Role of ruvAB genes in UV- and gamma-radiation and chemical mutagenesis in Escherichia coli.

Escherichia coli umuC122::Tn 5 was mutagenized with N-methyl-N'-nitro-N-nitrosoguanidine to isolate mutations that block the residual gamma-radiation mutagenesis observed in umuC strains. Two of these mutations were shown by transductional mapping and plasmid complementation to map in the ruvA and ruvB genes (i.e., ruvA200 and ruvB201). Whereas ruvA200 was complemented by ruvA+ plasmids, the only other known ruvA mutation, ruvA59::Tn10 required both the ruvA+ and ruvB+ genes to show complementation. The ruvA200, ruvB201, ruvA59::Tn10 and ruvB60::Tn10 mutations all reduced gamma-radiation-induced ochre reversion [argE3(Oc)----Arg+] to about 30% of the wild-type level, and they all reduced UV-radiation-induced ochre reversion to about 15% of the wild-type level. The ruvA200 and ruvB201 mutants also showed reduced gamma- and UV-radiation mutagenesis with two other assays [hisG4(Oc)----His+ and Rifs----Rifr]. Streptozotocin mutagenesis (Rifr) was reduced to about half of the wild-type level in ruv strains, but ethyl methanesulfonate mutagenesis was normal. While the umuC strain did not show the oxygen enhancement of gamma-radiation mutagenesis, the ruvA200 strain showed an oxygen effect that was similar to that shown by the wild-type strain. When the ruvA200 mutation was combined with the umuC mutation, gamma-radiation mutagenesis was further reduced to 5% of the wild-type level and cells showed a synergistic sensitization to UV- and gamma-radiation-induced killing. A mutational spectrum analysis indicates a general depression of both umuC-dependent and umuC-independent gamma-radiation mutagenesis in the ruvA strain, which is in contrast with the site-specific reduction in gamma-radiation mutagenesis that is observed in the umuC mutant. The reduced radiation mutagenesis in the ruvA strain could not be correlated with a reduction in transcription of the recA or umuC genes.