When Frank recently informed me that he planned to publish a guest article by atheist Tim Duck on the scientific evidence for neo-Darwinian evolution, I was immediately intrigued. As someone with some background and academic training in biology (I hold a degree in the field), I looked forward to reading what Tim had to say. When Frank forwarded me Tim’s final draft of his essay, however, the result was a tremendous anti-climax. The first half of the essay (which you can view here) was essentially wasted in laying out elementary concepts of biology known by every freshman undergraduate. When he finally did get around to presenting his case, the result was disappointing.
We were treated to a lengthy discussion of Michigan State University biologist Rick Lenski’s now-famous experimental work on E. coli (about which we are not ignorant). The only other identifiable positive argument for the claim in question was the assertion – without justification – that an indefinite extrapolation from micro- to macro- evolution is warranted. But since this is what Tim – allegedly – set out to prove, this constitutes a remarkable instance of begging the question.
But before getting into the specifics, allow me to highlight a few areas on which Tim and I are agreed. We agree that evolution possesses explicative power (we disagree over the extent). We agree that evolution does not entail atheism (one can accept evolution and remain a Christian theist). We agree that evolution, strictly speaking, has nothing to say on the origin of life. And we agree that argumentum ad consequentiam is a logical fallacy.
So, at which point does Tim err?
Tim’s first significant error relates to the false misconception – as prevalent as it may be – that the totality of traits possessed by an organism is ultimately determined at the gene level. This is somewhat of a simplistic view of development, and one can see quite clearly why one might naively come to think that the kind of evolutionary change required for the origin of novel body plans can simply be accomplished by the workings of microevolution on a grander scale.
In reality, however, the difference is not quantitative but qualitative. While DNA is responsible for the specification of protein structure (via an RNA intermediate), it does not alone determine the kind of spatial specificity required for proper cell-type differentiation, nor does it determine how these respective cell types are arranged into different tissues and organ systems, and ultimately the formation of an organism’s body plan. I have addressed this subject before, and readers are invited to read my previous writing on the subject for some explanation as to the immense problems with the DNA-centric understanding of development.
If, indeed, it is the case that DNA (and its interaction with the environment) is not the whole story as far as the morphogenesis of organismal form is concerned, then there is no reason to think that the extrapolation from ‘micro-evolution’ (which results from mutations affecting DNA) is at all justified. Indeed, we are only now learning that the 3D structure of the zygote itself plays a foundational role in producing an animal’s body plan. At any rate, given that an organism’s body plan is established right at the start of development, the situation looks bleak anyway because mutations affecting early development are the least likely kinds of mutations to be tolerated by animals (I explain why here and, in more detail, here).
After a full commentary on the process of natural selection and all that it entails, we are subsequently treated to a discussion of Richard Lenski’s famous laboratory work with E. coli. What we are not given, however, is a rebuttal to the numerous pertinent comments which have been given by ID proponents with regards to Lenski’s work. Michael Behe, for example, discusses Lenski’s work on pages 140-142 of his book, The Edge of Evolution, and — more recently — in a peer-reviewed article in the Quarterly Review of Biology. Behe has also been keeping tabs on Lenski’s work over on his Uncommon Descent blog.
As to the specific example of adaptive evolution given to us by Tim D., this same example — as I recall — was given by Richard Dawkins in his most recent popular book, The Greatest Show on Earth. The case of the citrate transporter seems, to me, to be a weak one because it has been documented that wild-type E. coli can already use citrate under low-oxygen conditions. Under these conditions, citrate is transported into the cell (Pos et al. 1998). The gene in E. coli specifies a citrate transporter. In the presence of high levels of oxygen, it is thought that the citrate transporter doesn’t function or is not produced. Thus, wild-type E. coli already possesses the genes necessary for the transportation of citrate into the cell and its subsequent utilisation. Indeed, Lenski et al. (2008) note that “A more likely possibility, in our view, is that an existing transporter has been co-opted for citrate transport under oxic [high oxygen level] conditions.” Such a scenario could take place by a loss of gene regulation (meaning that the gene is no longer expressed exclusively under low oxygen conditions) or a loss of transporter specificity.
Tim gives us one or two other uncontested examples of the occurrence of natural selection in the wild, reminding us that “[Evolution] is about divergence, not progression. To ‘evolve’ does not mean ‘to get stronger’ or ‘to get better,’ or to ‘improve’. It simply means to ‘change.'” Well, no one is going to dispute that living species change over time, or even that this change is, in part, facilitated by natural selection. But if one is to justify the stupendous extrapolation from natural selection and random mutation as an explanatory framework for microevolution within existing species, to be an all encompassing explanation for all of biodiversity, one has to demonstrate something just a tad more impressive than “species change over time.”
At the end of his essay, Tim states that “I know I haven’t addressed *all* of the criticisms that are out there.” I don’t think that Tim has really addressed any of them. Tim’s entire argument rests on the unjustified assumption that minor changes within existing species can be extrapolated to account for the origin of species. But this premise is merely asserted, and not justified. He has not given us an explanatory framework — within the paradigm of neo-Darwinism — which adequately accounts for structures which possess the quality of irreducible complexity, or for that matter even attempts to (see, for example, my discussion of flagellar assembly here), nor have we been given an explanation which would adequately account for the successful evolutionary search for sparse functional protein folds (which are extremely rare with respect to combinatorial sequence space), e.g. see Axe (2004) and Axe (2010a).
Moreover, as documented by Axe and Gauger (2011), even a seemingly trivial switch from Kbl to BioF function requires at least seven co-ordinated mutations, putting the transition well beyond the reach of a Darwinian process within the time allowed by the age of the earth. Their paper studies the PLP-dependent transferases superfamily. They identified a pair within the superfamily with close structural similarity but no overlapping function. The enzymes chosen were Kbl (which is involved in threonine metabolism) and BioF (which is part of the biotin synthesis pathway). And they used a three-stage process to identify which sequences were most likely to confer a change in function.
This three stage process involved:
1. Using structural and sequence comaprisons of the two enzymes to identify candidate amino acids most likely to be functionally significant.
2. Mutating these amino acids in BioF, making them like Kbl, and checking for loss of BioF activity.
3. Testing whether changing these groups in Kbl to look like BioF would enable the Kbl to substitute for the function of BioF.
And thus they estimated that seven or more mutations would be required to convert Kbl to BioF function.
Axe and Gauger’s paper is not an isolated result. One recent review in Nature reported that changing an enzyme’s chemistry may require multiple neutral or deleterious mutations.
“Interchanging reactions catalyzed by members of mechanistically diverse superfamilies might be envisioned as ‘easy’ exercises in (re)design: if Nature did it, why can’t we?…Anecdotally, many attempts at interchanging activities in mechanistically diverse superfamilies have since been attempted, but few successes have been realized.”
When these results are taken into account in the context of the predictions of population genetics with regards the waiting time for multiple co-ordinated non-adaptive mutations which are required to facilitate a given transition (e.g. see Axe 2010b), the situation for neo-Darwinism appears to be bleak.
I could continue on in a similar vein for some time. Suffice it to say for the time being that Tim has not given us any credible reason to think that these profound conundrums can be overcome. Should Tim desire to respond with some more substantive arguments, he will of course be most welcome to do so.
In summary then,
1) Richard Lenski’s work on E. coli, as fascinating as it is, does not demonstrate anything remotely like what Tim’s thesis requires.
2) There is not just an absence of evidence for the micro- to macro- extrapolation. There is also an evidence of absence — That is to say, there is positive evidence which militates against the claim that the extrapolation is justified (what I outline above is only the tip of the iceberg).
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