The Toll-like receptor (TLR), which has a detailed and well established function in immune function in vertebrates is a good example of this problem. As I've wrote previously (and hope to go into more detail in the future), the Toll receptor (what TLRs in vertebrates is named after) has different functions in invertebrates such as worms and the fruit fly Drosophila melanogaster (see update). Rather than being a direct part of the immune system of these organisms, Toll functions primarily as factors that aid development of the organism, essentially telling cells which way is 'up' and which way is 'down' so they develop properly. This signalling function in vertebrates is used for a different function, where the TLR has been hijacked for its signalling ability for recognising different 'bits' of pathogens, like lipopolysaccharide, DNA (CpG motifs) and other things to activate adaptive immunity. This is a classic example of co-option of a receptor with one function that has been adapted entirely for another (see the previous post for a good reference).
Of course, creationists obviously disagree and then have to come up with any contrived excuse to explain away this prediction. Interestingly, in a group of abstracts published by the Baraminology study group for a conference they held, which David Rintoul was kind enough to alert me to, one of the abstracts was talking about the invertebrate Toll. The abstract, Investigating the Presence of Toll-like Receptors on the Cell Surface of Earthworm Coelomocytes focuses in particular on those of invertebrates, which the authors seem to think somehow justified this rather spurious claim:
Non-disease fighting functions of Toll may be of interest to creationists since this may represent a remnant of Toll’s function in the pre-Fall environment.Now as I've said above, the problem with this statement isn't so much the fact that invertebrate Toll has non-disease fighting functions, which they very obviously do but the whole 'pre-fall' nonsense at the end. Firstly, it's important to consider what a TLR is actually doing in the human immune system at the moment. TLRs in humans are found on specific cells and usually specific TLRs to boot (we have around 14 of them, with probably more to be discovered). For example, macrophages and dendritic cells have the job of playing 'clean up crew' in the body and have batteries of TLRs to sense a wide array of pathogens. On the other hand, epithelial cells of the gut have TLRs as well but only a limited subset (usually involving detecting viruses) because they see less types of different pathogens.
This in itself deals a considerable amount of damage to the above hypothesis. In vertebrates, TLRs are almost exclusively linked to the adaptive immune system, which they are critical in the function of, and are usually found directly linked with cells of the immune system. They are not produced in every single cell in the body, noting that gut epithelial cells of the gut are an exception because those cells are directly on "the front lines" when it comes to seeing new pathogens. If TLRs before the 'fall' are used in non-immune functions in vertebrates as they are in invertebrates, why are they only found in such close association with cells involved in immunity and virtually nowhere else? There is somewhat of a logical disconnect between noting what is ultimately the evolutionary relationship of developmental TLRs to the present day immune TLR, to suddenly claiming that this non-immune function is what they were doing before disease 'existed'.
Of course, this obvious localisation of TLRs makes full sense unless you're a creationist. If these have a non-immune function, I wonder what the authors actually proposed they were doing in antigen-presenting cells and the like before there was disease. Taking up space? They aren't playing a role in overall development, as you can knock out TLRs to compromise immunity without hindering growth of normal every day cells. This does stuff numerous cells of the immune system however, but that should be fairly obvious considering the entire point of TLRs are to detect pathogens and stimulate immune cell maturation and differentiation.
This problem of the localisation of these TLRs is not the only one of course. For example, why is it that TLR 11 in humans is a useless pseudogene yet in other animals is completely functional? Why is there such an incredible variation among TLRs between different animals, some having among 30-40 while others such as us Humans having a much lower amount. Are other animals after the fall just more diseased than we are? Without engaging in majorly wierd mental gymnastics, it's just incredibly difficult to support the immune system being 'created' when there is no disease then suddenly 'poofing' into existence (mind, Professor Behe thinks 'poof' is a legitimate explanation for things). This poofing occuring in the correct cells with the correct receptor patterns to spot diseases that never existed, which coincidentally have themselves just popped into existence with factors that allow them to destroy/subvert the immune system that never existed before either.
Is it just me, or is that utterly non-sensical? Many creationists tell me evolution is full of impossible 'just-so' stories and then come out with things like the above quote.... Hmmm, I think I'll take the 'orthodox' co-evolutionary warfare of pathogens and host immune systems thanks, as at least it makes sense.
Reference
Roach J.C., G. Glusman, L. Rowen, A. Kaur, M.K. Purcell, K.D. Smith, L.E. Hood and A. Aderem (2005). The evolution of vertebrate Toll-like receptors. Proceedings of the National Academy of Sciences, 102,27;9577-9582.
Update: I should point out that the TLR in Drosophila melanogaster should really be identifed as a Toll receptor as that organism is where these molecules were originally named and discovered. The TLR is named as it is because of the similarities between the D. melanogaster Toll receptor and a family of immune modulating receptors found in vertebrates. It's rather silly to call the original Toll receptor a "TLR" considering it's the receptor everything is supposed to look like. I apologise for any confusion and I've also cleaned up the definitions in this post so that the distinction is clearer.
