Studies on mutagen-sensitive strains of Drosophila melanogaster: VI. The effect of DNA-repair deficiencies in spermatids, spermatocytes and spermatogonia irradiated in N 2 or O 2

Abstract

This study was aimed at ascertaining the extent to which paternal repair processes possibly deficient in mei-9 a, mei-41 D5 and mus-101 D1 genotypes would affect the recovery of radiation-induced recessive lethals in early spermatids, spermatocytes and spermatogonia. These germ cell stages were sampled in two 2-day broods from freshly hatched males, that were irradiated as 24-h old pupae in O 2, or N 2 followed by N 2 or O 2 post-treatment. Spontaneous mutation frequencies were higher in mei-9 and mei-41 males, and thus appropriate corrections were applied to the radiation data. Only with mei-9 males a clear and consistent increase of the radiation-induced mutation frequency was observed. The effect is somewhat more pronounced in brood B, presumably representing spermatogonia, than in brood A and is observed after radiation in either O 2 or N 2. The paternal repair process thus differs from the maternal one in that it also responds to radiation damage induced in O 2. The finding that, following irradiation under anoxia, post-treatment with O 2 (versus that with N 2), also lowers the mutation frequency in mei-9 males, indicates that the repair defect in mei-9 does not interfere with oxygen-dependent post-radiation repair. Thus there are two different paternal repair processes in these early stages of spermatogenesis: that is, one controlled by mei-9 and one depending on oxygen. Mei-41 and mus-101 do not appear to interfere with the paternal repair process. The frequency of translocations recovered from these stages was likewise not affected by mus-101.