Lehrbach P, Kung A H, Lee B T, Jacoby G A
J Gen Microbiol. 1977 Jan;98(1):167-76. doi: 10.1099/00221287-98-1-167.
The R factor pMG2 protects Pseudomonas aeruginosa against the lethal effects of ultraviolet (u.v.) and gamma irradiation, and methyl methanesulphonate and N-methyl-N'-nitro-N-nitrosoguanidine treatment. Enhanced survival occurs in strains of uvr+ rec+ (wild-type) genotype and a variety of uvr rec+ type mutants. No protection occurs in a rec A-type mutant. The plasmid also enhances u.v.-induced mutagenesis. These effects appear to be due to host-cell controlled plasmid-determined DNA repair function(s). Studies on P. aeruginosa strains deficient in DNA polymerase I (polyA) suggest that a plasmid-determined repair resynthesis function may be responsible for increased u.v.-survival and enhanced u.v.-mutability in pMG2-containing bacteria.
R 因子 pMG2 可保护铜绿假单胞菌免受紫外线(uv)、γ 射线照射以及甲磺酸甲酯和 N-甲基-N'-硝基-N-亚硝基胍处理的致死效应。uvr⁺ rec⁺(野生型)基因型菌株以及多种 uvr rec⁺ 型突变体中均出现存活率提高的情况。rec A 型突变体中未出现保护作用。该质粒还可增强紫外线诱导的诱变作用。这些效应似乎归因于宿主细胞控制的质粒决定的 DNA 修复功能。对缺乏 DNA 聚合酶 I(polyA)的铜绿假单胞菌菌株的研究表明,质粒决定的修复再合成功能可能是含 pMG2 的细菌紫外线存活率增加和紫外线诱变率提高的原因。