Two responses to ID propaganda

Last week, Science published an article by Bridgham et al., (2006) Evolution of hormone-receptor complexity by molecular exploitation. The paper shows how an irreducibly complex interaction between a receptor and its hormone that it binds to can evolve. Naturally, the DI got visibly upset over actual research, published in actual journals, performed in actual labs demolishing their claims they have put out in popular books made for the public. One of their responses, if you can call it that, can be found here and is about as incredulous as you would expect from the DI.

Since that, there have been two very good responses to the nonsense thrown out by the DI response. Firstly, I would point you to this excellent post by Carl Zimmer at the Loom. His commentary is particularly cutting but he makes one particularly brilliant point (emphasis mine):

Is it me, or is it strange that intelligent design advocates are telling biologists that they aren't working hard enough, that they are not getting enough results from their lab work? Remember, this is the same Michael Behe whose sole peer-reviewed paper in the past eight years was a computer model (and a pretty poor one, it turned out). Compare that to the work of Joe Thornton, the principal investigator on the new paper. In the past eight years he's published twenty papers on hormones and their evolution: he's been sequencing hormone receptor genes, working out how they respond to different hormones, determining how they're related to one another, and even resurrecting them after 450 million years of oblivion.

Ouch. I felt that one from all the way over here in New Zealand! Further, another response that is worth noting is from the Pandas Thumb (of course), where Ian Musgrave notes how slippery the definition of IC is. Additionally he also shows how the definition of IC isn't really that well defined to avoid any form of significant falsification.

Yet this “system” is precisely the thing that Behe uses in his exemplar for the Behe and Snoke paper, the binding of DPG to haemoglobin. And Behe has said in testimony to the Dover trial (3) that the Behe and Snoke paper on evolution of binding sites is about irreducible complexity. So if the evolution of the DPG binding site (where you only need two mutations to make a functioning DPG binding site) is an example of IC, then the evolution of the aldosterone binding site is also (note 2). As the BCT paper specifically cites the Behe and Snoke paper, you would expect they would look at the ideas contained in the paper, not “Darwins Black Box”. Behe has had a long history of citing examples of molecular IC. He has even called disulfide bond “irreducibly complex” (2). So his disavowal of an example that directly addresses the Behe and Snoke paper (3) is particularly disingenuous.

Not that Behe has ever thought much of actual scientific research anyway.