Studies on mutagen-sensitive strains of Drosophila melanogaster: IX. Modification of genetic damage induced by X-irradiation of spermatozoa in N 2, air or O 2 by 4 autosomal repair-deficient mutants

Abstract

The influence of defects in DNA repair on the recovery of X-ray-induced genetic damage in spermatozoa of Drosophila melanogaster was studied. Basc males were irradiated in N 2, air or O 2 and mated to females of 4 repair-deficient mutant types: mus(2)201 D1 (excision repair deficient), mus(3)306 D1 (excision repair deficient), mus(3)302 D1 and mus(3)308 D2 (both excision repair and post-replication repair deficient). The frequencies of sex-lined recessive lethals and of autosomal translocations in the F 1 progeny were determined following standard genetic procedures. The responses in the different crosses with repair-deficient females were compared to those with repair-proficient mei + females (maternal effects). The main findings are the following: (1) with excision repair-deficient females the frequencies of spontaneous recessive lethals tend to be higher than with mei + females; (2) with excision repair-deficient females the frequencies of recessive lethals induced in N 2 and air and often in O 2 are higher than with mei + females; (3) with post-replication repair-deficient mutants a maternal effect is found for X-ray-induced translocations - both increases and decreases occur depending on the specific mutant type. The data are explained as follows: excision repair deficiencies cause the processing of primary lesions to be diverted from the error-free excision repair to the error-prone post-replication repair pathways. This results in enhanced mutational yields. After irradiation in O 2 secondary effects cause selective elimination of potential recessive lethals in those mutants that exhibit lowered fertility ( mei-9, mus-302). Therefore those mutants have no differential maternal effect on the recovery of recessive lethals after irradiation in O 2. The changes in translocation yield with post-replication repair deficiencies are thought to be the result of defects in the repair of DNA breaks. These defects might cause the post-replication repair deficiency too. The group of post-replication repair mutants is heterogenous. The mutants with low fertility seem to cause decreased translocation frequencies by selective elimination through dominant lethality. The other mutants increase the frequencies.