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“The evolutionary puzzle becomes more complex at a higher level of cellular organization.” No kidding.

The January 25th issue of Nature carries a “Progress” paper by Poelwijk et al that’s touted on the cover as “Plugging Darwin’s Gaps,” and cited by its authors as addressing concerns raised by proponents of intelligent design. The gist of the paper is that some amino acid residues of several proteins can be altered in the lab to produce proteins with properties slightly different from those they started with. A major example the authors cite is the work of Bridgham et al (2006) altering hormone receptors, which I blogged on last year. That very modest paper was puffed not only in Science, but in the New York Times, too. It seems some scientists have discovered that one way to hype otherwise-lackluster work is to claim that it discredits ID.

Quite unsurprisingly, the current paper shows that microevolution can happen. Small changes in a protein may not destroy its activity. If you start out with a protein that does something, such as bind DNA or a hormone, it’s not surprising that you can sometimes find a sequence of changes that can allow the protein to do something closely similar, such as bind a second sequence of DNA or a second, structurally-similar hormone.
My general reaction to breathless papers like this is that they vastly oversimplify the problems evolution faces. Consider a very rugged evolutionary landscape. Imagine peaks big and small all packed closely together. It would of course be very difficult for a cell or organism to traverse such a landscape. Now, however, suppose an investigator focuses his gaze on just one peak of the rugged landscape and myopically performs experiments whose products lie very close to the peak. In that case the investigator is artificially reducing what in reality is a very rugged landscape to one that looks rather smooth. The results tell us very little about the ability of random processes to traverse the larger, rugged landscape.

The authors remark, “The evolutionary puzzle becomes more complex at a higher level of cellular organization.” No kidding. Nonetheless, they, like most Darwinists, assume that larger changes involving more components are simple extrapolations of smaller changes. A good reason to be extremely skeptical of that is the work of Richard Lenski, which they cite. Lenski and his collaborators have grown E. coli in his lab for tens of thousands of generations, in a cumulative population size of trillions of cells, and they have seen no building of new systems, just isolated mutations in various genes. Apparently, nature has a much more difficult time putting together new systems than do human investigators in a lab.

Poelwijk,F.J., Kiviet,D.J., Weinreich,D.M., and Tans,S.J. 2007. Empirical fitness landscapes reveal accessible evolutionary paths. Nature 445:383-386.
Bridgham,J.T., Carroll,S.M., and Thornton,J.W. 2006. Evolution of hormone-receptor complexity by molecular exploitation. Science 312:97-101.

Michael J. Behe

Senior Fellow, Center for Science and Culture
Michael J. Behe is Professor of Biological Sciences at Lehigh University in Pennsylvania and a Senior Fellow at Discovery Institute’s Center for Science and Culture. He received his Ph.D. in Biochemistry from the University of Pennsylvania in 1978. Behe's current research involves delineation of design and natural selection in protein structures. In his career he has authored over 40 technical papers and three books, Darwin Devolves: The New Science About DNA that Challenges Evolution, Darwin’s Black Box: The Biochemical Challenge to Evolution, and The Edge of Evolution: The Search for the Limits of Darwinism, which argue that living system at the molecular level are best explained as being the result of deliberate intelligent design.

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