Michael Behe writes about a new study from PNAS in Evolution News. (H/T Think Apologetics)

Excerpt:

A recent paper in PNAS confirms a key inference I made in 2007 in The Edge of Evolution. Summers et al. conclude that “the minimum requirement for (low) [chloroquine] transport activity … is two mutations.” This is the first of three posts on the topic.

[…]A major point of the book was that if evolution has to skip even one baby step to attain a beneficial state (that is, if even one intermediate in a long and relentlessly detailed evolutionary pathway is detrimental or unhelpful), then the probability of reaching that state decreases exponentially. After discussing a medically important example (see below), I argued that the evolution of many protein interactions would fall into the skip-step category, that multi-protein complexes in the cell were beyond the reach of Darwinian evolution, and that design extended very deeply into life.

However, at the time the book’s chief, concrete example — the need for multiple, specific changes in a particular malarial protein (called PfCRT) for the development of resistance to chloroquine — was an inference, not yet an experimentally confirmed fact. It was really an excellent, obvious inference, because resistance to chloroquine arises much, much less frequently than to other drugs. For example, resistance to the antimalarial drug atovaquone develops spontaneously in every third patient, but to chloroquine only in approximately every billionth one. About PfCRT I wrote, “Since two particular amino acid changes [out of four to eight total changes] occur in almost all of these cases [of chloroquine resistance in the wild], they may both be required for the primary activity by which the protein confers resistance.” The result would be that “the likelihood of a particular [malarial] cell having the several necessary changes would be much, much less than the case [for atovaquone] where it needed to change only one amino acid. That factor seems to be the secret of why chloroquine was an effective drug for decades.” Still, the deduction hadn’t yet been nailed down in the lab.

Now it has, thanks to Summers et al. 2014. It took them years to get their results because they had to painstakingly develop a suitable test system where the malarial protein could be both effectively deployed and closely monitored for its relevant activity — the ability to pump chloroquine across a cell membrane, which rids the parasite of the drug. Using clever experimental techniques they artificially mutated the protein in all the ways that nature has, plus in ways that produced previously unseen intermediates. One of their conclusions is that a minimum of two specific mutations are indeed required for the protein to be able to transport chloroquine.

I think when we are discussing evolution, we at least have to ask the Darwnian side to bear their burden of proof. If you’re saying that mutations can lead to improvements, then we need to see examples. And the examples have to have mutations that are likely to occur.

You can listen to a recent episode of the ID the Future podcast where Casey Luskin and Michael Behe went into more details about the new discovery.