Abstract
The mus206A1 mutation, previously identified in our laboratory on the basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data localize mus206 at 2-64.8. Sex-linked recessive lethal mutation tests indicate that mus206A1 exhibits significant alkylation-induced hypermutability, compared to the wild-type Oregon R progenitor strain, suggesting a defect in DNA repair function. Results of embryo viability tests show that mus206A1 and Oregon R embryos hatch to the first instar larvae at similar rates, indicating that the mus206A1 mutation does not confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated considerably less nucleotide incorporation following treatment with MMS, confirming that mus206A1 is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. Previous genetic investigations have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. This study brings to 7 the number of mus genes displaying alkylation excision-repair deficiency.
