Summary: Strains of deficient in post-replication recombination repair were more sensitive to bleomycin than wild-type, repair-proficient strains. Mutants lacking excision repair functions were no more sensitive to bleomycin than the wild-type strains, indicating that this pathway is not involved in the repair of bleomycin-damaged DNA. Plasmid R46 not only protected repair-proficient strains but also those with or genotypes, suggesting that R46 protection against bleomycin is independent of these host repair functions. However, R46 protection was abolished in or strains, indicating that these gene functions are necessary for plasmid-mediated protection. It is suggested that protection may be due to a -dependent interaction of a plasmid-encoded product with host DNA polymerase I, resulting in an increase in the DNA repair capacity of cells.


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