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(Permalink) Posted: July 22 2003,20:51   

Da next book:


NEW AS OF 22 July 2003
<> Uncommon Dissent: Intellectuals Who Find Darwinism Unconvincing. [22July03] Table of contents, introduction, and list of contributors to edited collection by William Dembski, due out with Intercollegiate Studies Institute early spring 2004.

Looks like some old stuff, some new.  Chances of actual biology being included: less than Dembski's UPB.

Link to table of contents and Dembski's intro:


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(Permalink) Posted: July 22 2003,21:34   

Why wasn't the book called, "Common Dissent?"  'Twould make more sense...

Anyhow, Dembski repeats his usual claim that:


The biological community has no detailed, testable proposals for how irreducibly complex systems might have arisen by Darwinian means but only a variety of wishful speculations...

But when confronted with just such proposals, for example for the complement cascade of the immune system, Dembski rather completely failed to even deal with the evidence or the literature:

Organisms using GAs vs. Organisms being built by GAs

Many other references:
AE immune system thread

Edited by niiicholas on July 22 2003,21:34


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(Permalink) Posted: July 22 2003,21:40   

Dembski writes, referring to the Lenski et al. (2003) paper:


This paper describes a computer simulation and thus contains no actual biology.

Wow.  This is true, but coming from Dembski, who has never dealt seriously with any actual biology (and who puts forward ridiculous random-assembly models for IC structures such as the flagellum, rather than the far more realistic mutation-and-selection model used by Lenski et al.), this statement puts a heavy strain on the irony-meter.


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(Permalink) Posted: July 22 2003,22:31   

Reposted from ISCID thread:

Dr. Dembski has recently put up his introduction to a soon-to-be published anthology of Darwinism skeptics: Uncommon Dissent.

Therein, he writes of the Lenski et al. (2003) simulation of the evolution of a complex, multiple-parts-required system,

This paper describes a computer simulation and thus contains no actual biology.  Go to the discussion section, and you'll read: "Some readers might suggest that we 'stacked the deck' by studying the evolution of a complex feature that could be built on simpler functions that were also useful.  However, that is precisely what evolutionary theory requires...."  In other words, the computer programmers artificially built into the simulation what they thought evolution needed in order to make it work.  The validity of this study therefore depends crucially on whether the simulation maps faithfully onto biological reality.

Unfortunately, it does not, and the study therefore doesn't prove a thing about real-life biological evolution.  By requiring of their simulation that complex features exhibiting complex functions can always be decomposed into simpler features exhibiting simpler functions, the authors of this article  begged precisely the point at issue with irreducible complexity in real-life biological systems.  There is no evidence that real-life irreducibly complex biochemical machines can be decomposed this way.
We will leave aside the irony of Dembski (author of the tornado-in-a-junkyard strawman for flagellar evolution, the closest thing to actual biology in No Free Lunch) accusing someone of not having any "actual biology" in their study.  The question that Dembski raises here is, can "complex features exhibiting complex functions" be "decomposed into simpler features exhibiting simpler functions"?  Dembski says that the simulation's validity "depends crucially" on this assumption, and further argues that Lenski et al.'s simulation is invalid because "There is no evidence that real-life irreducibly complex biochemical machines can be decomposed this way."

But, in responding to Ken Miller just a few months ago, Dembski conceded exactly this assumption about irreducibly complex systems: the Icon of ID, the flagellum, can in fact be decomposed into several subsystems with independent functions:


To this let me add: A system is irreducibly complex in Behe's sense if all its parts are indispensable to preserving the system's basic function. That an irreducibly complex system may have subsystems that have functions of their own (functions distinct from that of the original system) is therefore allowed in the definition. It seems that Miller is unclear about the distinction between a definition and an argument. Irreducible complexity is a well-defined notion that is appropriately and ascertainably applied to the bacterial flagellum. Miller's concern ultimately seems not over the definition but over its use as an argument to rebut Darwinism. Miller's point here generally is that if subsystems can be found with functions of their own (perforce different from that of the original system since otherwise the original system would not be irreducibly complex), then those subsystems and their functions can be grist for selection's mill and underwrite a Darwinian account of how the original system arose.

Source: Still Spinning Just Fine: A Response to Ken Miller
(Dembski then goes on to argue that the fact of functional subsystems doesn't disprove Behe's arguement, but that is not the point Dembski is contesting in his Uncommon Dissent critique of Lenski)

If that weren't enough, Dembski has been even clearer elsewhere:


You've charged me with moving the goalposts and adjusting the definition of irreducible complexity because I require of evolutionary biologists to "connect the dots" in a causally convincing way. The dots here are functional precursors that could conceivably have evolved into the final system of interest. You state that previously I claimed that the dots couldn't exist because they wouldn't be functional. Please show me in Michael Behe's writings or my own where we deny that IC systems can be made up of subsystems that can be functional in their own right. The point is not whether subsystems can be functional on their own but whether they can exhibit the same function in the same manner as the system in question. You misrepresent our position.

Source: ISCID thread, page 2: Organisms using GAs vs. Organisms being built by GAs
And he even says in one place that such subsystems "always" occur:


But any reasonably complicated machine always includes subsystems that perform functions distinct from the original machine.

Source: Evolution's Logic of Credulity: An Unfettered Response to Allen Orr
In other words, Dembski has already admitted that his own argument against the Lenski paper is wrong.  He has *already* admitted in print, repeatedly, that "complex features exhibiting complex functions can always be decomposed into simpler features exhibiting simpler functions."  And yet he criticizes Lenski for their assumption:

...the authors of this article  begged precisely the point at issue with irreducible complexity in real-life biological systems.  There is no evidence that real-life irreducibly complex biochemical machines can be decomposed this way.
...even though it is -- even according to Dembski himself -- biologically *realistic* and therefore "actual biology".

Dembski spends most of his introduction to Uncommon Dissent accusing scientists of adhering to evolutionary theory for all kinds of ideological reasons, rather than evidence.  Perhaps Dembski would be more successful in convincing them if he spent more time making sure his own arguments were self-consistent (let alone well-supported by evidence, a topic for another thread), and less time calling them names.


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(Permalink) Posted: July 22 2003,23:17   

II thread:

T.o.: thread


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(Permalink) Posted: July 23 2003,00:04   

Dembski's 'contains no actual biology' remark echoes Behe's remark in the Chronicle of Higher Education, where he was quoted as saying
But Michael J. Behe, a professor of biological sciences at Lehigh University who is one of the most vocal proponents of intelligent design, says that the simulation proves nothing. "If I were a Darwinist, I would be embarrassed for this paper to be published in Nature," he said.

"There's precious little real biology in this project," Mr. Behe said. For example, he said, the results might be more persuasive if the simulations had operated on genetic sequences rather than fictitious computer programs.

Dembski's comment about the Lenski, et al. study 'begging the point' because there were functional intermediates available in the simulation echoes some of the objections raised in the ISCID Literature Review Forum discussion of the paper.  There's no indication in his Introduction that Dembski learned anything from that discussion, though.

Finally, the inclusion of intermediates in the Lenski, et al., study was not an assumption or requirement; it was part of the experimental design.  They actually ran evolutionary runs with 38 different combinations of intermediates, including the extreme case of no simpler intermediates, the case with all 7 'simpler' functions (simpler than EQU), and 36 different conditions with one or a pair of the intermediates removed.  In 37 of the 38 conditions, lineages capable of performing the input-output mapping corresponding to EQU evolved; only in the condition in which there were no intermediates did the EQU mapping fail to appear in 50 runs.


Edited by RBH on July 23 2003,00:14

"There are only two ways we know of to make extremely complicated things, one is by engineering, and the other is evolution. And of the two, evolution will make the more complex." - Danny Hillis.


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(Permalink) Posted: July 23 2003,15:40   

Dembski has started a thread on ARN on the irreducible complexity/Lenski, et al portion of his Introduction here.  I provided a cross-reference from that thread to yersinia's posting on ISCID's Literature Review Forum.


"There are only two ways we know of to make extremely complicated things, one is by engineering, and the other is evolution. And of the two, evolution will make the more complex." - Danny Hillis.


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(Permalink) Posted: July 23 2003,18:24   

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 FAQ:

...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:;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:
    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:


    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):


    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.
    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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(Permalink) Posted: July 24 2003,03:23   

From the ARN thread:


In the passage that you cited, Inlay is rebutting some of Behe's assertions.  Behe argued that certain intermediate stages in the evolution of the immune system receptors would have been nonfunctional/useless, and therefore not selectable.

Inlay found (in the literature) examples of receptors doing just what Behe said would have been nonfunctional.  As for the origin of adaptive immunity, there is a pretty well supported hypothesis involving the insertion of a transposon (transposons are continually inserting into random spots in eukaryote genomes) into an Ig-receptor.  This is discussed elsewhere in Inlay's FAQ.

Here is a quote from the lit giving the basic situation:

Early on, it was suggested that the V(D)J recombination system might have arisen by the fortuitous integration of a transposable element into an ancestral antigen-receptor gene [14]. This hypothesis was strengthened by the discovery that the RAG genes are tightly linked [7], and by the finding that the RAG proteins can act as a transposase. Thus, a plausible model for the acquisition of the V(D)J recombination system during vertebrate evolution is the integration of a transposable element carrying the linked RAG genes into a primordial antigen-receptor gene in an ancestral jawed vertebrate, approximately 450 million years ago (reviewed in [1,11]). Presumably, this initial integration event created the first rearranging antigen-receptor gene; subsequent gene duplication events then created the multiple immunoglobulin and T-cell receptor loci.

An example article showing recent experimental support for the hypothesis:

Immunol Res. 1999;19(2-3):169-82.

Transposition mediated by RAG1 and RAG2 and the evolution of the adaptive immune system.

Schatz DG.

The RAG1 and RAG2 proteins together initiate V(D)J recombination by performing cleavage of chromosomal DNA adjacent to antigen receptor gene segments. Like the adaptive immune system itself, RAG1 and RAG2 are found only in jawed vertebrates. The hypothesis that RAG1 and RAG2 arose in evolution as components of a transposable element has received dramatic support from our recent finding that the RAG proteins are a fully functional transposase in vitro. This result strongly suggests that antigen receptor genes acquired their unusual structure as a consequence of the insertion of a transposable element into an ancestral receptor gene by RAG1 and RAG2 approx 450 million years ago.
There is a great deal of related literature on this evolutionary hypothesis.

The evolutionary model even made it into Nature:


Nature. 1998 Aug 20;394(6695):744-51.

Transposition mediated by RAG1 and RAG2 and its implications for the evolution of the immune system.

Agrawal A, Eastman QM, Schatz DG.

Immunoglobulin and T-cell-receptor genes are assembled from component gene segments in developing lymphocytes by a site-specific recombination reaction, V(D)J recombination. The proteins encoded by the recombination-activating genes, RAG1 and RAG2, are essential in this reaction, mediating sequence-specific DNA recognition of well-defined recombination signals and DNA cleavage next to these signals. Here we show that RAG1 and RAG2 together form a transposase capable of excising a piece of DNA containing recombination signals from a donor site and inserting it into a target DNA molecule. The products formed contain a short duplication of target DNA immediately flanking the transposed fragment, a structure like that created by retroviral integration and all known transposition reactions. The results support the theory that RAG1 and RAG2 were once components of a transposable element, and that the split nature of immunoglobulin and T-cell-receptor genes derives from germline insertion of this element into an ancestral receptor gene soon after the evolutionary divergence of jawed and jawless vertebrates.



Figure 7 RAG-mediated transposition and a model for the origins of split antigen-receptor genes. a, Parallels between RAG- and Tn10-mediated transposition. Tn10 transposase (T'pase) or the RAG proteins (shaded ovals) recognize and synapse the terminal sequences of the transposable element (blue and red triangles or rectangles) and then excise it from donor sequences (dashed lines). Target capture, strand transfer, and gap repair result in target-site duplications (green rectangles) flanking the elements (see text). b, Possible structure of the original transposable element that integrated into the germ line of an ancestral vertebrate. Dashed arrows indicate the direction of transcription of the RAG genes. c, The present 'split' nature of immunoglobulin and TCR genes is proposed to have arisen from transposition mediated by RAG1 and RAG2 (bottom left) of one or two SE/SE elements into a primordial receptor gene exon (top, dark green rectangle), thereby dividing the exon into two or three gene segments, each flanked by one or two recombination signals (blue or red triangles). These gene segments would represent the evolutionary precursors of current V, D and J gene segments (top). Other models for the generation of D segments can also be envisioned. Different patterns of gene duplication (right) would result in the 'mammalian' or 'cluster' configurations of gene segments characteristic of the heavy chain locus of mammals or cartilaginous fishes, respectively. The constant region exons © are represented as single grey rectangles. Similar models have been proposed previously [14,41].
As for the origin of various types of receptors, it's pretty clear that they're all related, since they are all built out of the same Ig-domain (immunoglobulin-domain) blocks:

  (each loop with an S--S link is a representation of the Ig-domain, relatives of which are found even in bacteria IIRC)

Here is another article on the topic:

The important thing here is not so much whether or not one completely understands this literature -- it is massive and technical.  The important question is whether Dembski understands it, let alone deals with it.  It is quite obvious that his pronouncements deny its existence completely, and that he is therefore without a leg to stand on until such time as he convincingly takes it on and refutes it.

But what Dembski does instead is simply assert, over and over, to anyone who will listen, that this scientific literature simply doesn't exist!  The existence of the literature has been pointed out to him on numerous occasions, and yet he repeats his wild assertions.

So, jon_e, don't you agree that scientists have very good reasons to be skeptical of Dembski?  He comes off as being some combination of wildly ignorant, a posturing blowhard, and deliberately misleading.  I'm sorry to put it that way, but it's the only conclusion that seems likely based on the differences between the actual literature, and Dembski's claims about it.


PS: jon, the innate (complement) system is indeed different from the adaptive (combinatorial) system; the innate system is older and found in organisms that lack adaptive immunity entirely.  Also, the evolution of the innate system has been traced in rather alot of detail; see Inlay's FAQ.


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(Permalink) Posted: July 24 2003,14:08   



Thanks, Nic. I'd like to refocus my question. Perhaps Dr. Dembski is a blowhard, or blathering idiot, or whatever; I don't know.
What I'd like to know concerns the concept of IC, my understanding of it, and what the questions should be.
I',m trying to understand your post. Is the literature you are citing positing a possible evolutionary pathway for T-cells and other antigen receptors? Does it also explain how the complete adaptive (combinatorial)system could have been "put together?" In other words, are we talking about the evolution of "parts" or "complete systems" (tightly integrated systems)? Dembski and Behe seem to question the presence in the literature of explanations of system development. Maybe I'm wrong, but you state that the innate system's evolution has been detailed (with a number of built-in assumptions, I might add), but what about the adaptive, combinatorial system (I mean the engineering of the system, not just the manufacture of its components)?

Neither Behe nor Dembski has ever been very precise about what constitutes a "part" and what constitutes the "system".  If you read Inlay's FAQ, you know that the skin can be seen as "part" of "the immune system".  There are all kinds of proteins involved in immunity, going in all directions, many not found in various organisms, others with multiple uses inside and outside immunity, etc.  It basically doesn't fit very well the simplistic models of clear biological "systems" favored by IDers.

What Behe did in DBB was pick three sets of molecular components in the immune system and call each of them an IC system.  One of these was adaptive immunity.  Basically what makes adaptive immunity different from other kinds of immunity is that the receptors re-arrange.  Signalling, replication of cells with successful antigen-binding receptors, etc. can all occur without rearranging receptors.  Even self-nonself recognition appears to predate the origin of rearranging receptors.  So yes, explanation of the origin of adaptive immunity is basically the origin of these re-arranging receptors.

Of course all of these different subsystems are continually co-evolving, and going in different directions in different lineages.  It would take books to explain it all, e.g.:

Origin and Evolution of the Vertebrate Immune System (Current Topics in Microbiology and Immunology, 248)
by L. Du Pasquier (Editor), G. W. Litman (Editor), Springer Verlag, May 2000

...although this one is already sorely out of date.  There are sample pages online at, you can take a look and see all the different topics that are discussed.

Here's my question: would you, if you read only Dembski's work, including his profligate pronouncements about the lack of literature on the evolution of IC systems, have ever found out about this book?  Something like 30+ academics, mostly with PhDs in immunology, contributed to that volume, and yet to the ID movement it simply doesn't exist.  There are far more biologists studying the evolution of the immune system, than there are IDists of any stripe seriously studying the origin of anything.

*This* is why the biological community at large is unimpressed with ID.  The only people ID can snowjob are folks like you, jon_e, who might not be aware of literature like this.  Don't you think that Dr. Dembski should retract his assertions regarding the literature until such time as he deals with the literature on the evolution of the immune system?

Actually, let's have a vote, people can say "yea" or "nay" as they desire:

Should Dr. Dembski retract his assertions regarding the literature until such time as he deals with the literature on the evolution of the immune system?


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(Permalink) Posted: July 24 2003,14:38   

PLA writes,


Question for Nic:

Do you think Melendez-Hevia et al. 1996 have explained the origin of the Krebs citric acid cycle? In other words, should the rest of the scientific community now consider that problem solved?
I would say that they achieved a reasonably detailed approximation of the True Full Explanation.  Like everything in science, improvements are always possible.  Also, not absolutely everything one might want to know should be expected to be in that single paper, it is built on a large number of papers cited, e.g.:


References [cutting those not specifically on the topic]

Baldwin JE, Krebs H (1981) The evolution of metabolic cycles. Nature 291:381–382

Buchanan BB, Arnon DI (1990) A reverse Krebs cycle in photosynthesis: consensus at last. Photosynth Res 24:47–53

Evans MCW, Buchanan BB, Arnon DI (1966) A new ferredoxindependent carbon reduction cycle in a photosynthetic bacterium. Proc Natl Acad Sci USA 55:928–934

Gest H (1981) Evolution of the citric acid cycle and respiratory energy conversion in prokaryotes. FEMS Microbiol Lett 12:209–215

Gest H (1987) Evolutionary roots of the citric acid cycle in prokaryotes. Biochem Soc Symp 54:3–16

Jacob F (1977) Evolution and tinkering. Science 196:1161–1166

Mason SF (1992) Chemical evolution. Clarendon Press, Oxford, pp 122–128

Mele´ndez-Hevia E (1990) The game of the pentose phosphate cycle: a mathematical approach to study the optimization in deisgn of metabolic pathways during evolution. Biomed Biochim Acta 49:903– 916

Mele´ndez-Hevia E, Isidoro A (1985) The game of the pentose phosphate cycle. J Theor Biol 117:251–263

Mele´ndez-Hevia E, Torres NV (1988) Economy of design in metabolic pathways: further remarks on the pentose phosphate cycle. J Theor Biol 132:97–111

Mele´ndez-Hevia E, Waddell TG, Shelton ED (1993) Optimization of molecular design in the evolution of metabolism: the glycogen molecule. Biochem J 295:477–483

Mele´ndez-Hevia E, Waddell TG, Montero F (1994) Optimization of metabolism: the evolution of metabolic pathways toward simplicity through the game of the pentose phosphate cycle. J Theor Biol 166:201–220

Mortlock RP (ed) (1992) Evolution of metabolic function. CRC Press, Boca Raton, FL

Schauder R, Eikmanns B, Thauer RK, Widdel F, Fuchs G (1986) Acetate oxidation to CO2 in anaerobic bacteria via a novel pathway not involving reactions of the citric acid cycle. Arch Microbiol 145:162–172

Thauer RK (1988) Citric acid cycle, 50 years on. Modifications and an alternative pathway in bacteria. Eur J Biochem 176:497–508

Waddell TG, Geevarghese SK, Henderson BS, Pagni RM, Newton JS (1989) Chemical evolution of the citric acid cycle: sunlight and ultraviolet photolysis of cycle intermediates. Orig Life 19:603–607

Waddell TG, Henderson BS, Morris RT, Lewis CM, Zimmermann AG (1987) Chemical evolution of the citric acid cycle: sunlight photolysis of a-ketoglutaric acid. Orig Life 17:149–153

Waddell TG, Miller TJ (1992) Chemical evolution of the citric acid cycle: sunlight photolysis of the aminoacids glutamate and aspartate. Orig Life 21:219–223

Weitzman PDJ (1985) Evolution of the citric acid cycle. In: Schleifer KH, Stackebrandt E (eds) Evolution of prokaryotes, Academic Press, London, pp 253–273
And research following this paper has advanced things even further:

Link to 175 related articles (some before, some after 1996)

A question for you, PLA: how much of this literature would you have expected to exist, if you relied on Dembski for your information?


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(Permalink) Posted: July 24 2003,22:51   


The bridge metaphor is pretty misleading, as M-H documented that functional organisms can exist without the full TCA cycle, that "shortcuts" across the cycle exist, etc.

But, since you asked, it appears that succinyl-CoA synthetase is part of a family of related enzymes:

Pfam CoA-ligase family entry

This article says that succinyl-CoA synthetase is homologous to acetyl-CoA synthetases and acyl-CoA synthetases:


J Biol Chem. 2000 Feb 25;275(8):5794-803.  
Acetyl-CoA synthetase from the amitochondriate eukaryote Giardia lamblia belongs to the newly recognized superfamily of acyl-CoA synthetases (Nucleoside diphosphate-forming).

Sanchez LB, Galperin MY, Muller M.

The gene coding for the acetyl-CoA synthetase (ADP-forming) from the amitochondriate eukaryote Giardia lamblia has been expressed in Escherichia coli. The recombinant enzyme exhibited the same substrate specificity as the native enzyme, utilizing acetyl-CoA and adenine nucleotides as preferred substrates and less efficiently, propionyl- and succinyl-CoA. N- and C-terminal parts of the G. lamblia acetyl-CoA synthetase sequence were found to be homologous to the alpha- and beta-subunits, respectively, of succinyl-CoA synthetase. Sequence analysis of homologous enzymes from various bacteria, archaea, and the eukaryote, Plasmodium falciparum, identified conserved features in their organization, which allowed us to delineate a new superfamily of acyl-CoA synthetases (nucleoside diphosphate-forming) and its signature motifs. The representatives of this new superfamily of thiokinases vary in their domain arrangement, some consisting of separate alpha- and beta-subunits and others comprising fusion proteins in alpha-beta or beta-alpha orientation. The presence of homologs of acetyl-CoA synthetase (ADP-forming) in such human pathogens as G. lamblia, Yersinia pestis, Bordetella pertussis, Pseudomonas aeruginosa, Vibrio cholerae, Salmonella typhi, Porphyromonas gingivalis, and the malaria agent P. falciparum suggests that they might be used as potential drug targets.
...and this article is about the origin of acetyl-CoA synthase:


Orig Life Evol Biosph. 2001 Aug-Oct;31(4-5):403-34.

The evolution of acetyl-CoA synthase.

Lindahl PA, Chang B.

Acetyl-coenzyme A synthases (ACS) are Ni-Fe-S containing enzymes found in archaea and bacteria. They are divisible into 4 classes. Class I ACS's catalyze the synthesis of acetyl-CoA from CO2 + 2e-, CoA, and a methyl group, and contain 5 types of subunits (alpha, beta, gamma, delta, and epsilon). Class II enzymes catalyze essentially the reverse reaction and have similar subunit composition. Class III ACS's catalyze the same reaction as Class I enzymes, but use pyruvate as a source of CO2 and 2e-, and are composed of 2 autonomous proteins, an alpha 2 beta 2 tetramer and a gamma delta heterodimer. Class IV enzymes catabolize CO to CO2 and are alpha-subunit monomers. Phylogenetic analyses were performed on all five subunits. ACS alpha sequences divided into 2 major groups, including Class I/II sequences and Class III/IV-like sequences. Conserved residues that may function as ligands to the B- and C-clusters were identified. Other residues exclusively conserved in Class I/II sequences may be ligands to additional metal centers in Class I and II enzymes. ACS beta sequences also separated into two groups, but they were less divergent than the alpha's, and the separation was not as distinct. Class III-like beta sequences contained approximately 300 residues at their N-termini absent in Class I/II sequences. Conserved residues identified in beta sequences may function as ligands to active site residues used for acetyl-CoA synthesis. ACS gamma-sequences separated into 3 groups (Classes I, II, and III), while delta-sequences separated into 2 groups (Class I/II and III). These groups are less divergent than those of alpha sequences. ACS epsilon-sequence topology showed greater divergence and less consistency vis-a-vis the other subunits, possibly reflecting reduced evolutionary constraints due to the absence of metal centers. The alpha subunit phylogeny may best reflect the functional diversity of ACS enzymes. Scenarios of how ACS and ACS-containing organisms may have evolved are discussed.
Or, we could just note that the CoA ligase family includes ATP-citrate lyase, which is a component of the rest of the TCA cycle.

(all of this is assuming I'm not making a terminological mistake somewhere, the naming of components is a bit confusing as enzymes get called different things depending on which way the reaction is being run, etc.)

Conclusion: succinyl-CoA synthetase didn't come from nowhere, homologous enzymes were present before the TCA cycle was completed.

PS: Dembski, I believe, raised this same argument in one of his debates with Ken Miller/Wes Elsberry.  Why didn't he look for the above literature first?

  11 replies since July 22 2003,20:51 < Next Oldest | Next Newest >  


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