response I have received from repeating Behe's claim about the evolutionary literature, which simply brings out the point being made implicitly by many others, such as Chris Dutton and so on, is that I obviously have not read the right books. There are, I am sure, evolutionists who have described how the transitions in question could have occurred.” And he continues, “When I ask in which books I can find these discussions, however, I either get no answer or else some titles that, upon examination, do not, in fact, contain the promised accounts. That such accounts exist seems to be something that is widely known, but I have yet to encounter anyone who knows where they exist.” David Ray Griffin - retired professor of philosophy of religion and theology
Well Nick, despite all your bluster, there are no new molecular machines to show for your beloved theory, how about just a single novel functional protein fold???
Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.ncbi.nlm.nih.gov/pubmed/15321723 Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact - Cornelius Hunter - July 2011 Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude. http://darwins-god.blogspot.com/2011/07/response-to-comments-proteins-did-not.html Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681
Shoot Nick, though you never will admit it, you ain't even in the right ballpark to begin with with the materialistic neo-Darwinian framework. Dr. Stephen Meyer comments at the end of the preceding video,,,
‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009)
etc.. etc.. etc..bornagain77
January 12, 2012
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Hey Nick- can a company lose money of each sale and make it up on volume, ie selling more? The following offers the argument pertaining to anti-biotic resitance: Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change? But all that is moot because you are still stuck on the silly strawman that ID is anti-evolution- hump that baby NickM! BTW how can we test the premise that the tetrapod jaw involved the loss of functionality in the gills? Can we mutate the heck out of fish embroys and see that?Joe
January 12, 2012
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