Radiation and transposon-induced genetic damage in Drosophila melanogaster: X-ray dose-response and synergism with DNA-repair deficiency.

The interaction of X-ray-induced and transposon-induced damage was investigated in P-M hybrid dysgenesis in Drosophila melanogaster. The X-ray dose-response of 330-1320 rad was monitored for sterility, fecundity and partial X/Y chromosome loss among F2 progeny derived from the dysgenic cross of M strain females xP strain males (cross A) and its reciprocal (cross B), using a weaker and the standard Harwich P strain subline. The synergistic effect of P element activity and X-rays on sterility was observed only in cross A hybrids and the dose-response was nonlinear in hybrids derived from the strong standard reference Harwich subline, Hw. This finding suggests that the lesions induced by both mutator systems which produce the synergistic effect are two-break events. The effect of increasing dose on the decline of fecundity was synergistic, but linear, in hybrids of either subline. There was no interaction evident and thus no synergism in X/Y nondisjunction and in partial Y chromosome loss measured by the loss of the Bs marker alone or together with the y+ marker. Interaction was detected in the loss of the y+ marker alone from the X and Y chromosomes. The possible three-way interaction of X-rays (660 rad), post-replication repair deficiency and P element mobility was assessed by measuring transmission distortion in dysgenic males derived from the II2 P strain. X-Irradiation of spermatids significantly increased the preferential elimination of the P-element-bearing second chromosome in mei-41, DNA-repair-deficient dysgenic males, but had no effect in their DNA-repair-proficient brothers. These findings indicate that the post-replication repair pathway is required for processing lesions induced by the combined effect of P element mobility and X-rays, and that the unrepaired lesions ultimately lead to chromosome loss.