Evolution Street Is One Way Only
Evolutionary biologists have long wondered whether it was possible for evolution to reverse direction; in other words, whether the proteins that make up an organism could “devolve” back to a previous shape or purpose. Carl Zimmer has an interesting piece on new research that strongly suggests evolution is a one-way street.
Evolutionary biologists have long wondered if history can run backward. Is it possible for the proteins in our bodies to return to the old shapes and jobs they had millions of years ago?
Examining the evolution of one protein, a team of scientists declares the answer is no, saying new mutations make it practically impossible for evolution to reverse direction. “They burn the bridge that evolution just crossed,” said Joseph W. Thornton, a biology professor at the University of Oregon and co-author of a paper on the team’s findings in the current issue of Nature. …
Dr. Thornton and his colleagues took a close look at the possibility of reverse evolution at this molecular level. They studied a protein called a glucocorticoid receptor that helps humans and most other vertebrates cope with stress by grabbing a hormone called cortisol and then switching on stress-defense genes.
By comparing the receptor to related proteins, the scientists reconstructed its history. Some 450 million years ago, it started out with a different shape that allowed it to grab tightly to other hormones, but only weakly to cortisol. Over the next 40 million years, the receptor changed shape, so that it became very sensitive to cortisol but could no longer grab other hormones.
During those 40 million years, Dr. Thornton found, the receptor changed in 37 spots, only 2 of which made the receptor sensitive to cortisol. Another 5 prevented it from grabbing other hormones. When he made these 7 changes to the ancestral receptor, it behaved just like a new glucocorticoid receptor.
Dr. Thornton reasoned that if he carried out the reverse operation, he could turn a new glucocorticoid receptor into an ancestral one. So he and his colleagues reversed these key mutations to their old form.
To Dr. Thornton’s surprise, the experiment failed. “All we got was a completely dead receptor,” he said.
