niiicholas
Posts: 319
Joined: May 2002
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Dr. Dembski,
Scientists will begin to believe IDist claims about the literature only when IDists actually begin addressing it.
Immune system
For example, exactly what you say you want, detailed proposals in peer-reviewed literature about the evolution of the vertebrate immune system, were provided for you in a handy talkdesign.org FAQ:
http://www.talkdesign.org/faqs/Evolving_Immunity.html
...and yet in an immensely long ISCID thread, neither you, nor collegues such as Paul Nelson, managed to defend Behe's assertion that the evolutionary literature had no answers about the origin of the immune system:
http://www.iscid.org/ubbcgi/ultimatebb.cgi?ubb=get_topic;f=6;t=000152
There are more references on the evolution of the immune system listed here.
Ken Miller
As for Ken Miller, his four examples of literature on the evolution of "biochemical machines" consisted of two proteins (which he, among many others, calls machines in their own right), a six-part pump, and the Krebs cycle.
- I'll conceed that individual proteins are not usually considered IC (although the claim has been made in various places, and the evolutionary origin of new proteins is very commonly doubted by IDists despite the massive evidence in favor of the common origin of new proteins).
- Miller's next example is:
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Evolution of the cytochrome c oxidase proton pump.
Musser SM, Chan SI.
J Mol Evol. 1998 May;46(5):508-20.
The superfamily of quinol and cytochrome c terminal oxidase complexes is related by a homologous subunit containing six positionally conserved histidines that ligate a low-spin heme and a heme-copper dioxygen activating and reduction center. On the basis of the structural similarities of these enzymes, it has been postulated that all members of this superfamily catalyze proton translocation by similar mechanisms and that the CuA center found in most cytochrome c oxidase complexes serves merely as an electron conduit shuttling electrons from ferrocytochrome c into the hydrophobic core of the enzyme. The recent characterization of cytochrome c oxidase complexes and structurally similar cytochrome c:nitric oxide oxidoreductase complexes without CuA centers has strengthened this view. However, recent experimental evidence has shown that there are two ubiquinone(ol) binding sites on the Escherichia coli cytochrome bo3 complex in dynamic equilibrium with the ubiquinone(ol) pool, thereby strengthening the argument for a Q(H2)-loop mechanism of proton translocation [Musser SM et al. (1997) Biochemistry 36:894-902]. In addition, a number of reports suggest that a Q(H2)-loop or another alternate proton translocation mechanism distinct from the mitochondrial aa3-type proton pump functions in Sulfolobus acidocaldarius terminal oxidase complexes. The possibility that a primitive quinol oxidase complex evolved to yield two separate complexes, the cytochrome bc1 and cytochrome c oxidase complexes, is explored here. This idea is the basis for an evolutionary tree constructed using the notion that respiratory complexity and efficiency progressively increased throughout the evolutionary process. The analysis suggests that oxygenic respiration is quite an old process and, in fact, predates nitrogenic respiration as well as reaction-center photosynthesis. |
The paper is freely available online, and looks pretty complex and detailed to me. Here is their figure 3:
Musser and Chan (1998) highlight the important fact that, while this multipart machine has 6 parts in humans, it has only 2 parts in bacteria, and Musser and Chan showed that the increasing complexity in parts could be explained by their proposed tree. They spend 2-3 pages, plus a long caption, explaining their scenario. I won't pretend to understand the paper as I have not studied this topic, but certainly the ball is in your (Dembski/Behe's) court, and has been since 1998. The only response, anywhere, to this paper from an IDist is in Behe's Irreducible Complexity and the Evolutionary Literature and is but a short paragraph. Behe basically says that the paper is not detailed enough, and that electron transfer might not be an IC function because one protein can do it. On this logic, the flagellum isn't IC either because Brownian motion can move bacteria around all by itself. As for "detail", Behe has never put forward any reasonable criteria for what constitutes "detailed enough"; Dembski's flailing on the issue of what constitutes detail, and who needs to have it, was gloriously revealed in this ISCID thread:
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As for your example, I'm not going to take the bait. You're asking me to play a game: "Provide as much detail in terms of possible causal mechanisms for your ID position as I do for my Darwinian position." ID is not a mechanistic theory, and it's not ID's task to match your pathetic level of detail in telling mechanistic stories. If ID is correct and an intelligence is responsible and indispensable for certain structures, then it makes no sense to try to ape your method of connecting the dots. |
In other words, you consider dozens/hundreds of peer-reviewed articles a "pathetic" level of detail, and yet the "level of detail" in your own hypothesis is far, far, below pathetic. And elsewhere on that page you say, basically, that evolutionists have to have a time machine and trace every single mutation, while IDists don't have to do squat but say "IDdidit" and declare the problem solved. You are never going to convince scientists with this attitude -- you're asking them to stop doing science.
Until Behe or Dembski deals with Musser and Chan's electron pump in at least as much detail as Musser and Chan do, this point goes to the evolutionists, and constitutes a counterexample to all of Dembski's wild and uninformed assertions about the evolutionary literature.
The evolution of the TCA cycle is an oft-cited counterexample to Behe/Dembski. Here is the paper (also freely online):
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The puzzle of the Krebs citric acid cycle: assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution.
Melendez-Hevia E, Waddell TG, Cascante M.
J Mol Evol. 1996 Sep;43(3):293-303.
The evolutionary origin of the Krebs citric acid cycle has been for a long time a model case in the understanding of the origin and evolution of metabolic pathways: How can the emergence of such a complex pathway be explained? A number of speculative studies have been carried out that have reached the conclusion that the Krebs cycle evolved from pathways for amino acid biosynthesis, but many important questions remain open: Why and how did the full pathway emerge from there? Are other alternative routes for the same purpose possible? Are they better or worse? Have they had any opportunity to be developed in cellular metabolism evolution? We have analyzed the Krebs cycle as a problem of chemical design to oxidize acetate yielding reduction equivalents to the respiratory chain to make ATP. Our analysis demonstrates that although there are several different chemical solutions to this problem, the design of this metabolic pathway as it occurs in living cells is the best chemical solution: It has the least possible number of steps and it also has the greatest ATP yielding. Study of the evolutionary possibilities of each one-taking the available material to build new pathways-demonstrates that the emergence of the Krebs cycle has been a typical case of opportunism in molecular evolution. Our analysis proves, therefore, that the role of opportunism in evolution has converted a problem of several possible chemical solutions into a single-solution problem, with the actual Krebs cycle demonstrated to be the best possible chemical design. Our results also allow us to derive the rules under which metabolic pathways emerged during the origin of life.
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Behe's response to this, cited by Dembski, is that the Krebs cycle is a metabolic pathway and that these are not IC. Behe's original logic in Darwin's Black Box was that *some* metabolic pathways might not be IC, if they could be evolved by duplication of one original protein (the model Horowitz introduced in 1945). But this escape does not work for Behe because (a) the Krebs cycle is a *cycle*, not a linear pathway that could be extended from a single component, (b) its parts actually came from diverse sources, and © two steps in the Krebs cycle are catalyzed by multienzyme complexes, which are as IC as anything gets.
There are other IC metabolic pathways, namely toxin degradation pathways, that also require multiple components to work. Unfortunately for Behe and Dembski, their evolution is also well-documented (within recent times, as these toxins are abiotic compounds such as pesticides). Mike Gene concedes that these prove that IC by itself is not a barrier to evolution. When are Behe and Dembski going to give up the "those are just metabolic pathways" co-out and admit that IC regularly evolves by natural processes? Why should anyone take Dembski's assertions about the literature seriously when neither Behe nor Dembski has ever grappled with this literature?
Ken Miller's other examples
Dembski also does not acknowledge that, after Miller's four examples, Miller then moved on to give explanations for the evolutionary origin of both vertebrate blood-clotting and decapod blood clotting. Behe never dealt with the decopod system at all, but regarding vertebrate blood-clotting, Behe again complained that there was not enough detail. So, Miller posted his unedited longer version of the origin of blood-clotting, which neither Behe nor Dembski has ever dealt with. They have similarly never dealt with the extensive peer-reviewed literature on the topic (Behe chose critique a speech by Doolittle in DBB), even though some recent literature has even been brought to their attention on ISCID.
Why should scientists take Dembski's assertions about the literature seriously, when he doesn't ever acknowledge it, let alone address it in any detail?
I think Dembski mythed something.
Edited by niiicholas on July 24 2003,03:24
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(each loop with an S--S link is a representation of the Ig-domain, relatives of which are found even in bacteria IIRC)