The effect of the mus309 mutation, defective in DNA double-strand break repair, on crossing over in Drosophila melanogaster suggests a mechanism for interference.

The mus309 gene in Drosophila melanogaster encodes a RecQ helicase which is involved in DNA double-strand break (DSB) repair. In a brood pattern analysis, it was observed that in mus309 mutant females, the frequency of single crossovers in the central cv - v interval of the X chromosome was decreased in young females but returned to the level of the wild type control as the females aged. In the proximal v - f interval, the frequency of single crossovers was increased during the whole experimental period. In particular, it was observed that the frequency of double crossovers, as well as the coefficient of coincidence first increased but then gradually decreased, finally reaching the level of the control flies, as the females aged. Map distances increased due to the mus309 mutation in both gene interval studies, but they did not change as the females aged, a result suggesting that the mus309 gene controls the distribution of DSBs to be repaired as crossovers instead of non-crossovers. The results are consistent with the hypothesis that in general the DSBs are initially independently distributed on the chromosome but non-randomly repaired so that the distribution of crossovers in the mutant flies becomes uniform, but uneven in wild-type flies. The results are consistent with the counting number model of crossover interference, based on genetic distance. On the other hand, the data are not consistent with the reaction-diffusion model based on physical distance. Consequently, the view that crossover interference in Drosophila is tightly tied to genetic distance is supported.