Isolation and Properties of Strains of Micrococcus (Deinococcus) radiodurans Unable to Excise Ultraviolet Light-induced Pyrimidine Dimers from DNA: Evidence for Two Excision Pathways

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Abstract
A mutant of D. radiodurans (formerly M. radiodurans) (strain 302, mutant in mtcA) sensitive to the lethal effect of mitomycin C and the mutagenic effect of simple alkylating agents, but having wild-type resistance to UV light, was treated with the mutagen N-methyl-N''-nitro-N-nitrosoguanidine in an attempt to isolate strains deficient in the ability to excise UV-induced pyrimidine dimers. Three strains were isolated that were UV-sensitive, but had wild-type resistance to the lethal effect of methyl methanesulfonate, and all were unable to excise pyrimidine dimers. These 3 strains (UVS9, UVS25 and UVS78) had, besides the mutation in mtcA, mutations in loci designated uvsC, uvsD and uvsE, respectively. When the mutant mtcA gene was replaced by its wild-type allele in all 3 strains they became UV- and mitomycin C-resistant. On incubating the double mutants UVS9, UVS25 and UVS78 with wild-type DNA, $ 50% of the transformants selected for UV resistance were mitomycin C-sensitive and .apprx. 50% resistant depending on whether the mutant mtcA or the uvsC, D or E genes had been replaced by their wild-type alleles. Although strains mutant singly in uvsC, D or E were UV-resistant, the pyrimidine dimer excision rates differed among them and were slower in all of them than in the wild-type strain 302. Thus, wild-type D. radiodurans evidently possesses 2 pathways for the excision of pyrimidine dimers and mutational blocks in both must exist for the excisionless phenotype to be expressed.

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