THE MUS206 GENE OF DROSOPHILA-MELANOGASTER IS REQUIRED IN THE EXCISION-REPAIR OF ALKYLATION-INDUCED DNA LESIONS

The mus206(A1) mutation, previously identified in our laboratory on th e basis of increased sensitivity to methyl methanesulfonate (MMS), has undergone further analysis. Genetic recombinational mapping data loca lize mus206 at 2-64.8. Sex-linked recessive lethal mutation tests indi cate that mus206(A1) exhibits significant alkylation-induced hypermuta bility, compared to the wild-type Oregon R progenitor strain, suggesti ng a defect in DNA repair function. Results of embryo viability tests show that mus206(A1) and Oregon R embryos hatch to the first instar la rvae at similar rates, indicating that the mus206(A1) mutation does no t confer embryonic lethality. Unscheduled DNA synthesis (UDS) studies with primary embryonic cell cultures subsequently demonstrated conside rably less nucleotide incorporation following treatment with MMS, conf irming that mus206(A1) is deficient at or before the resynthesis step of alkylation-induced DNA excision repair. previous genetic investigat ions have provided indirect support that at least 15 Drosophila genes which display MMS sensitivity are deficient in DNA repair functions. T his study brings to 7 the number of mus genes displaying alkylation ex cision-repair deficiency. (C) 1997 Elsevier Science B.V.