The mechanism of intragenic recombination.

Abstract

The prudent scientist keeps his hypothesis simple. He endows it with only enough complexity to account for the observations. He stands stubbornly by his simple hypothesis, resisting the complicating results of other peoples' experi­ ments, until there can be no further doubt of their validity. Then he retreats a very short way, taking up a new position with only enough added complexity to accommodate the unwanted findings. There he digs in and prepares for the next attack of the anarchists. The siege on the mechanism of genetic recombination has been particularly long and telling. For many years it appeared that the event could be described in the simplest terms: a single, reciprocal exchange between two homologous chromosomes which could occur (with similar likelihood) at the junction between any two adjacent genes. From this it followed that measurements of recombination frequency generated genetic maps that revealed the order of successive sites and even an approximation of the distances between them. When it was discovered that recombination could take place at a site within a functional (1, 2), some modification of the model was required. The discoverers of intragenic recombination found that this event could not be explained by a single, reciprocal exchange. It required two or three exchanges in a very short distance to account for some of the products. Furthermore, tetrad analysis showed that these exchanges were not exactly reciprocal. Segregating sites in the immediate vicinity of a recombination event showed frequent 3: I (or 1 :3) segregations. This was called gene conversion. (Indeed, one way to interpret the production of a wild-type recombinant in a cross between allelic mutants was to say it did not involve exchange at all but was the result of conversion of one of the mutant alleles to wild type.)