Gap-filling repair synthesis induced by ultraviolet light in a Bacillus subtilis Uvr- mutant.
Deoxyribonucleic acid repair synthesis was studied in one wild-type and two mutant strains of Bacillus subtilis that are defective in excision of pyrimidine dimers. The cells were irradiated with ultraviolet light, and 6-(p-hydroxyphenyl-azo)-uracil was used to block replicative synthesis, allowing only repair synthesis. One of the mutations (uvs-42) resulted in a severe inhibition of incision, dimer excision, and repair synthesis. In contrast, the other mutant (uvr-1) slowly incised and excised dimers and did repair synthesis in patches which appear to be several-fold longer than those in the wild-type strain, apparently because large gaps are produced at excision sites. The results indicate that the primary defect in uvs-42 cells is in initiation of dimer excision, whereas the uvr-1 mutation appears to be a defect in the exonuclease normally used to complete dimer excision.
D001412:Bacillus subtilis / Q000235:genetics* / Q000378:metabolism / Q000528:radiation effects; D004260:DNA Repair; D004269:DNA, Bacterial / Q000096:biosynthesis*; D005796:Genes; D009154:Mutation; D011740:Pyrimidine Dimers / Q000378:metabolism*; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D011740:Pyrimidine Dimers