...the contention made by Behe is quite different from this – it is that evolution cannot explain the flagellum in principle (because its multiple components have no selectable function). By demonstrating the existence of such functions, even in just a handful of components, we have invalidated the argument.
1. Note the tacit abandonment of classical Darwinian direct evolution along a linear axis in the attempt explain these machines.
2. The ability to imagine such alternate funtions is not evidence that they existed. Is there any reason to suspect these alternate functions really existed, and are not just vague, ad hoc appeals to cooption?
3. The appeal to raw chance necessary to the coicidental cooption of alternative functions removes the explantory power:
3. Cooption of Alternative Function (CAF)
This explanation best exploits the logical flaw in the "IC = evolution is impossible" argument. That is, since the existence of A, B, C, and D need not be F-dependent, CAF simply proposes that A, B, C, and D did indeed exist prior to F, whereby these components performed some alternative, original function. As such, this is really the only evolutionary explanation that has the potential to explain the origin of an IC system. Thus, let's take a closer look at it.
This explanation would look as follows:
where G, H, I, and F are functions that previously employed components A, B, C, and D, respectively. A, B, C, and D could be directly donated into the newly formed IC system if functions G - J become disposable. Or, a gene duplication may occur for each of the gene products, allowing the duplicates to be recruited into the newly formed IC system. Or, gene products A - D could exist and now carry out dual roles in the cell.
While such a scenario provides a working explanation for the origin of the IC system, a serious investigator will want to know if there is reason to think this scenario is relevant to the origin of any particular IC system in question (the mere ability to imagine such scenarios is not evidence that such a scenario happened). Put simply, we need evidence to think this scenario applied.
Back in 1997, Julie Thomas posted an analysis of IC to the talk.origins newsgroup that is relevant here. Thomas describes what is needed when considering component (player) C, but keep in mind the same analysis would apply for A, B, and D:
However, in order for alternative activity to pose a serious challenge to the IC status of actual player C, several things must be demonstrated:
1. Evidence must exist that indicates the similar activity is older. Since this explanation proposes the acquisition of function F after the existence of the similar activity, alternative activity fails as an objection to IC if the similar activity post-dates function F. Put simply, the secondary activity must reflect a more ancient state and not a recent by-product of actual player C's role.
2. The similar activity should exist at biologically relevant states. This is important as in vitro evidence can be misleading. For example, if actual player C is a DNA-binding protein, but binds to RNA in the test tube under conditions that are not seen in the cell, the similar activity is biologically suspect and may simply be an artifact of the unnatural in vitro conditions.
3. Is the alternative activity present in the organism with the IC system in question? Similar activities, detected by in vitro tests using extracts from two very different organisms is of questionable biological relevance since the lineage of the organism with the IC system in question may have never possessed anything like the alternative activity.
4. The similar activity should not be part of another IC system. Otherwise, the argument travels in a circle. For example, single-stranded binding (ssb) proteins are involved in DNA replication and DNA recombination. If one explains away the role of ssb proteins in replication by appealing to recombination, yet explains away the role of ssb proteins in recombination by appealing to replication, we have gotten nowhere and have only the appearance of a refutation of actual player C's role in an IC system.
Such analyses will go a long way in resolving IC claims. If the similar activity post-dates player C's role, it fails as an explanation. If it is found only in test tube assays, the explanation is severely weakened. If the similar activity is part of another IC system, the original role may be in question, but some IC role remains.
However, even if a particular system successfully overcomes these obstacles, it is not clear CAF applies. CAF makes an assumption about cell biology than is increasingly untenable, namely that the cell is basically a soup. This soupy aspect of the cell is needed for A, B, C, and D to escape their original functional states in order to fortuitously interact. Yet it is becoming increasingly clear than many machine components are assembled into the complex very quickly after being synthesized and/or targeted to specific sites of assembly. For example, it's becoming more and more clear that certain metabolic enzymes are secured in various places and interact as tightly fitting complexes that directly hand-off product/substrate. Where they are found and how they are arranged is just as important as their existence. This was beautifully illustrated with some mutant work in Drosophila that showed a specific glycolytic isozyme was required for flight, as the existence of another isozyme was not functional due to its mislocation. As one reviewer of this study commented, "The presence of catalytically functional proteins alone is therefore not adequate; they must be properly located." Therefore, for the CAF scenario to work, the alternative function should not anchor the component-to-be-borrowed and if it does, some cellular change must be invoked to liberate it.
Yet the most basic problem with CAF is its complete reliance on chance. If we return to the originally proposed pathway above, we are asked to believe that while A, B, C, and D have long been shaped by selection to carry out their original alternative functions, a fortuitous interaction among them all would spontaneously emerge a brand new function. Selection might be invoked to fine-tune and improve this new function, but the bottom line remains in that raw chance is being credited for the creation of a novel function. I explained this elsewhere as follows:
"Co-option is the most commonly cited non-teleological means to generate an IC system. Yet, it is essentially a return to raw coincidence to account for apparent design. The brilliance of Darwin was to minimize the role of chance in apparent design. But once we turn to the co-option explanation, we leave this explanatory appeal behind, as chance reasserts itself into a place of prominence. For it is chance that determines whether the various gene products just happen to come together to form a new functioning system, as selection was previously pruning these gene products in accord with various different functions. If one is to invoke co-option, good supporting evidence is required."
The problem of invoking chance to explain the origin of a new function is quite serious when dealing with IC molecular machines. For these machines to work, their components are usually tightly fitted into a whole through the interactions of their complementary conformations. It would be unlikely for four various proteins, pruned by selection to carry out their original functions, just happened to have sufficient conformational complementarity to assemble into a novel machine with a novel function (which explains why no one has ever observed cooption to spawn a new molecular machine). Unless, of course, certain machines were designed to channel evolution by cooption, meaning that certain cooption events were rigged to occur...
IC revisited
Cordially,