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Hypermutation: evolutionary fast track?

Hypermutation: Evolutionary fast track?

Two years ago, Boston scientists committed an evolutionary heresy of sorts by suggesting that certain bacteria can mutate on demand to suit themselves (SN: 9/10/88, p.166; 3/10/90, p. 149). Their research report, based on laboratory experiments, questioned a basic tenet of neo-Darwinian theory: that all mutations arise spontaneously without regard to environmental pressures.

Other researchers soon issued reports challenging the so-called "directed" mutation. Now, evolutionary biologist Barry Hall of the University of Rochester, N.Y., says he has evidence that refutes some of their doubts while suggesting a new explanation of how the bacteria accomplish "this very interesting and evolutionarily important trick."

Hall started with special strains of Escherichia coli that require external supplies of the amino acid tryptophan, but that have the potential to mutate in order to synthesize their own. He grew the bacteria in a culture medium provisioned with a three-day ration of tryptophan, then "starved" them of tryptophan for the next nine to 11 days. During that period, the numbers of bacteria mutating to produce their own tryptophan jumped 3- to 30-fold, he says.

Through a rigorous series of controls, Hall adds, he showed that this mutation did not arise before the tryptophan deprivation and did not occur in bacteria starved of a different amino acid, thus helping to refute some of the arguments raised against the 1988 experiments led by John Cairns at the Harvard School of Public Health.

"But the key thing I found," he told SCIENCE NEWS, "was that when I looked in those old colonies, I looked at other genes, and asked: Are there more mutations elsewhere? The answer was no."

"The phenomenon that Cairns describes is real," he asserts. "Mutations that occur more when they're useful than when they're not: That I can document any day, every day, in the laboratory."

Hall's findings will appear in the September GENETICS, along with his hypothesis to explain why only specific mutations would increase so dramatically. Hall proposes that some cells, when stressed by starvation, enter a "hypermutable" state in which mutations of all sorts abound; but only those cells with the specific mutation that solves the immediate problem (in this case, the inability to synthesize tryptophan) survive. The rest, no matter how useful their other mutations might be in the longer run, die before they have a chance to pass on those traits, he suggests.

But evolutionary scientists need not scrap their books just yet. "At the moment, this phenomenen has only been shown in bacteria," observes Cairns. "What about people? That, of course, is another ballgame altogether."
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Author:Stolzenburg, William
Publication:Science News
Date:Jun 23, 1990
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