Summary: bacteria have a higher spontaneous mutability and are 4·6 times more u.v.-sensitive than isogenic wild-type bacteria. Bacteria deficient in dimer excision () are 15 times more u.v.-sensitive than isogenic bacteria. Double mutant bacteria are only 1·5 times more u.v.-sensitive than bacteria and double mutant bacteria were as u.v.-sensitive as bacteria, suggesting that there exists a - and - dependent repair pathway which is blocked by the mutation. We suggest that the mutation affects primarily the excision repair pathway. Strict additivity of the and mutations on u.v. sensitivity suggests that -mediated repair acts in part of repair pathway different from excision repair. U.v.-induced DNA degradation in the bacteria is only slightly greater than that in bacteria and the mutation does not affect the ‘reckless’ character of u.v.-induced DNA breakdown in the bacteria. The and or double mutants have spontaneous mutation frequencies similar to that of the single strain.


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