Model Madness: Axe vs. Lynch and Abegg

I recently blogged about a paper by Lynch and Abegg 2010, which I thought was an important paper. It showed that, yes, there was time enough for evolution, mainly because neutral and even maladaptive variations could accumulate in sufficient numbers until they finally coalesced into a new beneficial function.

Douglas Axe, a leading scientist within the ID community, responded to the challenge inherent in this paper. Axe's position and research agenda has long been that there is not time enough for evolution.

At this point, I have to say that even though I disagree with Dr Axe, I give him credit for being the most professional and rigorous pro-ID scientist I have ever read. Yes, professional scientists can work themselves into a corner that eventually becomes crank science as they refuse to abandon a position - witness the Rubin group at the University of Oregon on "birds are not dinosaurs". Yes, I do think Axe is in this position, but he is trying in a principled, scientific way to address the issues. As such, he has demonstrated far more professional integrity than Stephen Meyer or William Dembski, neither of whom is a scientist.

Axe's response is The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations, which attempts to criticize Lynch and Abegg and to propose an alternative model.

For now, I'd like to focus on the differences in the models. Lynch and Abegg use a model assuming sexually reproducing diploid populations. Axe tries to refute them with an asexually reproducing haploid island population model. Are those differences appropriate?

One way to answer would be to look at the biochemistry that is being discussed, and ask when did it evolve. Is it eukaryotic or prokaryotic in origin? As I pointed out in my last post on this, eukaryotic sexual species with large populations have been around for a billion years. The larger portion of the biochemistry we operate with is eukaryotic - not shared with bacteria.

That calls into question the basic assumption of Axe's model. Another way to look at the issue is to question the realism of the asexual population genetic abstraction. We now know that in real life, as opposed to the test tube or a mathematical simplification, bacteria exchange genes rapidly. The process might be based in conjugation, or it might be through viral infection. In either case, the binary fission model of where genes come from isn't relevant.

Axe's model also incorporates an effective population size that is quite small - 10^9, a billion bacteria. This is justified by appealing to the island model dynamics of Maruyama and Kimura 1980. Even accepting these dynamics, a gene's eye view of the world has to incorporate the reservoirs afforded by other species and viruses. So I would argue that Axe's effective population size is too small.