[Effect of neocarzinostatin on E. coli mutants deficient in DNA repair]

The colony forming ability of E. coli mutants defective in DNA repair was compared to that of the parent strain AB 1157 after neocarzinostatin treatment. A recA and a recB mutant were most sensitive. The suppression of the recB mutation in the recBC sbcBC mutant, which is as sensitive as the parent strain, indicates that recB is not the primary pathway by which lesions after NCS treatment are repaired. The survival curve of the recBC recF sbcBC mutant, corresponding to that of the recF mutant, further supports this interpretation. The relative resistance of the recBC recF sbcBC mutant suggests that NCS lesions are not only repaired by the recF and recB pathway. An alternative pathway could be the SOS induction, as a lexA mutant also is sensitive to NCS. The sensitivity of the uvrA and polA xthA mutants, however is explained by the involvement of the uvrA and polA gen products in rec repair.