Joined: May 2002
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:
An example article showing recent experimental support for the hypothesis:
|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 . This hypothesis was strengthened by the discovery that the RAG genes are tightly linked , 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.|
There is a great deal of related literature on this evolutionary hypothesis.
|Immunol Res. 1999;19(2-3):169-82.|
Transposition mediated by RAG1 and RAG2 and the evolution of the adaptive immune system.
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.
The evolutionary model even made it into Nature:
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:
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].
(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.