Recombinational Repair of Mitomycin C Lesions in Phage T4

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Treatment of phage T4-host adsorption complexes with mitomycin C (MMC) doubled the frequency of recombination between two rII markers. The rate at which MMC delivered lethal lesions to cells infected by two or more phage (multicomplexes) was 10-fold less than the rate at which they were delivered to singly infected cells (monocomplexes). Thus there was very strong multiplicity reactivation (MR) of MMC lesions. Four out of five phage mutants tested which were defective in recombination functions were deficient in MR. Mutants defective in genes 46 and 47 lost most of their MR capacity whereas gene 32 and y mutants had a smaller loss. A mutant defective in uvs X had the wild-type level of MR. Mutants defective in two genes with functions unrelated to recombination had no loss of MR. These results suggest that MR of MMC lesions is a recombinational repair process. Mutants defective in genes 46, 47, uvsX, and y, which are involved in recombination, also showed clearly reduced survival in monocomplexes compared to wild type after MMC treatment. This suggests that recombinational repair of MMC lesions occurs in monocomplexes as well as in multicomplexes.