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Author
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Topic: Organisms using GAs vs. Organisms being built by GAs
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William A. Dembski
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Member # 7
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posted 13. September 2002 19:08
It seems clear that organisms employ GAs to solve many of the tasks of living (cf. the immune system). But why should that provide confirmation for organisms being the result of GAs (e.g., through a Darwinian evolutionary process). It seems that the immune system, for instance, is a general purpose GA that targets an interloper, sets up a gradient that tracks the interloper, and then runs a GA adapted to that gradient whose output is a molecular assemblage that vanquishes the interloper. All of this sounds very high-tech and programmed. What's more, none of this contradicts my work in NFL. GPGAs (General Purpose Genetic Algorithms) show all the hallmarks of design.
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yersinia
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Member # 324
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posted 13. September 2002 21:08
Dr. Dembski,
quote:
It seems that the immune system, for instance, is a general purpose GA that targets an interloper, sets up a gradient that tracks the interloper, and then runs a GA adapted to that gradient whose output is a molecular assemblage that vanquishes the interloper.
Interesting idea. However, it creates a paradox, as innumerable microorganisms have complex -- usually irreducibly complex -- systems that they use to avoid, subvert, or destroy the immune system (or that help the microorganism to do so). The flagellum of No Free Lunch fame is one of these [1], as is the Type III secretion system [2].
Note that this is not an "argument from evil", rather it is a simple logical paradox: putatively "high-tech" designs are working in direct opposition to each other. Unless the paradox is resolved the probability of the design hypothesis would appear to be lessened.
quote:
All of this sounds very high-tech and programmed. What's more, none of this contradicts my work in NFL. GPGAs (General Purpose Genetic Algorithms) show all the hallmarks of design.
The difficulty here is that the immune system shows numerous hallmarks of evolution, and indeed there are numerous extant organisms getting by with only pieces of this irreducibly complex system. Study of these organisms has resulted in a reasonably detailed, and highly testable, outline of the evolution of the vertebrate immune system [3]. That this has been done for one of the premier IC systems would appear to have sobering implications for the design hypothesis.
(1) Giron JA, Torres AG, Freer E, Kaper JB. The flagella of enteropathogenic Escherichia coli mediate adherence to epithelial cells. Mol Microbiol 2002 Apr;44(2):361-79
(2) Cornelis GR, and Frédérique Van Gijsegem. Assembly and function of Type III secretory systems. Annu. Rev. Microbiol. 2000. 54:735-774.
(3) Inlay, Matt (2002). "Evolving Immunity: A Response to Chapter 6 of Darwin's Black Box". Talk.design archive. See especially the extensive references listed.
[ 13 September 2002, 21:26: Message edited by: yersinia ]
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Frances
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Member # 169
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posted 14. September 2002 18:56
As Yersina has argued, the immune system shows a lot of evidence of natural design. Perhaps we should ask the better question: How did intelligent design implement the approaches so succesfully applied by natural design? Perhaps we are approaching the whole issue from the wrong direction?
May I also ask Dembski about the relevance of the recent findings that NFL theorems may not even apply to evolutionary algorithms. It seems to me that the NFL theorems by itself are not sufficient to show that GAs combined with random mutations cannot generate CSI.
On Classes of Functions for which No Free Lunch Results Hold
Christian Igel Marc Toussaint
quote:
Abstract
In a recent paper it was shown that No Free Lunch results hold for any subset F of the set of all possible functions from a finite set X to a finite set Y iff F is closed under permutation of X. In this article, we prove that the number of those subsets can be neglected compared to the overall number of possible subsets. Further, we present some arguments why problem classes relevant in practice are not likely to be closed under permutation.
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Martin F. Poenie
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Member # 10
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posted 14. September 2002 21:49
Yesinia wrote:
“The difficulty here is that the immune system shows numerous hallmarks of evolution, and indeed there are numerous extant organisms getting by with only pieces of this irreducibly complex system. Study of these organisms has resulted in a reasonably detailed, and highly testable, outline of the evolution of the vertebrate immune system [3]. That this has been done for one of the premier IC systems would appear to have sobering implications for the design hypothesis.”
Something needs to be clarified here because as it stands, the statement above is quite misleading, no doubt due to the influence of the article by Mark Inlay
1. The combinatorial or adaptive immune response is first seen in sharks and not in lower agnathans and lower eukaryotes. Agnathans have neither spleen nor thymus although they do have presumptive gut lymphoid tissue. This is in itself interesting because Spi genes, a marker for B lymphocytes, have been detected in lampreys. Even so, these presumptive lymphocytes do not have the elements of the combinatorial immune system and their actual function is not known.
Shintani, S., J. Terzic, A. Sato, M. Saraga-Babic, C. O'HUigin, H. Tichy, and J. Klein. 2000. Do lampreys have lymphocytes? The Spi evidence. Proc Natl Acad Sci U S A. 97:7417-22.
2. At the heart of the combinatorial immune system are the RAG1 and RAG2 genes. These genes are:
A. Not related to each other.
B. Highly conserved in vertebrates
C. Responsible for the only known site specific recombination in vertebrates
D. Not present in agnathans or lower eukaryotes.
The similarity of RAG1 to bacterial transposases, the absence of introns in the RAG genes and their abrupt appearance in sharks has led to the suggestion that these jumped into the genome as a lateral gene transfer event. If so this is a remarkable story – that two different genes jumped into the germs cells of an agnathan, integrate into an Ig molecule and then generate the diversity of antibody and TcR molecules. At essentially the same time we get the MHC genes (see below) and probably the jaw and thymus to boot.
Gellert, M. 2002. V(D)J recombination: rag proteins, repair factors, and regulation. Annu Rev Biochem. 71:101-32.
Bartl, S., D. Baltimore, and I.L. Weissman. 1994. Molecular evolution of the vertebrate immune system. Proc Natl Acad Sci U S A. 91:10769-70.
Laird, D.J., A.W. De Tomaso, M.D. Cooper, and I.L. Weissman. 2000. 50 million years of chordate evolution: Seeking the origins of adaptive immunity. Proc. Natl. Acad. Sci. U.S.A. 97:6924–6926.
3. The MHC class 1 and class 2 genes that function in antigen presentation appear just as abruptly in sharks as do the RAG genes.
Klein, J., and A. Sato. 1998. Birth of the major histocompatibility complex. Scand J Immunol. 47:199-209.
4. The TcR and Ig genes make their first appearance in Sharks. With respect to finding ancestral sequences to these genes I quote directly from Laird et al., (2000) and include their citations.
“Many investigations have approached the hypothesized primordial receptor by searching for relics of Ig-type molecules in classes of organisms that diverged before agnathans. Sequences isolated from hagfish (15, 16), tunicate (17), and sponge (14, 18) aligned with canonical Ig domains produce a similarity score that falls into the ‘twilight zone’ of questionable homology’’
Laird, D.J., A.W. De Tomaso, M.D. Cooper, and I.L. Weissman. 2000. 50 million years of chordate evolution: Seeking the origins of adaptive immunity. Proc. Natl. Acad. Sci. U.S.A. 97:6924–6926.
Citations from Laird et al., (2000)
14. Blumbach, B., Diehl-Seifert, B., Seack, J., Steffen, R., Muller, I. M. & Muller, W. E. G. (1999) Immunogenetics 49, 751–776.
15. Varner, J., Neame, P., Litman, G. W. (1991) Proc. Natl. Acad. Sci. USA. 88, 1746–1750.
16. Raison, R. L. & Hildemann, W. H. (1984) Dev. Comp. Immunol. 8, 99–108.
17. Pancer, Z., Diehl-Seifert, B., Rinkevich, B. & Muller, W. E. (1997) DNA Cell Biol. 16, 801–806.
18. Pancer, Z., Skorokhod, A., Blumbach, B.&Muller W. E. (1998) Gene 207, 227–233.
19. Doolittle, R. F. (1987) URFs and ORFs: A Primer on How to Analyze Derived Amino Acid Sequences
5. There is much continuity between the innate immunity of lower eukaryotes and vertebrates but to say that there “are numerous extant organisms getting by with only pieces of this irreducibly complex system” seems to confuse the two systems
(innate versus adaptive immunity) one of which seems to have a long evolutionary history and the other that arises dramatically and suddenly in an event appropriately dubbed the “Immunological Big Bang” (Schluter et al., 1999). This is not to say that there are no developments after the initial emergence of the combinatorial immune system but the basic system is all present in sharks.
Schluter, S.F., R.M. Bernstein, H. Bernstein, and J.J. Marchalonis. 1999. 'Big Bang' emergence of the combinatorial immune system. Dev Comp Immunol. 23:107-11.
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yersinia
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Member # 324
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posted 15. September 2002 04:21
Dr. Poenie,
I think that, on Dembski's irreducible complexity argument (where maintaining function of a system with a minimum number of parts is the primary criterion), the adaptive immune system must be considered as part of the whole immune system. The function is protection from harmful pathogens, or more precisely, distinguishing self from non-self and eliminating non-self.
The problem is that the adaptive immune system is clearly not a "necessary part" for the function of immunity, as numerous organisms have immunity without having the adaptive immune system. Sure, if you define functions narrowly enough you can create an irreducibly complex system for anything in biology (the IC function of system X is X-dependent function), but the point of the IC argument was that there could be no functional precursors. The adaptive immune clearly has functional precursors in the innate immune system.
That the adaptive immune system emerged (probably) after the divergence of lampreys and before the common ancestor of cartilaginous fish and the rest of vertebrates is well-known, and is indeed stated in paragraph 2 of (Matt) Inlay's article.
In support of my contention, that the "adaptive immune clearly has functional precursors", I cite:
1) Your point #1, where you reference (as does Inlay) the presence of B lymphocytes in agnathans as discussed by Shintani et al. Inlay puts it thus:
quote:
Recent data also suggests that lampreys have lymphocytes, but since lymphocytes in all other vertebrates utilize rearranging antigen receptors, their role in lamprey immunity remains unclear (Shintani, Terzic et al. 2000).
In other words, lampreys have a part that is used in adaptive immunity, except that they don't have adaptive immunity (apparently; I do wonder if they have some beginnings of it). Clear case of a "precursor" if I ever saw one. Even if we treated the adaptive immunity sub-system as the IC system, this constitutes a precursor which, despite missing parts, is still functional.
2) Regarding your point #2, on the origin of the Recombination Activating Gene (RAG) proteins; first, non-rearranging receptors are indeed useful as they are found both in animals with and without the adaptive immune system; second, while you note the similarity to transposons:
quote:
The similarity of RAG1 to bacterial transposases, the absence of introns in the RAG genes and their abrupt appearance in sharks has led to the suggestion that these jumped into the genome as a lateral gene transfer event. If so this is a remarkable story -- that two different genes jumped into the germs cells of an agnathan, integrate into an Ig molecule and then generate the diversity of antibody and TcR molecules. At essentially the same time we get the MHC genes (see below) and probably the jaw and thymus to boot.
...but you don't acknowledge that this "story" is in fact a well-supported hypothesis with just the kind of support in the literature (dozens/hundreds of articles) that Dembski has asked for in numerous recent ISCID threads. (I would also note that there are rather a lot of extinct placoderms and such that should be taken into account when considering the "suddenness" of the transitions that occurred between jawless and jawed fish.
Inlay notes that the original article in which the transposon hypothesis was proposed (Sakano et al. 1979) has been cited by 706 other research articles. And in fact Inlay documents that recent observations have refined and strengthened the hypothesis:
quote:
V(D)J recombination shares a lot of similarity to transposition (Lewis and Wu 1997; Lewis 1999; Schatz 1999). The RAG genes are closely linked on the mammalian genome, being only 8 kb apart (Oettinger, Schatz et al. 1990). Additionally, each gene is encoded by a single exon. This type of genomic organization is rare for higher eukaryotes, but common for genes contained within transposons. Additionally, the RSS sequences are similar to the inverted repeat sequences used by many transposons (Dreyfus 1992). The reaction itself has many features similar to transposition (Spanopoulou, Zaitseva et al. 1996). For instance, the cleavage reaction mediated by the RAGs leads to the formation of a DNA hairpin intermediate structure (Roth, Menetski et al. 1992). Transposases, such as the Tn10 transposase in bacteria, can also generate similar hairpin intermediates (Kennedy, Guhathakurta et al. 1998). This feature is also shared by retroviruses during integration (Van Gent, Mizuuchi et al. 1996). However, the strongest piece of evidence favoring a transposase origin for V(D)J recombination was the demonstration of transposase activity by RAGs in vitro (Agrawal, Eastman et al. 1998; Hiom, Melek et al. 1998). Two research groups independently discovered that purified RAG proteins in vitro could not only excise a DNA region flanked by RSSs, but also reinsert that region into another location (transposition). The ability to transpose a region of DNA to a new genomic location has no use in V(D)J recombination, and does not occur in vivo. With that discovery, there can be little doubt that the similarities between the two processes are more than coincidental.
You can call it a "remarkable story" if you like but let us be clear that your argument is not with me but with a rather large number of immunologists and their literature.
Even the articles you cite support the transposon hypothesis:
Gellert, M. 2002. V(D)J recombination: rag proteins, repair factors, and regulation. Annu Rev Biochem. 71:101-32.
quote:
The RAG proteins are also capable of transposing RSS-ended fragments into new DNA sites. This transposition helps to explain the mechanism of RAG action and supports earlier proposals that V(D)J recombination evolved from an ancient mobile DNA element.
Bartl, S., D. Baltimore, and I.L. Weissman. 1994. Molecular evolution of the vertebrate immune system. Proc Natl Acad Sci U S A. 91:10769-70. (Full text online BTW)
...is of course a brief 2-page review article that Behe mistakenly took as the "best" available one putting forth the transposon hypothesis when he wrote Darwin's Black Box (discussed in detail by Inlay)...
Laird, D.J., A.W. De Tomaso, M.D. Cooper, and I.L. Weissman. 2000. 50 million years of chordate evolution: Seeking the origins of adaptive immunity. Proc. Natl. Acad. Sci. U.S.A. 97:6924-6926. (Also full text free online)
...is a commentary on the Shintani et al. article discussed above. Looks like Dembski has an entire field of people he has to deal with if he is to continue asserting that testable models do not exist for the origins of complex systems:
quote:
With the unavailability of either fossilized Cambrian nucleic acid or time travel, evolutionary immunologists primarily rely on comparative tools using extant species. Recent investigations into the phylogenetic origin of this complex system derive from four different approaches: (i) the study of the evolution of rearranging receptors, (ii) the study of the origin and assembly of MHC, (iii) the study of the origins of self-nonself recognition systems such as histocompatibility, and (iv) the study of lymphocyte phylogeny. A paper in this issue of PNAS by Shintani et al. (4) advances our understanding of the cellular mediators of adaptive immunity by tracing the origins of the Spi family of lymphocyte-specific transcription factors in the jawless fish. Here we attempt to situate this finding from the laboratory of Jan Klein within the field of evolutionary immunology.
...and it looks like Laird et al.'s opinion on the transposon hypothesis is quite favorable as well:
quote:
Rearranging Antigen Receptors. Much attention has focused on the epicenter of rearrangement, RAG1/2, the lymphocyte-specific proteins that create nicks between germline chromosomal V, D, and J components of Igs and TCR. The curious genomic proximity of RAG1 and -2, their absence of introns (5), and their detection in sharks but not protochordates first inspired the hypothesis of their origin by horizontal transfer to a vertebrate ancestor (6). Similarity between the mechanisms of DNA cleavage for RAG recombination, retroviral integration, and transposition corroborated the hypothesis that RAG1 and RAG2 entered together on a retrotransposon (7-11). It is thought that a retrotransposon containing RAG1 and -2 integrated into a large cis promoter element. Once translated, RAG proteins mediated transposition of a gene segment flanked by short recombination signal sequences (RSS) into a primordial receptor gene, first splitting the gene into fragments that became V, D, and J through duplication (12). Whether RAG fortuitously planted itself into a uniquely lymphoid promoter or acquired specificity later is unclear.
...and in fact Laird et al. also comment rather more on the origin of TcR and Ig genes (by looking for potential non-rearranging precursors) than is shown by the quote you give (more below in point 4).
3) Regarding MHC genes, the very Laird et al. article that you quoted above gives us some evidence of precursors, although apparently research into the origins of the MHC genes is just beginning. Following up on some of the further research that is hinted at in the Laird article, we get:
quote:
Magor BG, De Tomaso A, Rinkevich B, Weissman IL. Immunol Rev 1999 Feb;167:69-79
Allorecognition in colonial tunicates: protection against predatory cell lineages?
The MHC molecules have been historically perceived as transplantation antigens, though it is now recognized that their primary, if not sole, role is in eliminating parasites and in surveillance and clearance of aberrant self. Indeed, pregnancy in mammals would represent the closest to a natural transplantation process that occurs in vertebrates. However, among the immediate ancestors to the vertebrates, natural intraspecific allorecognition processes are common. Among members of the colonial tunicate Botryllus schlosseri, two individuals that share a single allele of the highly polymorphic fusibility/histocompatibility (Fu/HC) locus are able to fuse with one another. Could this Fu/HC be related to the MHC such that the MHC really did have its origins as a transplantation antigen? Presently we review the genetics and biology of natural transplantation processes in colonial tunicates, comparing it with allorecognition as mediated through the vertebrate T-cell receptor, killer cell inhibitory receptor/Ly49, and MHC. Experimental approaches to determining if the molecules regulating allorecognition in tunicates have any ancestral relationship to the vertebrate MHC are discussed, as is a genomic approach to isolating novel mediators of allorecognition. We also explore the biological basis for allorecognition in colonial tunicates and recent work that highlights the costs of not maintaining a system for allorecognition.
...and...
quote:
Flajnik MF, Kasahara M. Immunity 2001 Sep;15(3):351-62
Comparative genomics of the MHC: glimpses into the evolution of the adaptive immune system.
MHC gene organization (size, complexity, gene order) differs markedly among different species, and yet all nonmammalian vertebrates examined to date have a true "class I region" with tight linkage of genes encoding the class I presenting and processing molecules. Three paralogous regions of the human genome contain sets of linked genes homologous to various loci in the MHC class I, class II, and/or class III regions, providing insight into the organization of the "proto MHC" before the emergence of the adaptive immune system in the jawed vertebrates.
4) Dr. Poenie writes
quote:
4. The TcR and Ig genes make their first appearance in Sharks. With respect to finding ancestral sequences to these genes I quote directly from Laird et al., (2000) and include their citations.
"Many investigations have approached the hypothesized primordial receptor by searching for relics of Ig-type molecules in classes of organisms that diverged before agnathans. Sequences isolated from hagfish (15, 16), tunicate (17), and sponge (14, 18) aligned with canonical Ig domains produce a similarity score that falls into the ‘twilight zone’ of questionable homology"
You treat this like it is some great point against the existence for Ig precursors, but after 500 million+ years of independent evolution it is not particularly surprising that sequence similarity is weak. And in fact if we look up e.g. ref 15, we find that the identification of a molecule as an immunoglobulin homolog is based on much more than just weak sequence similarity (although they can do great stuff with just this these days anyhow, see the extensive thread on PSI-BLAST and weak but consistently recoverable sequence similarity )
E.g., ref 15 abstract:
quote:
We have isolated, characterized, and partially sequenced immunoglobulin from the most primitive extant nonvertebrate craniate, the hagfish, a jawless fish that may have diverged from the vertebrate lineage more than 500 million years ago. The 160-kDa protein, which is a minor serum component, is composed of two different heavy chains of 69 and 74 kDa and a light chain of 29 kDa and resembles known immunoglobulin on the basis of an equimolar ratio of heavy and light chains, N-linked glycosylation of heavy chains, presence of intra- and interchain disulfide bonds, and polydispersity of each peptide chain. High molecular mass (polymeric) as well as low molecular mass (monomeric) forms were isolated from serum. The hagfish immunoglobulin is unique in that each heterodimer is composed of two different heavy chains and two light chains. The partial peptide maps and amino acid compositions of the two heavy chains differ; the chains do not crossreact immunologically. Slight crossreactivity of the 74-kDa heavy chain with antisera against purified shark immunoglobulin and some conservation of amino acid sequences, including those surrounding a cysteine, suggest that the isolated protein is an immunoglobulin.
Returning to Laird et al., in addition to the quote you include, directly before it we have Laird et al. citing more evidence of Ig and TCR precursors:
quote:
Ig and TCR molecules feature a structural motif comprised of ß-pleated sheets, known as the “Ig fold,” whose archtypical presence in receptors and adhesion molecules through phylum Chordata and even in invertebrates (13, 14) dates it before the entrance of RAG.
...and right after the quote we have still more evidence cited:
quote:
Another line of investigation begins with the analysis of vertebrate non-rearranging Ig-like receptors in hopes of gleaning information about the structure of the ancestral pre-RAG receptor. [etc.]
Just for kicks, here is yet another article documenting precursors of the adaptive immune system, here immunoglobulin homologs in sponges:
Muller WE, Blumbach B, Muller IM. Evolution of the innate and adaptive immune systems: relationships between potential immune molecules in the lowest metazoan phylum (Porifera) and those in vertebrates. Transplantation 1999 Nov 15;68(9):1215-27
quote:
"Precursors" of the second type of immune response in mammals, the adaptive immune system, have been traced in sponges. It is shown that the expression of a lymphocyte-derived cytokine from mammals is up-regulated during non-self-recognition in S. domuncula. Finally, in G. cydonium, two classes of receptors that comprise Ig-like domains have been identified: the receptor tyrosine kinases and the non-enzymic sponge adhesion molecules. They contain two polymorphic Ig-like domains that are grouped to the variable set of immunoglobulins. The expression of these molecules is also up-regulated during the grafting process. It is concluded that sponges are already provided with a series of elements used in higher vertebrates for both the innate and the adaptive immune recognition.
Summary
To sum up, I conclude that in each of the four areas that Poenie mentions, there is indeed good evidence in the literature supporting my statement that:
quote:
[T]he immune system shows numerous hallmarks of evolution, and indeed there are numerous extant organisms getting by with only pieces of this irreducibly complex system
...and that this is true whether or not we are talking about the immune system in general or the adaptive immune system in particular.
To reemphasize one of my two Main Points in this thread: Dembski has been hinging his arguments on the purported non-existence of testable, well-supported pathways in the literature for the origins of IC systems. Indeed, he recently told ICSID readers that:
quote:
If evolutionary biologists can discover or construct detailed, testable, indirect Darwinian pathways that account for the emergence of irreducibly and minimally complex biological systems like the bacterial flagellum, then more power to them -- intelligent design will quickly pass into oblivion. But until that happens, the eliminative induction that attributes specified complexity to the bacterial flagellum constitutes a legitimate scientific inference.
I argue that this has substantially been done by scientists in the case of the vertebrate immune system. Hundreds of articles on the evolutionary origin of the immune system have been published, numerous predictions have been made and confirmed, much more supporting evidence has been gathered in the 6 years since Behe published Darwin's Black Box (and Behe missed most of the literature even then), and there is a clear path for future research. The only quibble is about how "detailed" is "detailed enough" for Dembski -- I would assert that the relevant criterion should be "detailed enough to be readily testable", and this is manifestly the case for the vertebrate immune system (and this compares rather favorability with the lack of detail and testability in the typical design explanation, "IDdidit").
All of this for a system that Behe highlighted as a premier example of irreducible complexity. And as Dembski argued in No Free Lunch that IC is a special case of specified complexity (and actually the key special case where cumulative evolutionary origin can be ruled out), evolutionary immunology has "dissolved" the putative specified complexity for a very, very complex, "designed-looking", biological system.
Ergo, the "eliminative induction that attributes specified complexity to the bacterial flagellum" or other complex "IC" systems no longer "constitutes a legitimate scientific inference".
yersinia
Leftover references not listed in-text:
Sakano, H., K. Huppi, et al. (1979). "Sequences at the somatic recombination sites of immunoglobulin light-chain genes." Nature 280(5720): 288-94.
Shintani, S., J. Terzic, A. Sato, M. Saraga-Babic, C. O'HUigin, H. Tichy, and J. Klein. 2000. Do lampreys have lymphocytes? The Spi evidence. Proc Natl Acad Sci U S A. 97:7417-22.
[ 15 September 2002, 04:30: Message edited by: yersinia ]
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William A. Dembski
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posted 15. September 2002 08:55
Yersinia,
Could you lay out schematically what your "hallmarks of evolution" are? As you know I have my own "hallmarks of design." From what you've written, the only hallmarks of evolution that I see are that components of supposedly evolved systems (evolved w/o design that is) have homologues in other systems. I don't see any detailed testable evolutionary pathways connecting the systems. In that case, we're back to the familiar conundrum -- is it common descent or common design?
Do enlighten us about your "hallmarks of evolution."
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Martin F. Poenie
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posted 15. September 2002 10:37
Yersinia
First I think my post was either not clear or taken in wrong way. I was supporting the idea that the RAG genes represent a lateral gene transer event. What I think that this illustrates is the way that the conventional line of thought, that adaptive immunity is merely derivative of innate immunity, breaks down. One might have presumed that RAG genes were derived from precursors in lower eukaryotes but all the evidence indicates that they are not.
In a similar vein, there are a lot of examples of tissue rejection reactions in lower eukaryotes such as in the case of tunicates. Here we might also look for a relationship between those histocompatability molecules and the MHC of vertebrates. Here also there appears to be no connection (at least according to J. Klein).
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Frances
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posted 15. September 2002 11:38
Dr Dembski,
It pleases me to hear that you seem to have taken my advice when you state that in absence of detailed pathways for evolution, we now have the conundrum common design or common descent. I find it encouraging that you seem to have taken my advice to not automatically infer design in absence of detailed evolutionary pathways.
But I do not believe that there is a dichotomy here, common descent could have a common designer, whether this is a natural or intelligent designer remains to be seen. Certainly OOL research has proposed several pathways, perhaps not to the full detail you seem to require, but perhaps you could enlighten us with some pathways used for intelligent design?
Perhaps to clarify, what do you consider to be hallmarks of __intelligent__ design? I would argue that IC and CSI mayu be hallmarks of design but do not help us distinguish perse between intelligent and natural design. To make this determination we need detailed pathways that describe a natural and intelligent design and perform the necessary math to determine which of these explanations is the better one.
[ 15 September 2002, 11:39: Message edited by: Frances ]
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yersinia
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posted 15. September 2002 14:32
Dr. Dembski,
quote:
Yersinia,
Could you lay out schematically what your "hallmarks of evolution" are? As you know I have my own "hallmarks of design." From what you've written, the only hallmarks of evolution that I see are that components of supposedly evolved systems (evolved w/o design that is) have homologues in other systems.
In other words, what we have is parts--numerous parts of an IC system (on Behe's authority) that are functional nonetheless. This is precisely what the IC/ID logic says cannot exist.
It is, on the other hand, what natural evolution (random mutation, natural selection, etc.) -- or natural design if you prefer -- predicts.
For a previous discussion about confirming the action of natural processes in ancient events, see this thread on ARN, gene duplications in chordate evolution.
The basic summary of what, to me, constitute "hallmarks of (natural) evolution":
(1) Modernly-observed RM&NS mechanisms should be detected in the ancient data. That is, processes that we observe today should leave evidence in the molecular data -- gene duplication, deletions, insertions, etc. We see this kind of thing in the study of the immune system, in spades.
(2) Inferred events in the ancient data (e.g. polyploidy) should be detectable in modern/ recent organisms in the lab and the wild. An example of this is the study of transposons in modern organisms by the evolutionary immunologists.
(3) Natural evolution, not having foresight, and not being able to design anything from scratch, can only make use of variation that mutation (broadly defined to include gene duplications, insertions, etc.) tosses up. Since the capabilities of chance alone are very very limited, this means that basically selection is limited to acting on modifications of previous systems. Therefore the hallmarks of evolution include (1) cooption of parts, (2) specialization of rudimentary functions, and therefore (3) close study of "innovations" should reveal precursors in more basally-divergent systems; new stuff is modified old stuff.
And again, we see these in spades in the evolution of the immune system.
quote:
I don't see any detailed testable evolutionary pathways connecting the systems. In that case, we're back to the familiar conundrum -- is it common descent or common design?
That's because you haven't read the literature; start here: Evolving immunity by Matt Inlay. Or, if you don't want to read his nice user-friendly introduction to the topic, you can type "evolution immune system" into PubMed and read things like this recent review article from July 2002:
quote:
Cohn M. Immunol Rev 2002 Jul;185(1):24-38
The immune system: a weapon of mass destruction invented by evolution to even the odds during the war of the DNAs.
Living systems operate under interactive selective pressures. Populations have the ability to anticipate the future by generating a repertoire of elements that cope with new selective pressures. If the repertoire of such elements were transcendental, natural selection could not operate because any one of them would be too rare. This is the problem that vertebrates faced in order to deal with a vast number of pathogens. The solution was to invent an immune system that underwent somatic evolution. This required a random repertoire that was generated somatically and divided the antigenic universe into combinatorials of determinants. As a result, it became virtually impossible for pathogens to escape recognition but the functioning of such a repertoire required two new regulatory mechanisms: 1) a somatic discriminator between Not-To-Be-Ridded ('Self') and To-Be-Ridded ('Non-self') antigens, and 2) a way to optimize the magnitude and choice of the class of the effector response. The principles governing this dual regulation are analyzed in the light of natural selection. [outline]
...and of course the 102 related articles (not a comprehensive list by any means) could be browsed for starters.
[edited to fix link-yersinia]
The only other possibility is that current ideas are not detailed enough for you, but then again you have never specified or justified any criteria as to what constitutes a sufficient level of detail. I have proposed that the relevant criterion is "detailed enough to be testable", and that this criterion has been meant easily in the case of evolutionary immunology.
quote:
Do enlighten us about your "hallmarks of evolution."
Listed above. It wasn't a wildly difficult thing to do, now was it?
yersinia
[ 16 September 2002, 02:46: Message edited by: yersinia ]
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rafe gutman
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posted 15. September 2002 23:51
quote:
by dembski:
the only hallmarks of evolution that I see are that components of supposedly evolved systems (evolved w/o design that is) have homologues in other systems. I don't see any detailed testable evolutionary pathways connecting the systems.
try agrawal and schatz's 1998 nature paper: "Transposition mediated by RAG1 and RAG2 and its implications for the evolution of the immune system.",
or hiom and gellert's 1998 cell paper: "DNA transposition by the RAG1 and RAG2 proteins: A possible source of oncogenic translocations."
their model is that the rag genes appeared through co-option of a transposase. their prediction was that the rag gene products may have retained some of their transposase activity. they looked for it, and found it. is this not a confirmed prediction made from an evolutionary model? what detailed testable models can ID give us for the origin of the adaptive immune system?
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Mike Gene
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posted 16. September 2002 00:49
Yersinia: Since the capabilities of chance alone are very very limited, this means that basically selection is limited to acting on modifications of previous systems.
Might you explain why the capabilities of chance alone are very very limited? Why is natural selection under such constraint?
Therefore the hallmarks of evolution include (1) cooption of parts, (2) specialization of rudimentary functions, and therefore (3) close study of "innovations" should reveal precursors in more basally-divergent systems; new stuff is modified old stuff.
Interesting. And the bacterial flagellum appears to lack any of these hallmarks. Is it safe to assume you don't accept evolution as an explanation for the origin of the flagellum? After all, your hallmarks have teeth, don't they?
BTW, are you suggesting evolution always entails cooption of parts? And it is possible that design might involve cooption of parts?
[ 16 September 2002, 01:54: Message edited by: Mike Gene ]
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yersinia
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posted 16. September 2002 02:13
quote:
Might you explain why the capabilities of chance alone are very very limited? Why is natural selection under such constraint?
Just to be clear, what I mean is that the capabilities of "chance" in terms of i.e. random assembly or random mutation acting alone are very limited. The capabilities of RM&NS together are on the other hand impressive. Surely the reasons that the capabilities of mutation alone are considered limited are well-known to everyone from Dawkins to Dembski, do I really have to repeat it here?
quote:
Therefore the hallmarks of evolution include (1) cooption of parts, (2) specialization of rudimentary functions, and therefore (3) close study of "innovations" should reveal precursors in more basally-divergent systems; new stuff is modified old stuff.
Interesting. And the bacterial flagellum appears to lack any of these hallmarks. Is it safe to assume you don't accept evolution as an explanation for the origin of the flagellum? After all, your hallmarks have teeth, don't they?
You're a bit behind on your literature, Mike, just in late 2001 your statement above was falsified, and plausible precursors for the MotA and MotB proteins of the bacterial flagellum were found:
Kojima S, Blair DF. Conformational change in the stator of the bacterial flagellar motor. Biochemistry 2001 Oct 30;40(43):13041-50
quote:
The occurrence of significant conformational change in the stator has implications not only for the present-day mechanism but also for the evolution of the flagellar motor. A membrane complex that undergoes proton-driven conformational changes could perform useful work in contexts other than (and simpler than) the flagellar motor, and ancestral forms of the MotA/MotB complex might have arisen independently of any part of the rotor. We queried the sequence database using the sequence of the best-conserved part of MotA (the segment containing membrane segments 3 and 4) from Aquifex aeolicus, a species whose lineage is deeply branched from other bacteria. In addition to the expected MotA homologues, the search returned a protein sequence from the archaeal species Methanobacterium thermoautotrophicum (protein MTH1022) that shows significant sequence similarity not only to MotA but also to the protein ExbB (Figure 9). ExbB is a cytoplasmic-membrane protein that functions in conjunction with ExbD, TonB, and outer-membrane receptors to drive active transport of certain essential nutrients across the outer membrane of Gram-negative bacteria. The energy for this transport comes from the proton gradient across the inner membrane. Thus, MotA and ExbB are both components of systems that tap the proton gradient to do work some distance away (at either the rotor-stator interface or the outer membrane; Figure 9).
Other features also point to a connection between the Mot and Exb systems. MotA functions in a complex with MotB, which as noted contains the critical residue Asp32 near the cytoplasmic end of its single membrane segment. ExbB functions in a complex with ExbD, which likewise has a single membrane segment with a critical Asp residue near its cytoplasmic end (Asp25 in ExbD of E. coli; ref 59). Although ExbB has only three membrane segments in contrast to the four in MotA, the membrane segments that show sequence similarity have the same topology. The protein TonB is also present in the complex with ExbB and ExbD (59, 60) and would provide an additional membrane segment to round out the topological correspondence (Figure 9). ExbB contains a well-conserved Pro residue (Pro141 in E. coli ExbB) that is the counterpart of Pro173 of MotA. Although MotB and ExbD do not share close sequence similarity apart from the critical Asp residue, in certain positions in the membrane segment the residues most common in MotB proteins are also common in ExbD proteins. Finally, like the MotA/MotB complex the ExbB/ExbD complex contains multiple copies of each protein (61). Together, these facts make a reasonable case for an evolutionary connection between the Mot proteins of the flagellar motor and the Exb proteins of outer-membrane transport (and by extension the TolQ/TolR proteins, which are related to ExbB/ExbD but whose functions are less understood).
This recent evidence directly refutes a statement that you made in your 3rd flagellum essay stating that
quote:
MotA/MotB, on the other hand, could plausibly exist as some ion channel prior to the existence of the flagella, but there is no evidence of this.
...but now there is. Ain't the advance of science great?
Given that for the archaeal flagellum we also have some homologous, functional, phylogenetically basal precursors (in the Type IV secretion system), and that (contra Behe's IC argument) a subset of the bacterial flagellum (different from the MotAB proteins) is functional as a secretion system (although a phylogenetically basal Type III secretion system has not been discovered...yet) -- and all of this has been discovered just since ~1994 -- I'd say that evolutionary biology is doing reasonably well on this case. Things are progressing. Compared to our understanding of the evolution of the immune system we have a long ways to go, but then the first articles on the evolution of the immune system were published back in the 1970's, and the flagellum is billions of years older than the immune system and only recently has a reasonably complete understanding of the system been reached.
But excepting Kojima and Blair 2001 you and I have been over the flagellum numerous times, Mike. The question in this thread is whether or not the immune system supports Dembski's arguments about IC and SC. Both Dembski and Behe have pretty explicitly asserted that:
(1) (to quote Dembski)
quote:
If evolutionary biologists can discover or construct detailed, testable, indirect Darwinian pathways that account for the emergence of irreducibly and minimally complex biological systems like the bacterial flagellum, then more power to them -- intelligent design will quickly pass into oblivion.
and (2) (more Dembski)
quote:
But until that happens, the eliminative induction that attributes specified complexity to the bacterial flagellum constitutes a legitimate scientific inference.
The existence of piles -- gobbs -- of literature on the evolution of the immune system, including books and articles in numerous top peer-reviewed journals, and including numerous advances just in the last few years, I am arguing, satisfies Dembski's point #1.
Thus, according to Dembski's point #2, the existence of other complex systems such as the bacterial flagellum no longer constitutes good evidence for design. If RM & NS can produce the vertebrate immune system in all of it's glorious, IC (Behe 1996) complexity, then asserting that some extra factor such as ID must be introduced to explain the flagellum is unparsimonious.
I am aware that Mike-Gene-ID is prepared to concede the natural evolution of certain complex, IC things like blood clotting and the immune system and yet maintain the ID inference for other cases of complexity such as the flagellum where the origin events are far more remote and the available evidence is much spottier, but (a) I think that is highly unparsimonious and (b) in any case, this kind of inconsistency is not a part of Dembski's argument, which is what we're talking about.
yersinia
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William A. Dembski
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posted 16. September 2002 11:09
Yersinia,
By your great mass of words and facts you've lost the train of the argument. The issue is not whether pieces exist for cooption (whether in the same organism or, with the immune system, even in different organisms) but whether those pieces can properly be coordinated to produce the final function in the IC system under examination. For cooption to work there has to be coordination. Design is known to have the capability to effect such coordination. You're claiming that natural selection does as well, but there is no evidence of that. The only evidence is of isolated pieces waiting to be coordinated. That's why I insist on **detailed** Darwinian pathways (and no, you haven't provided them). Pathways are continuous trajectories that connect the dots. The issue is not whether the dots are in place but how to connect them. You've offered no evidence that natural selection can do that -- or is your evidence simply that it couldn't have been design and therefore natural selection is all that's left? That sounds like an argument from ignorance.
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Martin F. Poenie
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posted 16. September 2002 12:48
I followed this thread for a short bit and would like to add a few parting comments
1. I do not think that Yersinia made their case in any direct sense. I pointed out two examples where predictions did not hold.
A. The RAG genes are not derivative from lower eukaryotes
B. The vertebrate class I and II MHC do not show homology to molecules in lower eukaryote rejection reactions
This seems to be irrelevant to the argument and it is easy to see why as I show below.
With respect to the RAG genes the argument then takes a turn to show that RAG genes are stand alone transposases and therefore that shows … what? Of course the RAG genes are derived from something. The argument that RAG genes functions as stand alone transposases strengthens the argument that this is a lateral gene transfer event. That is because they are not exactly like bacterial transposases and so one was not sure of the connection or their possible function. The demonstration that they were stand alone transposases showed that they were functional and I think, further strengthens the argument for a lateral gene transfer event. However, as an argument pro or con against evolution, what difference would it make if they were stand alone enzymes or not. I think it would not make a bit of difference.
But the futility of this thread and the arguments go deeper.
A. First, I think the argument of irreducible complexity is well nigh impossible to defend, regardless of the possible truth or falsity of its premise. It will always be subject to the creativity of “this or that might have happened”. Thus I would not want to enter into a defense of that notion.
B. Second, I believe that the arguments made by Yersinia and most antagonists in this debate carry with them a hidden assumption. That assumption is this: any scenario wherein the DNA of an organism might have been altered, whether known now or yet to be discovered is in the domain of natural evolution, natural design or whatever one wants to call it and, by the same token, not it the domain of a designer. Thus insertion of two functional genes due to lateral gene transfer falls under the rubric of random mutation and natural selection because any means of altering the DNA falls under the rubric of mutation and natural selection. In taking this approach, a designer is defined out of the possibility of acting. So what is there to discuss? There is no designer by definition. Mind you, one could not get at the truth or falsity of the premise of a designer by defining it out of existence. The only possibility left is some sort of instant materialization of genes or organisms that one could prove had no origin other than by instant materialization. I for one would not want to find myself arguing for that. Is that what the poles of this discussion are about?
I would like to add to the above the idea that if sudden introduction of new information in terms of new fully functional genes (even though they exist somewhere else in the biosphere) is required for big transitions such as seen in the origin of combinatorial immunity, that would in a way (at least from my perspective) fit with Bill Dembski’s point of view. Perhaps it is more naturalistic than he would like but it still seems to fit.
Finally, there was this bit about the flagella. The argument of the flagella hinges on where Aquifex is located in the scheme of things. From my perspective this is simply impossible to sort out. Doolittle has demonstrated what a mess that lateral gene transfer makes to ancient phylogenies. Phillipe and Forterre have demonstrated what a mess that long branch attraction makes of these phylogenies. Phillipe and Forterre did what seemed to be a very reasonable approach to getting around these problems and came up with eukaryotes at the root of the tree of life. Furthermore, Forterre made what I think is a great argument that the reverse gyrase present in all hyperthermophiles is due to a gene fusion event and thus derivative, calling into question how ancient they are. This was followed by a number of articles suggesting prokaryotes are derivative of eukaryotes, some based on the idea that eukaryotes contain more “relics” of an RNA world.
I do not pretend to be an expert in these issues nor would I like to decide whose idea of the phylogeny of prokaryotes and eukaryotes is correct. However, given the status of things, hinging an argument on deriving the flagella from “older” Aquifex or something like that seems weak. I am not calling this into question as a defense of irreducible complexity, I am simply commenting on the character of these arguments.
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yersinia
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posted 16. September 2002 15:58
Dr. Dembski writes:
quote:
Yersinia,
By your great mass of words and facts you've lost the train of the argument. The issue is not whether pieces exist for cooption (whether in the same organism or, with the immune system, even in different organisms) but whether those pieces can properly be coordinated to produce the final function in the IC system under examination. For cooption to work there has to be coordination. Design is known to have the capability to effect such coordination. You're claiming that natural selection does as well, but there is no evidence of that.
There are no two ways about it, this is false. I think that even Peonie and Mike Gene would agree with me on this one. There are dozens of examples of the origin of new genes and even multigene systems in either modern times or geologically recently enough that the direct evidence of natural selection remains in the genome, and *very* detailed pathways, on the level of individual nucleotide changes, have been traced in many instances.
A few of the examples are described here.
Here is a list, just off the top of my head. References can be found easily by searching PubMed so I trust you will not mind if for the purposes of space I just list some of the cases I know about without giving refs for all of them.
The recent-origin Drosophila genes jingwei and sdic
Nylon degradation genes (multiple independent origins)
Recent origin of antifreeze genes in fish (and plants)
Antibiotic and antipesticide genes
Here is a case of the origin of an autotransporter (AT) gene, lav by domain shuffling; I quote just a bit, the whole rather long article with all of their documenting evidence is freely online at pubmed:
quote:
A mosaic origin for lav was inferred from a G+C content transition at the boundary of its presumed passenger domain with the linker and -barrel domains. Similarly, the junction of nonhomology between lav and las coincides with the G+C transition and inferred domain boundaries of both genes. On the basis of quite different evidence (discordance between phylogenies based on individual domains), Loveless and Saier have proposed that AT proteins evolve by domain shuffling (28). A functionally novel AT can arise by linking a new passenger activity to a generic -barrel pore. Our analysis provides independent evidence for the combinatorial origin and subsequent reshuffling of at least one AT protein.
[...]
As biotype aegyptius strains and Int1 belong to different phylogenetic subgroups, it is unlikely that they inherited lav from a common ancestor. Rather, it is likely that the first H. influenzae clade to acquire the gene passed it to one or more other clades by transformation and homologous recombination within flanking DNA. Once a laterally transferred fragment has been acquired by a population of naturally transformable bacteria, it can readily be assimilated into the species by co-opting linked homologous sequence and uptake signals. Interstrain and interspecies transfer implies a shared selective advantage in certain host environments.
For the evolution of multigene systems, even those with multiple-parts -required, see:
Mortlock, R. P., editor (1992). The Evolution of Metabolic Function Boca Raton Fla., CRC Press, pp. 1-339.
Table of contents:
quote:
1) Experiments in the Evolution of Catabolic Pathways Using Modern Bacteria
2) Natural and Experimentally Evolved Pathways for the Utilization of D-Arabinose in Enteric Bacteria
3) The Development of a Catabolic Pathway for Ethylene Glycol
4) Evolution of [alpha]-Aminoadipate Pathway for the Synthesis of Lysine in Fungi
5) Common Ancestry of Escherichia coli Pyruvate Oxidase and the Acetohydroxy Acid Synthase of the Branched-Chain Amino Acid Biosynthetic Pathway
6) Evolution of Bacterial Alcohol Metabolism
7) Microbial Metabolism of Mandelate: Occurence, Function, Properties, and Evolution of Mandelate Dehydrogenases and Other Enzymes of the Mandelate Pathway
8) Evolution of the Bacterial Phosphoenolpyruvate: Sugar Phosphotransferase System
Section I: Physiologic and Organismic Considerations
Section II: Molecular Considerations
9) An Emerging Outline of the Evolutionary History of Aromatic Amino Acid Biosynthesis
10) Life Before DNA: The Origin and Evolution of Early Archean Cells
11) The Prebiotic Evolution of Complex Molecules: A Central Role for Catalyzed Cells
...and lots of articles published since 1992, e.g.:
On atrazine resistance (lots of articles here)
The degradation of pentachlorophenol by the recent assembly of a multiple-parts-required pathway, e.g.:
Copley SD. Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach. Trends Biochem Sci. 2000 Jun;25(6):261-5.
Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD. Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol. Biochemistry. 2000 May 9;39(18):5303-11.
An even more sophisticated example is Johnson et al.'s (2002) article, "Origins of the 2,4-Dinitrotoluene Pathway". 2,4-dinitrotoluene (DNT) is another recently human-introduced compound, and yet bacteria have assembled a quite complex pathway for its degradation. The summary of the reconstructed evolution of the pathway is also quite complex (and detailed):
quote:
Inferences from the comparison of the structural genes of the 2,4-DNT pathway suggest that the pathway came together from three sources. The initial dioxygenase appears to have originated from a naphthalene degradation pathway like that of strain U2 (17). A large portion of the salicylate hydroxylase oxygenase component is retained but is not functional. The MNC monooxygenase was probably derived from a pathway for degradation of chloroaromatic compounds. The presence of the vestigial (with respect to 2,4-DNT degradation) ortho-ring fission dioxygenase is consistent with its recruitment from a pathway for chloroaromatic compounds. The true ring fission enzyme for 2,4-DNT degradation has a different origin. The sequence of DntD is quite dissimilar to all other described meta-ring fission enzymes, including those from naphthalene and chloroarene degradative pathways. The distinctive sequence of the ring cleavage enzyme reflects the substrate specificity observed for the THT oxygenase (28). The distant relationship between homogentisate dioxygenase and DntD and the association with homologs from amino acid metabolism (dntE and dntG) indicate that the lower pathway operon arose from a gene cluster for amino acid degradation.
The disparate origins of the various dnt and associated genes described in this study are consistent with the difficulties that bacteria face to achieve efficient metabolism of synthetic compounds like 2,4-DNT. The organization of the pathway genes suggests there is a progression towards a compact region en-coding the entire pathway. In that progression, remnants from assembly persist, such as the benzenetriol oxygenase (ORF3), putative maleylacetate reductase (ORF10), and putative trans-posase (ORF4). No role in nitroarene degradation is apparent for the remnants; their presence might indicate an intermediate point in the evolution of an optimal system or perhaps some of the proteins could be used in other pathways when another substrate is available.
And numerous review articles that review the topic of cooption:
Otto SP, Yong P. The evolution of gene duplicates. Adv Genet 2002;46:451-83 Related Articles, Links
Betran E, Long M. Expansion of genome coding regions by acquisition of new genes. Genetica. 2002 May;115(1):65-80.
Kondrashov FA, Rogozin IB, Wolf YI, Koonin EV. Selection in the evolution of gene duplications. Genome Biol 2002;3(2):RESEARCH0008 (free online)
Eizinger A, Jungblut B, Sommer RJ. Evolutionary change in the functional specificity of genes. Trends Genet 1999 May;15(5):197-202
Hughes A. Adaptive evolution after gene duplication. Trends Genet 2002 Sep;18(9):433
Ganfornina MD, Sanchez D. Generation of evolutionary novelty by functional shift. Bioessays. 1999 May;21(5):432-9.
Long M. Evolution of novel genes. Curr Opin Genet Dev 2001 Dec;11(6):673-80
True JR, Carroll SB. Gene Co-Option in Physiological and Morphological Evolution. Annu Rev Cell Dev Biol. 2002
Here's a case of cooption in a slightly different sense, but returning to one of my original points: microbes "designed" to subvert the immune system:
quote:
Immunology 2001 Jan;102(1):2-7
Co-option of endocytic functions of cellular caveolae by pathogens.
Shin JS, Abraham SN.
It is increasingly becoming clear that various immune cells are infected by the very pathogens that they are supposed to attack. Although many mechanisms for microbial entry exist, it appears that a common route of entry shared by certain bacteria, viruses and parasites involves cellular lipid-rich microdomains sometimes called caveolae. These cellular entities, which are characterized by their preferential accumulation of glycosylphosphatidylinositol (GPI)-anchored molecules, cholesterol and various glycolipids, and a distinct protein (caveolin), are present in many effector cells of the immune system including neutrophils, macrophages, mast cells and dendritic cells. These structures have an innate capacity to endocytoze various ligands and traffic them to different intracellular sites and sometimes, back to the extracellular cell surface. Because caveolae do not typically fuse with lysosomes, the ligands borne by caveolar vesicles are essentially intact, which is in marked contrast to ligands endocytozed via the classical endosome-lysosome pathway. A number of microbes or their exotoxins co-opt the unique features of caveolae to enter and traffic, without any apparent loss of viability and function, to different sites within immune and other host cells. In spite of their wide disparity in size and other structural attributes, we predict that a common feature among caveolae-utilizing pathogens and toxins is that their cognate receptor(s) are localized within plasmalemmal caveolae of the host cell.
In other words, like the evidence for the evolution of the immune system, the evidence for cooption by natural processes has gobbs of evidence and literature behind it. Yet Dembski asserts that there is "no evidence" for it.
quote:
The only evidence is of isolated pieces waiting to be coordinated. That's why I insist on **detailed** Darwinian pathways (and no, you haven't provided them). Pathways are continuous trajectories that connect the dots. The issue is not whether the dots are in place but how to connect them.
The previous claim of the IC argument was that the dots couldn't exist because they wouldn't be functional. Now you're conceding that they exist, but quibbling over how "detailed" the reconstructed pathways are, and yet you still refuse to explicitly say what counts as "detailed" for you or to justify that level of detail as an appropriate standard of judgement of evolutionary explanations. The goalposts are on wheels. The standard in science is clear however: testability and passed tests, and this is the one I advocate, and which I think all evolutionary immunologists would argue is being successfully applied in the field. Compared to "IDdidit" (where's your details there, Dr. Dembski?) the reconstructed origin of the immune system is quite detailed, and getting more so all of the time.
quote:
You've offered no evidence that natural selection can do that -- or is your evidence simply that it couldn't have been design and therefore natural selection is all that's left? That sounds like an argument from ignorance.
Nope, the known natural processes of mutation and selection make predictions about what should be seen in the data, which I outlined in a previous post, and in this thread I'm arguing that the evidence and the literature on the origin of the IC immune system supports those predictions. Some have made suggestions in the thread that, basically, maybe ID did it even though it looks like natural processes (employing small changes, cooption etc. predicted by RM&NS) were responsible; this cannot of course be ruled out, but my point is that ID does not *predict* these observations while RM&NS does.
[ 16 September 2002, 17:07: Message edited by: yersinia ]
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