The cilium evolved into part of the “irreducibly complex” chordate eye
How do we get theories, and what is their purpose? Is a theory something that we have after every phenomenon encompassed by the theory is completely explained? Why would we even need a theory in biology, if we knew everything that happens in the past and present according to physics, and its theories?
Of course Behe and the other IDists’ understanding of (or at least rhetoric about) theory is as flawed as their understanding of everything else in science. This is not the post for a long discussion about why theories exist, yet it is worth pointing out, yet again, that theories exist to guide research and to organize knowledge, and are not catalogs of everything that has happened, is happening, and will happen. This is why evolutionary theory is a crucial theory, because it acknowledges the constraints that exist in biology and thus explains the limits of biological change. This would even be true if Behe’s mutation-causing God were responsible for some mutations, because in any case this “God” does not transcend the limits of heredity and of mutation, or at best (we have to trust Behe to discuss this claim, since he supplies no evidence for this mutator) only pushes the limits of mutation without doing anything that we understand as design-like (such as giving radio communication to organisms).
The above follows up on my last two posts involving DBB, here, and here, and it introduces the following discussion of how the structures of cilia provided opportunity and constraint in evolution after the cilium first became a fixed eukaryotic structure. No, not everything about the origin of cilia is known, nor is everything about the evolution of cilia into parts of sensory structures understood, but only evolution makes any kind of sense at all of the distributions and modifications of cilia that we find in noses, in eyes, and in the motility of ciliated cells, in addition to its origin.
Sensory reception via cilia appears to be evolutionarily ancient (Mitchell), so the fact that cila comprise parts of the vertebrate eye, olfaction, and of taste buds is not especially surprising. Presumably, cilia have had a sensory role from very early in evolution both because they provide extensions into extracellular media, and because they can set up currents in liquids in order to sense media which would otherwise be beyond the reach of the ancestral free-living cell. Nevertheless, the evolution from what were probably moving cilia to the outer portions of the rods of our eyes is the kind of transformation that we would not suspect, if the evidence of it were not so clear. Here is a photograph (bottom) of a rod cell of the eye, with a cilium clearly visible as part of it.
The transformation of part of the cilium into stacks of lamellae, and the role played by the cilium as a photoreceptor, indicate a rather extensive evolutionary change of this supposedly “irreducibly complex” organelle. Indeed, most (perhaps all) of the “irreducibly complex” visual biochemical pathway that Behe discusses in DBB chapter one (see figue on p. 20) occurs exactly in the region of the rods which are made up substantially of cilia, although these originally evolved for quite different purposes (motility and chemoreception).
My point here is not to go through the complexities of these matters (which can be found on the web quite easily), but rather to show that we have “nested” complexities which reveal successive evolutionary events–not the sudden creation at the Cambrian hinted at by Behe and other IDists–having all of the accidents (hereditary and mutational/selectional) expected in evolution, and highly complex modifications of previously evolved complexities. Importantly, evolution proceeds just as predicted by evolutionary theory, with evolved complexity itself almost certainly providing a major constraint on the evolution of later complexity (of P. falciparum, for instance), so that the complexity of the cilium is utilized by the chordate eye in order to supply the complexity needed for photoreception.
What is perhaps at least as interesting is that the modification of the cilium to function for the eyesight of chordates was not the only solution to the problem of photoreception. We have ciliary photoreceptors, while many animals have rhabdomeric photoreceptors, which apparently evolved from the same cells from which retinal ganglion cells are derived (Evolution of eyes and photoreceptor cell types). Again, the story is of accident, where no design reason can be given for our ciliary photoreceptors, and it is the accidental (initial and subsequent) evolution of cilia that gives us any reason for such an odd switch from rhabdomeric photoreceptors to ciliary photoreceptors in the chordate line. That anyone would try to claim that such obvious accident is the result of “design” strains any notion of design that reasonable people have.
I do not plan to revisit the evolution of the eye after this, since the incorporation of the “irreducibly complex” cilium into the “irreducibly complex” vertebrate eye while all of the hereditary and mutational/selectional constraints of evolution apply, is the only possible, and easily sufficient, evidence that unguided evolution is responsible. Complexity builds upon complexity in the same sorts of evolutionary (cladistic) patterns as exist in microevolutionary processes, and only a fool would fail to match up cause and effect in both microevolution and in macroevolution.
However, since this is probably the only substantial discussion I will have of eye evolution (at least while discussing Behe’s books), I’d like to point to a some more evidence of the evolution of the eye from simple to complex that may be found in the last link/reference. Never mind Behe’s peculiar and unjustified demands for evidence, here is some of the reasoning (from evidence) and conclusion for evolution from simple to complex:
The prevalence of pigment-cup eyes in Bilateria, and their stereotype, simple design, tells us that eyes started off with merely two cell types, photoreceptor cells that associated with pigment cells to detect the direction of light (…). Additional cell types were added during subsequent eye evolution, such as lens cells, various kinds of support cells, muscle cells etc. that also formed part of the eyes. Cell type diversity reached its maximum in the vertebrate and cephalopod camera eye, as well as in the arthropod compound eye. Evolution of eyes and photoreceptor cell types
Opsin homologies go back at least to before the evolution of bilateral animals (“bilaterians”), such as ourselves:
On the molecular level it is long known that all eye photoreceptor cells so far described use a vitamin-A-based light-sensitive photopigment, comprising a chromophore and an apoprotein, opsin. Phylogenetic analysis approves that all opsins trace back to one opsin precursor molecule that predated bilaterians. Evolution of eyes and photoreceptor cell types
Beyond that, the homologies are extensive throughout vertebrate eyes, and yet however common a gene like pax6 may be in animal eye development, it, too, appears to be so due to accidents of heredity, for it is neither exclusive to eye development, nor needed for the development of all animal eyes:
In the vertebrates, pax6 is required for the formation of virtually all retinal cell types…. In Drosophila, the pax6 orthologs eyeless and eye gone are required for the formation of the entire eye disc (…), which gives rise to all ommatidial cell types including the photoreceptor cells. Eyeless and another pax6 ortholog, twin of eyeless are also expressed in precursor cells of the photoreceptive Bolwig organ and ocelli (…), and in the late Bolwig organ (…). In line with a general affiliation with photoreceptor cell specification, pax6 expression also covers the early eye anlagen in cephalopods (…), planarians (…) (…), nemertines (…), and polychaetes (…). However, and even if pax6 started off as an early photoreceptor specification gene in pre-bilaterians, in none of the species investigated is pax6 photoreceptor cell-specific, or even eye-specific (…). This means that the ancestral function of pax6 in cell type specification or differentiation (whatever it was) is not exclusively required in photoreceptor cells. It is also clear that in few cases photoreceptor cells can form in the complete absence of pax6, such as the Hesse eyecups in Branchiostoma (…). Evolution of eyes and photoreceptor cell types
The animal eye is an exquisite adaptation, an organ that is extremely important to the lives of most animals that have eyes, and so eyes are finely-honed instruments. A very crucial point to the use and intellectual sense of the achievement of understanding, however, is how to account for all of the accidents of heredity and apparently of mutation/selection. Thus, we like to know why the chordate eye is a complex of preceding parts, such as cilia, and in turn, why cilia are composed of parts of cytoplasmic transport systems which preceded the cilia.
None of these questions are asked by IDists, for they know that they have no answers via design. Accident is the antithesis of design, despite the fact that Behe tries by analogy to claim that apparent accidents are within the realm of “design” (DBB 193-194). Of course he tries to do so, since he knows that life is shot through with evident accident, including complex accidents (coupled, of course, with natural selection) like ciliary eyes. He does the only thing he can do, however, which is to try to claim that some complexes of accidental characteristics are too complex to be the result of accident, then to claim design without any actual evidence in favor of design.
Actually, though, complexes of accident ought to be accepted as being the result of accident (plus ordering principles, like natural selection) so long as design characteristics (purpose and rationality being the biggest) cannot be demonstrated. For the fact is that when you have the sequential accidents found in life, like oxygenic photosynthesis producing the necessary oxygen for the Ediacaran and the Cambrian “explosions”, or cilia being composed of intracellular transport biochemicals and then cilia hosting crucial photoreceptor biochemical pathways, you really can only honestly conclude that the accidental effects are due to accidents which natural selection filters, not to design.
For, again, design is itself the opposite of accident, if not totally devoid of accident. That is, design filters out most accidents, leaving primarily non-accidental rational organization–at least when it is good design. When it comes right down to it, natural selection only refines accident–it really only filters organic traits out of the accidents of mutation, duplication, deletion, and environmental contingencies–for an incomplete list–and however many accidents are excluded, only accidents remain. Because we see only accident and natural selection behind the integrated complexities of life, we must pick evolution as the cause of life’s configurations.
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.Explore posts in the same categories: Darwin's Black Box comment below, or link to this permanent URL from your own site.