Repair of UV-induced DNA damage in recombination-deficient strains of Bacillus subtilis.
To clarify the role of gene products for genetic recombination which might be concerned in excision repair, the repair of DNA lesions induced by ultraviolet (UV) irradiation was examined under non-growing conditions with a variety of recombination deficient (Rec-) mutants of Bacillus subtilis. The extent of repair was estimated by the recovery of transforming activity of DNA extracted from the cells during the post-irradiation incubation period (the assay method was termed as marker-repair experiment). The marker repair seemed to be accomplished by the excision repair as assumed from the effects of inhibitors. Among Rec- mutants tested, a mutant strain UVS80TH (rec-80) exhibited a normal level of marker repair activity, whereas strains GSY1025 (recA1), GSY1028 (recB2) and GSY908 (rec-4) exhibited reduced marker repair activities. These results and the data on UV sensitivity of the mutants indicate that (1) the products of all these Rec genes are related to UV resistance of the cell viability and are factors functioning through mechanisms other than excision repair, (2) the products of recA, recB and rec-4 genes display some roles in maintenance of a level of excision repair activity, and (3) the product of the rec-80 gene does not participate at all in excision repair.
D000167:Acriflavine / Q000494:pharmacology; D001412:Bacillus subtilis / Q000502:physiology* / Q000528:radiation effects; D002110:Caffeine / Q000494:pharmacology; D004260:DNA Repair; D004269:DNA, Bacterial; D005838:Genotype; D009154:Mutation / Q000528:radiation effects*; D009268:Nalidixic Acid / Q000494:pharmacology; D010641:Phenotype; D011831:Radiation Genetics; D011995:Recombination, Genetic; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D000167:Acriflavine; D009268:Nalidixic Acid; D002110:Caffeine