Molecular basis for genetic recombination.

HE past few decades have witnessed the successive description in biochemiTcal-or “molecular”-terms of the great formal entities of classical genetics. The lickage group was early identified with the objectively seen chromosome, then the gene itself, in its wild and mutant forms, more and more closely related to the linear DNA regions thereof. We have seen the identification of the gene product or “physiological gene” with proteins and polypeptide units, and then the exciting unraveling of the widespread protein biosynthetic mechanisms and their control by the broadly applicable genetic code. A last great genetic formalism-the interaction of homologous DNA regions with each other, o r genetic recombination-is now coming under detailed analysis as to its biochemical mechanism. It will be impossible to summarize here details of these highly technical studies; rather I shall attempt to portray what I see as the chief principles by which answers are sought from this approach. On the one hand, the successful unified schemes for biosynthesis and its genetic control have encouraged a dream of a single idealized process, “the mechanism of genetic recombination”. On the other hand, the comparative analysis of different genetic systems by modern geneticists has seemed to bring us a large series of different aberrations of random recombination and to suggest therefore a varied series of underlying mechanisms. I t will be my purpose to argue here that these are indeed visualizable as merely various manifestations of a broadly uniform genetic process, modified only in non-essential ways by the diverse enzymatic endowments of the different organisms and systems. What are in fact the various so-called abnormalities of recombination-the map distortions, map expansions, non-additivities, positive and negative interferences, gene conversions and polarities? All of them can be described as the observance of a greater or lesser number of recombinants within a particular subpopulation than were expected, on some previously assumed basis. As a single example, let us recall that gene conversions are properly claimed when a full recovery of primary segregants, from meiosis in an ascomycete or an attached duplication, shows one parental allele-or small region-in excess over its homolog. Now, we do not have the right to claim gene conversion in these or other organisms, when the primary products are submerged in a population that is derived from mass matings. But let us suppose we have so interacted two genomes