New York Times science writer Ken Chang reported this week on how “scientists have pinpointed mutations in an ancient protein that transformed its shape and function more than 400 million years ago.” One of the researchers even claims to have discovered “how evolution sculpted the protein structure to produce a new function.”

Really? With such claims having been bandied about before with little basis in reality, I sought out a biologist working in a research lab and asked her about this paper and she responded:

Chang has misrepresented what the paper in fact demonstrates. This paper says nothing about how one protein fold might evolve into another fold with a different 3-dimensional structure. Rather, it describes one hypothetical set of changes that might convert the mineralocorticoid receptor (MR) to a glucocorticoid-specific receptor (GR). To change MR to GR does not require anything like unraveling the fold. The protein backbone still follows the same course, and the vast majority of its amino acids are unaltered. In fact the “evolved” MR started out able to bind to both hormones, as Ortland et al acknowledge in their paper, so relatively few changes were able to boost recognition of cortisol in preference to aldosterone. Even then, most changes they tested were non-functional, and in at least one case, required a second mutation to restore activity…

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As noted in the above, Behe has made some comments on this in his blog. Here’s a relevant passage:

Of course, getting a single amino acid mutation by chance is not a problem. But in order to have the mutation be positively selected, it has to benefit an organism. The authors (and news stories) completely ignore that – the authors didn’t measure whether duplicating the ancestral gene, and then modifying it, would benefit an organism that was used to relying on just one protein (admittedly that would be hard to do). What’s more, in order to be confident that a multi-mutation scenario reconstructs a Darwinian process, all subsequent mutations have to be positively selected, too.

But they aren’t. Although they test none of the mutations in actual organisms, the authors themselves feel that the very particular mutations they deliberately introduced, which strengthen the protein but don’t affect hormone binding, would have been neutral. That makes those mutations much, much less likely to spread in a population, to be available later for when the beneficial mutations came along. In other words, the authors themselves think the scenario involves a big stroke of luck. In the New York Times Chang quotes Thornton: “‘These very exquisitely adapted bodies we have represent a role of the dice,’ Dr. Thornton said. ‘And they could have turned out very differently.'”

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