Mutagen sensitivity of Drosophila melanogaster. VI. Evidence from the excision-defective mei-9AT1 mutant for the timing of DNA-repair activity during spermatogenesis.
The sex-linked recessive lethal test has been used to compare mutation induction by ethyl methanesulfonate and methyl methanesulfonate in spermatogenic stages of the DNA repair-deficient mei-9AT1 mutant and a repair-proficient control strain. For both agents, the data demonstrate that induced mutation rates are similar in both strains for the meiotic and post-meiotic broods. Conversely, for spermatogonial broods, the data indicate that the excision-deficient strain exhibits a 4-8 fold increase in induced mutation rate in comparison to the excision-proficient control strain. These experiments suggest that the low mutability of gonial cells normally observed for these agents is due to effective excision-repair processes which function until the commencement of meiosis. From alkylation mutagenesis experiments with repair-deficient E. coli strains, we note that the mei-9 strain exhibits pleiotropic mutant phenotypes very similar to those displayed by the uvr D mutant. By analogy with these studies, we speculate that mei-9, like uvr D, is deficient in a DNA unwinding protein.
D000818:Animals; D004260:DNA Repair; D004331:Drosophila melanogaster / Q000235:genetics*; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D005804:Genes, Lethal; D005808:Genes, Recessive; D008297:Male; D008540:Meiosis / Q000187:drug effects; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D009153:Mutagens / Q000494:pharmacology*; D013091:Spermatogenesis / Q000187:drug effects*; D013997:Time Factors
D009153:Mutagens; D005020:Ethyl Methanesulfonate; D008741:Methyl Methanesulfonate