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Abstract
Summary: 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 uvrA + bacteria. Double mutant uvrA6 uvr502 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 uvr502 mutation. We suggest that the uvr502 mutation affects primarily the excision repair pathway. Strict additivity of the uvr502 and recB21 mutations on u.v. sensitivity suggests that recB +-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 ဘrecklessမ character of u.v.-induced DNA breakdown in the recA56 bacteria. The avr502-uvrA6 and uvr 502 rec A56 or uvr502recB21 double mutants have spontaneous mutation frequencies similar to that of the single uvr502 strain.
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