Evolution of Adaptive Immunity V–Complexity evolves, isn’t copied

Behe has basically one arrow in his quiver–life is really complex. Unfortunately for him, complexity is hardly diagnostic of design.  Still, it is fair to say that evolutionary theory must address complexity.  Considered collectively, indeed, life is far more complex than it would ever have to be if it were designed.  That is because evolution is very good at coordinating complex simultaneous and sequential changes.  And it has no ability to do what a designer can do, which is to take what works in one organism and copy it (with any necessary modifications) to work in another organism. 

While horizontal gene transfers are the exception to the rule that evolution does not copy from distantly-related taxa, such transfers can generally be inferred from the evidence, and these events typically do not affect metazoan evolution much.  So although the transposon genes which gave rise to RAG1 and RAG2 genes in gnathostomes (jawed vertebrates) may have transferred from bacteria into eukaryotes, evolution of adaptive immunity had to rely almost entirely upon genes that were vertically transferred, or at least that had been for a very long time.

The adaptive immune system of the agnathans (jawless vertebrates–lampreys and hagfish) is not nearly as well characterized as is the adaptive immune system of gnathostomes.  That it is very different from our immune system is well-understood, however, and some of its evolutionary origins can be understood as well.  Both adaptive immune systems developed largely out of the innate immune sytem, and are highly integrated with innate immunity (the integration is more an educated guess in the case of agnathan adaptive immunity, but well-demonstrated in the case of our own).  And what we see with agnathan adaptive immunity is the ability of evolution to evolve new systems over and over to meet an important need (immunity is one of the most important requirements), and its utter inability to copy anything complex if lateral transfers of genetic material are rare to non-existent.

And of course the usual predictions of evolution (which are not predictions of design, naturally), that similarities between each adaptive immune system which date back to before we diverged from the agnathan line, along with considerable differences arising since then, are to be found when the two immune systems are compared.  I have already quoted the text below in a previous post, but I do so again to establish here the homologies between agnathan and gnathostome immune systems:

Many of the genes for transcription factors involved in gnathostome lymphocyte development can be found in agnathans. SPI-B, IKAROS, EBF, GATA, PAX-2/5/8, and BACH2 gene relatives have all been identified in the lamprey (Rothenberg and Pant, 2004).  Since many of the signaling pathways involved in inflammatory responses, such as the NF-κB pathway, exist in insects, it is not surprising that lymphocyte-like cells in lampreys possess NF-κB and STAT signaling-cascade components. Many additional genes that our lymphocytes use for activation purposes are expressed by lamprey lymphocytes (Mayer et al., 2002 and Pancer et al., 2004b).  These include genes for the CD45 transmembrane protein tyrosine phosphatase, SYK protein tyrosine kinase, Src family members, and the HS-1 adaptor molecule. Lamprey lymphocyte-like cells also express relatives of the CXCR4 chemokine receptor and its SDF-1 ligand, the cytokine interleukin 8 (IL-8) and its receptor, and the IL-17 receptor.  The Evolution of Adaptive Immunity

In my last post, and in many others, I pointed to Behe’s correct statement that Darwinian evolution requires “physical precursors” (DBB, 45), and noted in the last post how gnathostome immunity meets this test (which Behe fails to apply).  Clearly agnathan adaptive immunity meets this test as well, and is thus beholden to inherited accidents.  The flip side of evolutionary prediction states that further development of lines that have diverged will not follow the same pathways, that they are subject not only to natural selection, but also to the contingencies and accidents of mutation–and even of selection (natural selection is also variable).  Which means that anything as complex as gnathostome adaptive immunity essentially could not re-evolve in agnathans, or vice-versa.  However and in whatever sequence the two adaptive immune systems evolved, at least one of the divergent lines simply missed out on the evolution of immunity in the other, and even though the two adaptive immune systems are considered to be “convergent,” they are very different since the two systems diverged.

Here is a diagram and caption explaining the very different recombinatorial functions of agnathan and gnathostome adaptive immune systems. Very simply, the difference is that instead of rearranging V(D)J sections of the TCR/BCR genes, a VLR (variable lymphocyte receptor) gene with three coding segments separated by large non-coding sites (introns) is translated, and–this is one of the most important aspects–LRR (leucine rich repeats) are randomly incorporated into the germline VLR gene.  See the above link, and The Evolution of Adaptive Immunity for a more full explanation, as it is the evidence for the evolution of a very different complex system that is to be discussed here.

While the exact phylogenetic relationships between the LRR-containing genes has not been untangled, many are associated with “innate immunity”, and these include Toll-like receptors in our immune system.  One might expect LRR-containing genes from innate immunity to be the source for the agnathan VLR gene, and of course this may be the case.  The following would tend to suggest as much:

An abundance of ancestral LRR genes were available for the evolutionary development of the VLR recombinatorial immune system seen in lampreys and hagfish. LRR proteins are found in unicellular organisms and throughout the animal and plant kingdoms, where they are used for a variety of purposes, including microbial invasion and host defense responses (Buchanan and Gay, 1996). Well-known examples include the bacterial internalins (Cabanes et al., 2002), plant disease-resistance R proteins (Dangl and Jones, 2001), and Toll-like receptors of the innate immune system (Akira et al., 2006). Due to the large interaction areas provided by their elongated and curved shape, LRR proteins may bind their ligands with very high affinities. These favorable structural and functional characteristics, coupled with the presence of a large number of LRR genes in cephalochordates (Pancer and Cooper, 2006), would have made the different LRR modular units an attractive substrate for generating diversity given the development of a recombinatorial mechanism for randomly assembling them in an agnathan ancestor.  The Evolution of Adaptive Immunity

However, one of best of the currently-known evolutionary links is with vertebrate platelet receptor glycoproteins.  See:  Evolutionary link between agnathan VLRs and vertebrate platelet receptor glycoproteins (From: Evolution and diversification of lamprey antigen receptors: evidence for involvement of an AID-APOBEC family cytosine deaminase, Nature Immunology).  A more recent study finds that same glycoprotein, hagfish VLRB.59 (unsurprisingly), and a human Slit protein to be most closely related to a particular lamprey VLR-antigen complex (Byung Woo Han, et al. “Antigen Recognition by Variable Lymphocyte Receptors,” 26 Sept. 2008 Science  321:1834-1837).

The same source states:

So far, only the binding mode of the TLR[Toll-like receptor]4-MD2 complex is similar to that of antigen recognition by VLRs, in that residues on the concave surface of the N-terminal and central domains of TLR4 interact with MD2.  However, no interaction is seen between LRRCT [C-terminal leucine-rich receptor capping region] of TLR4 and MD2 as observed between the highly variable insert in LRRCT of VLRs and antigens.  Because we do not yet have sufficient VLR [variable lymphocyte receptor] and TLR [Toll-like receptor] complex structures to make statistically significant conclusions, and the number of LRR modules in TLRs is much greater than in VLRs, it may be too early to infer evolutionary relationships between VLRs and TLRs.  (Ibid.)

The general link between the evolution of VLRs and genes containing LRRs seems to be beyond any reasonable doubt, however.

Once again, the predicted evolutionary patterns play out in the evolutionary histories of the two adaptive immune systems.  Homologies exist between the two systems via the “physical precursors” which must exist for “Darwinian” evolution to occur.  Without much lateral transfer of genes, however, accident and contingency interact with natural selection to make quite different adaptive immune systems after the two diverge. 

Mindlessly, the IDists complain that evolution “can’t predict” future evolution, apparently without realizing that one of the predictions of evolution is that much of evolution is not predictable.  This should be understood as an extension of chaos theory, wherein complexity cannot be predicted.  Nevertheless, causal factors can be predicted to produce different patterns.  Design of any type we know would use rationality for a purpose, and would be unhindered by the genetic barriers between taxa, hence would be expected to transfer the design of one organism to another one without any “physical transfer” (actually, as we understand design scientifically, the physical transfer would take place via the designer, but IDists like to pretend that intelligence is non-physical).

Evolution cannot do this, but it can evolve different types of complexity again and again.  Both evolution’s unpredictability vis-a-vis the specific forms that will evolve, and its predictability regarding the homologies that will nevertheless exist via common ancestry, point to only one mechanism, that of evolution.  As Isaac Newton put it:

Rule I. We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances.

To this purpose the philosophers say that Nature does nothing in vain, and more is in vain when less will serve; for Nature is pleased with simplicity, and affects not the pomp of superfluous causes.

Rule II. Therefore to the same natural effects we must, as far as possible, assign the same causes.

As to respiration in a man and in a beast, the descent of stones [meteorites] in Europe and in America, the light of our culinary fire and of the sun, the reflection of light in the earth, and in the planets.  From Principia Mathematica

I went with Newton because, as a theist, he clearly is not trying to do away with God with his rules.  But using just those two rules, we could hardly allow that anything other than unguided evolution gave us the forms of life (building upon the starting form(s) of life, of course), since we cannot bring in extra causes when we have sufficient cause–and especially we cannot bring in causes which are not expected to result in the effects we observe.  Even more, via Rule II, we cannot assign different causes to similar effects, so that when we ascribe homologous “physical precursors” and unrelated accidents and natural selection producing the hierarchies and homologies that we see in “microevolution,” we can only conclude that the same causes produced essentially the same patterns and results in “macroevolution.”  At least this is true if one knows of no causes that give similar effects as unguided evolution, and of course intelligence is presumed by any reasonable person to produce quite different results than do unintelligent processes (indeed, IDists want this to be so by insisting on a “designer,” but they completely fail to scientifically differentiate between the results of design and those of unguided evolution).

Others have dealt more closely with Behe’s “challenge” regarding adaptive immunity.  I have been far more focused on demonstrating that nothing in adaptive immunity is what one would expect of design, and upon facts like the one that we can follow the apparently gradualistic evolution of a myriad of biochemicals involved in innate immunity as they came to serve adaptive immunity.  Furthermore, genes coding for biomolecules specifically performing the adaptive functions of gnathostome recombination, like TCR genes and part of the BCR gene, along with RAG1, exist in organisms related to gnathostomes, like lampreys and lancelets.  Correspondingly, the LRRs of the agnathan VLR gene have numerous counterparts both inside and outside of innate immunity.

That is how science is done, by identifying similar causes by observing similar effects.  It is no wonder that Behe is on record at Dover wishing to change science, because by no means is finding similar patterns of homology via the last common ancestor of a group of organisms, plus dissimilarity since they diverged (again, where the organisms do significantly laterally share genes), in “microevolution” and in “macroevolution”, to be ascribed to different causes.  Doing so would make a mockery not only of science, but of the processes of justice (akin to claiming that the expected similarities of father’s and child’s genes were due to the miracle of the Holy Spirit).

The fact is that of all of the fundamental biochemical pathways, adaptive immunity is especially good at confirming the predictions of evolution–that complexity evolves due to accidents of heredity, mutation, and environment (selection itself is contingent, but non-accidental in crucial ways), and it is not copied into groups like agnathans and gnathostomes.  Copying would be indicative of design in such a case, and we never find copying where a designer would have to be the cause of such replication.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

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