In the latest edition of Science, Michael Gray, Julius Lukes, et.al, tackle what they see as a big dilemna for Darwinism: “gratuitous complexity”. The first two sentences of their short piece are these: “Many of the cell’s macromolecular machines appear gratuitously complex, comprising more components thatn their basic functions seem to demand. How can we make sense of this complexity in the light of evolution?” I’ll translate: “Based on directional selection, there’s way more proteins at work in these ‘machines’ that we can possibly explain.” So, ‘adaptionist’ and ‘selectionist’ explanations will not do. How big then is the problem? Well, when it comes to the spliceosome, they tell us: “The spliceosome uses five small nuclear RNAs and hundreds [my emphasis] of proteins to do the same job that some catlytic introns (called ribozymes) can do alone.” That’s some kind of problem: where did the ‘hundreds’ of proteins come from? And how did they become functionally integrated into the spliceosome? Or, as they put it: “For the addition of some of these proteins, selection probbly did drive increased complexity, but there is no basis to assume that this explains all, or even most, of the increased complexity of these machines.”(My emphasis again)[Note the continual use of the word ‘machine’.]
Well, how do the Darwinists get out of this one? The authors begin their journey to the Promised Land by citing the work of Michael Lynch, who invokes the “fixation of neutral or slightly deleterious features as a general and unavoidable source of complexity in taxa with small populations.” Such “non-selective processes” can lead to “neutrally fixed complexities”, but, of course, if selection is not involved, then these ‘complexities’ can be “neutrally ‘unfixed'” through random inversion. So, what is a evo-biologist to do? Here they turn to a “ratchet mechanism” proposed by Maynard Smith and Szathmary in the early nineties termed “contingent irreversibility”, which says “previously independent evolutionary units” can become “interdependent . . . for ‘accidental reasons that have little to do with the selective forces that led to the evolution of the higher entity in the first place” [J. Maynard Smith, E. Szathmary, The Major Transitions in Evolution (Oxford Univ. Press, Oxford 1995)]
The basic idea is that some kind of evolutionary novelty arises (how? they don’t tell us—see below and TEoE), and then this novelty becomes embedded through subsequent ‘neutral’ mutations that cause the embedded structure to bind more strongly and thus not allowing disassociation (it is a very rough idea). As examples they cite the symbiosis of mitochondria and plastids that become ‘harbored’ to cells, and the presence of tyrosyl tRNA synthetase as a splicer in Neurospora whose mitochondria have “self-splicing” introns. (Notice we come down from “hundreds” of extra proteins to just one.) Well, how might this synthetase have come about, and why is it still there? The authors state that the usual explanation is this: the interaction [with the synthetase] arose “‘to compensate for structural defects acquired’ by the intron sequences.”
Now, quite interestingly, the authors go on to make this observation: “But this order of events puts the cart before the horse: Introns bearing such defects would be at an immediate selective disadvantage and would not likely be fixed in populations before they TyrRS (synthetase) binding evolved to suppress their deleterious effects.” Well, join the club. This is exactly what critics of neo-Darwinian say all the time. This has now become obvious to the Darwinists (that is, they’re willing to state it out loud!) only because they now think they have a solution. And what is that solution: “If the order of events is reversed, then there would be no deleterious intermediate. Specifically, if the binding interaction arose first—fortuitously or for some reason unrelated to splicing—its existence could allow the accumultation of mutations in the intron that would have inactiviated splicing, were the protein not bound. Because the compensatory or suppressive activity of the protein is imagined to exist fortuitously before any intron mutation, this might be called “presuppression,” and the acquisition of protein dependence by the intron could be selectively neutral ( or, even slightly disadvantageous), and yet also inevitable, in finite populations.”
I like the phrase they use for how this protein function came about: “fortuitously or for some reason unrelated to splicing”. When was the last time you read an article that contained both the words “gratuitous” and “fortuitous”? I “imagine” it’s been a while. Well, this is where the Designer comes in handy. You see, I, too, can imagine that the Designer has “fortuitously” inserted this new function, and that later mutations were just neutral accretions. So I propose that we heretoforward respond to Darwinists as to “how” the Designer designs by answering that the Designer uses “contingent irreversibility”!
Amazingly, these scientists, who I presume to be highly regarded in their fields, can’t see their flight of fancy for what it is: a mythical prance to the Promised Land of macroevolutionary theory. Is “imagining” things to exist, and to have come to be “fortuitously” really the language of science?!
Additionally, let us point out that in all of what they present, in the mechanism/process they propose, positive selection is not included; only negative selection, and, the unbridled power of neutral drift. How is it possible to work within a putative Darwinian structure and at the same time do an end-run around NS? Take NS away from Darwinism and what do you have left? DESIGN! How can I make such a bold statement? Because Dawkins assures us that though all of nature appears to be supremely designed, in fact, it is not. Instead, non-randomness—order—enters through NS. But wait a second . . . these authors aren’t invoking NS as their mechanism. Instead they’re proposing “fortuitious” interventions to explain the “gratuitously complex” machines that are found in the cell. So, sorry Dawkins, nature is designed. And we even know how He designs: through “contingent irreversibility”!!
Lastly, you’ll again notice that (1) we went from 100 proteins to 1, and (2) we’re talking about “protein binding sites”. Does that sound familiar? It should. It is this that is precisely Michael Behe’s quest in The Edge of Evolution. And what is Behe’s conclusion: that Darwinian evolution would be hard pressed to come up with one binding site, let alone two. And, in the case of the spliceosome how many proteing binding sites need explanation? 100-1=99. So, how do you explain the rise of the spliceosome? And if you can’t explain the rise of the spliceosome, then how can you explain the evolution of higher taxa that rely on it? You see, if one invokes the Designer, at least it’s easy to explain “fortuitous” events. I wonder if the Darwinists will give us that much?