No. 72: Nov-Dec 1990
The year 1988 saw a flurry of excitement over the purported discovery of "directed mutation" in the laboratory; that is, mutations of organisms that seemed goal-directed rather than random and independent of environmental pressures. The concept of directed mutation is counter to prevailing biological dogma, and, naturally, this research bore severe scrutiny. Objections and arguments against directed mutation arose, but the original research was never shown to be faulty.
New experiments along this line, by B. Hall at the University of Rochester, have supported the original Harvard work and refuted some of the objections that had been leveled. Working with a special strain of Escherichia coli, Hall starved the bacteria of a certain amino acid, (tryptophan) that they usually got from the environment and could not synthesize. In the days that followed, many of the bacteria mutated so that they could synthesize their own tryptophan. Hall concluded: "Mutations that occur more when they're useful than when they're not: That I can document any day, every day, in the laboratory."
Rather than assign any "conscious" goal-seeking attributes to the bacteria, Hall prefers to think that the environmental stress induced a state of "hypermutation." In this state all sorts of mu-tations occurred in abundance. Only those that synthesized tryptophan survived the starvation program; even potentially favorable mutations died quickly. (Stolzenburg, W.; "Hypermutation: Evolutionary Fast Track," Science News, 137:391, 1990.)
Comment. Besides the implication that environmental stresses have initiated the mutations that gave us today's fauna and flora, we see that the idea of hypermutation is merely an acceleration of standard evolutionary processes. But how do environmental stresses turn on the biological switch that starts the mutation machine going? What sort of environmental stresses would cause humans to mutate? What would we turn into if, say, global temperatures rose 5°?
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