Attfield P V, Pinney R J
J Gen Microbiol. 1982 Mar;128(3):539-47. doi: 10.1099/00221287-128-3-539.
Strains of Escherichia coli 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 recB, recC, uvrA or lig genotypes, suggesting that R46 protection against bleomycin is independent of these host repair functions. However, R46 protection was abolished in recA or polA strains, indicating that these gene functions are necessary for plasmid-mediated protection. It is suggested that protection may be due to a recA+-dependent interaction of a plasmid-encoded product with host DNA polymerase I, resulting in an increase in the DNA repair capacity of cells.
与野生型、具备修复能力的菌株相比,缺乏复制后重组修复功能的大肠杆菌菌株对博来霉素更为敏感。缺乏切除修复功能的突变体对博来霉素的敏感性并不高于野生型菌株,这表明该途径不参与博来霉素损伤DNA的修复。质粒R46不仅能保护具备修复能力的菌株,还能保护具有recB、recC、uvrA或lig基因型的菌株,这表明R46对博来霉素的保护作用独立于这些宿主修复功能。然而,在recA或polA菌株中,R46的保护作用消失,这表明这些基因功能对于质粒介导的保护作用是必需的。有人提出,保护作用可能是由于质粒编码产物与宿主DNA聚合酶I的recA +依赖性相互作用,导致细胞的DNA修复能力增强。