Evolution on a Crash Course

Many readers are no doubt familiar with our frequent emphasis on the “direction” of genetic change: all observed mutations—the supposed foundation of evolution—either hold constant or reduce the amount of information in an organism’s genome. This is in direct contrast to what the grand story of evolution (i.e., from inorganic compounds to complex life in millions of years) needs: a mechanism to introduce new information in the genome. Naturally, then, news that evolution “doesn’t make U-turns” (in the words of ScienceNOW’s Michael Torrice) caught our attention.

News that evolution “doesn’t make U-turns” caught our attention.

A team led by evolutionary biologist Joseph Thornton of the University of Oregon reports new findings in Nature (“An Epistatic Ratchet Constrains the Direction of Glucocorticoid Receptor Evolution”). The team examined a protein called glucocorticoid receptor (GR), which helps control animals’ responses to the stress hormone cortisol. They hoped GR would help them answer the question of whether evolution can “go backward.” (The ScienceNOW report intriguingly notes that problems predating the study included a “lack [of] sufficient information about ancestral traits or how present-day traits evolved.”)

The researchers discovered that in its most “ancient” form, GR responded to two hormones, cortisol and aldosterone. But a more “recent” form responds only to cortisol. The team found thirty-seven amino acid differences between the two versions, but only two that were required to deactivate the aldosterone response. To answer their question (whether evolution can go backward), the scientists reverted the amino acids in the cortisol-only version of GR, hoping to “re”-enable the aldosterone response. However, the reversion not only failed to enact the aldosterone response; it destroyed GR’s ability to recognize any hormone (including cortisol)!

It seems that the GR protein has lost function over time.

The problem was five of the remaining thirty-five amino acid differences: they played a part in knocking out the aldosterone-response ability as well; left unfixed, they caused the entire protein to fail after the scientists made their revisions. But because they cannot enable the aldosterone response themselves, natural selection could not act to preserve the changes in the unlikely event they “fixed themselves” (i.e., all spontaneously mutated back to the original/fully-functioning form). “They burn the bridge to return back to the ancestral function,” explained Thornton.

Thus, it seems that the GR protein has lost function over time, which affirms the creationist understanding of genetic evolution. That said, the research was partially based on “resurrecting” the ancient GR form based on the evolutionary tree of life; it may be that some organisms do not need the aldosterone response, and thus that the GR versions are each tailored designs.

If, however, some or all of the cortisol-only GR versions once had the aldosterone-response ability as well, that indeed backs up creationist teaching about the “downward” direction of mutations. The difficulty the team had repairing the protein underscores this. It is relatively easy to break the sophisticated instructions and machinery of living cells, and mutations have an excellent track record of doing just that. What scientific reason is there for believing, in spite of the evidence, that mutations could have generated the incredible biology we see all around us?

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