Studies on mutagen-sensitive strains of Drosophila melanogaster: IV. Modificaiton of genetic damage induced by X-irradiation of spermatozoa and spermatids in N 2 or O 2 by mei-9a, mei-41 D5 and mus(1)101D1

Abstract

The influence of defects in DNA repair processes on X-ray-induced genetic damage in post-meiotic male germ cell stages of Drosophila melanogaster was studied using the ‘maternal effects approach’. Basc males were irradiated in N 2, air or O 2 either as 48-h-old pupae (to sample spermatids) or as 3–4-day-old adults (to sample mature spermatozoa) and mated to females of 3 repair-deficient strains ( mei-9 a: excision-repair-deficient; mei-41 D5 : post-replication-repair-deficient; mus(1)101 D1: post-replication-repair-deficient and impaired in DNA synthesis). Simultaneous controls involving mating of males to repair-proficient females ( mei +) were run. The frequencies of sex-linked recessive lethals and of autosomal translocations were determined following standard genetic procedures. The responses elicited in the different crosses with repair-deficient females were compared with those in mei + crosses. The main findings are the following: (1) with mei-9 females, the frequencies of recessive lethals are higher after irradiation of spermatids in N 2, but not after irradiation in air of O 2 (relative to those in the mei + crosses); this result is different from that obtained in earlier work with spermatozoa, in which cell stage, higher yields of recessive lethals were obtained after irradiation of males in either N 2 or air; (ii) in the mei-9 crosses, there are no significant differences in response (relative to mei +) after irradiation of either spermatozoa or spermatids in O 2; (iii) the translocation frequencies in the mei-9 crosses are similar to those in the mei + crosses, irrespective of the treated germ cell stage or the irradiation atmosphere; (iv) irradiation of either spermatozoa or spermatids in N 2, air or O 2 does not result in any differential recovery of recessive lethals in the mei-41 relative to mei + crosses; (v) irradiation of spermatids in N 2 and of spermatozoa in air leads to a higher recovery of translocations in the mei-41 crosses; and (vi) after irradiation of spermatids or spermatozoa in any of the gaseous atmospheres, the frequencies of recessive lethals and of translocations are lower in the mus-101 crosses. The differences in responses (between cell stages, in different gaseous atmospheres and with different repair-deficient females) are explained on the basis of both qualitative and quantitative differences in the composition of the initial lesions and the extent to which their repair may be affected by the defects present in the different repair-deficient females. Several discrepancies between expectations based on biochemical results and the genetic results are pointed out. Thus it is made clear that not all the genetic results can be easily explained on the basis of the available biochemical information. On the basis of these and other data from experiments on maternal effects with the repair-deficient mutants, a scheme is presented. This scheme envisages the existence of at least 6 classes of qualitatively different types of initial lesions and of at least as many repair pathways through which these lesions are processed.