The relationship between radiation-induced and transposon-induced genetic damage during Drosophila spermatogenesis.

The combined effect of transposon mobility and X-rays on X-linked recessive lethals and dominant lethals was measured in the germ line of F1 male hybrids in the P-M system of hybrid dysgenesis. X-Linked lethal mutation rate was measured in the chromosome derived from the P-strain father of the M X P cross. Mutations induced in irradiated dysgenic males were compared to those of unirradiated males, as well as to irradiated nondysgenic males derived from M X M crosses. Three four-day broods of sperm were tested for both X-linked lethals and dominant lethals. X-Linked lethal mutation rate in dysgenic control males was 6.38%, 6.36% and 4.55% in broods 1, 2 and 3 respectively, thus showing a decrease in older males. The mutation rate in the same broods of irradiated, nondysgenic control males was 3.66%, 4.46% and 6.38%, respectively. The rate obtained in dysgenic irradiated males was 10.33, 11.16 and 7.97 in the same 3 broods. These results demonstrate that when X-rays and P element mobility were combined as a source of mutagenesis, a strictly additive effect on genetic damage was observed in the first two broods of sperm which represent primarily mature sperm and spermatids respectively. The third brood, representing mostly spermatocytes showed a less than additive effect, probably due to germinal selection. In contrast, the induction of dominant lethals showed a clearly synergistic effect in the last two broods of sperm tested, when X-rays and transposon mobility were combined. The X-ray component of dominant lethality in brood 1, representing mostly mature spermatozoa, was negative, indicating a lower than expected lethality induced by X-irradiation in the presence of P element mobility. The X-ray-induced component of dominant lethality, was expressed as the per cent of embryo lethality after adjusting the results obtained with each brood of sperm from nondysgenic and dysgenic males to their respective unirradiated controls. These values were 32.3%, 30.5% and 64.7% for brood 1, 2 and 3 respectively from nondysgenic males, and 14.1%, 56.1% and 71.4% for the same broods from dysgenic males. Thus the differential effect of X-rays in sperm broods 1, 2 and 3 was -18.2, +25.6 and +6.7% respectively. These results suggest that the synergistic effect may be due to the common component of X-ray and P element-induced genetic damage, namely chromosome breaks, and that the interaction of these lesions resulted in a greater than additive number of of unrestituted chromosome breaks and nonviable chromosomal rearrangements.