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Escherichia coli uvr502 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 (uvrA6) are 15 times more u.v.-sensitive than isogenic uwAf bacteria. Double mutant uvrA6uvr5oz bacteria are only 1.5 times more u.v.-sensitive than uvrA6 bacteria and double mutant uvr502recA56 bacteria were as u.v.-sensitive as recA56 bacteria, suggesting that there exists a uvrA+-and recA+-dependent repair pathway which is blocked by the u v r~o z mutation. We suggest that the uvr5oa mutation affects primarily the excision repair pathway. Strict additivity of the uvr502 and recB21 mutations on U.V. sensitivity suggests that red+-mediated repair acts in part of repair pathway different from excision repair. U.v.-induced DNA degradation in the uvr502 bacteria is only slightly greater than that in uvr+ bacteria and the uvr502 mutation does not affect the 'reckless' character of u.v.-induced DNA breakdown in the recA56 bacteria. The uvr5oa-uvrA6 and uvr502recA56 or uvr5ozrecB21 double mutants have spontaneous mutation frequencies similar to that of the single uvr~oa strain.

Summary. The frequency of direct and reverse mutations at several chromosomal loci increased in UV sensitive uvr502 strains of E. coll. Both UV sensitivity and mutator (Mut-) phenotype are due to the single uvrS02 mutation. In uvr+/uvrS02 merodiploid the Mutphenotype is recessive.

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