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  Topic: Co-option/change of function, Citations of this in the literature< Next Oldest | Next Newest >  

Posts: 319
Joined: May 2002

(Permalink) Posted: Feb. 17 2003,19:06   

I'd forgotten that I'd accumulated these, they were posted originally in the ISCID immune system thread:

Dr. Dembski writes:



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:


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:

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):

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:


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.  


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.


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.

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