Khmel I A, Kopylov V M, Vorobjeva I P, Polyanin V P
Mol Gen Genet. 1981;181(1):101-6. doi: 10.1007/BF00339012.
The presence of colicinogenic plasmids ColIb-P9 and ColIa-CA53 in E. coli K-12 cells, wild-type with respect to repair, enhanced the survival of cells after UV irradiation and increased the frequency of UV-induced argE3 and his-4 reversions, while the presence of ColV-K30 negatively affected repair and mutagenesis. The plasmid ColIb-P9 showed a UV-protective effect in E. coli cells carrying mutations in genes uvrA, uvrB, uvrC, polA, recB, recF, though in none of the mutants did cell survival reach the wild-type level. The effect of ColIb-P9 on mutagenesis did not depend on the uvrA or recB genes. The plasmid's protective effect and the enhancement of mutagenesis depended on the recA+ lexA+ genotype. The frequency of 2-aminopurine-induced mutations was not affected by ColIb-P9 or ColV-K30. The presence of ColIb-P9 decreased the ability of ColE1-carrying cells to induce colicin E1 synthesis caused by DNA-damaging agents: UV, MNNG, mitomycin C, whereas ColV-K30 increased the percentage of colicin E1-producing cells. These plasmid effects on the level of induction of colicin E1 synthesis were not observed in the case of induction caused by chloramphenicol which did not depend on the products of recA and lexA genes.
在修复方面为野生型的大肠杆菌K-12细胞中，产大肠杆菌素质粒ColIb-P9和ColIa-CA53的存在提高了紫外线照射后细胞的存活率，并增加了紫外线诱导的argE3和his-4回复突变的频率，而ColV-K30的存在则对修复和诱变产生负面影响。质粒ColIb-P9在携带uvrA、uvrB、uvrC、polA、recB、recF基因突变的大肠杆菌细胞中表现出紫外线保护作用，不过在任何一个突变体中，细胞存活率都未达到野生型水平。ColIb-P9对诱变的影响不依赖于uvrA或recB基因。该质粒的保护作用和诱变增强作用依赖于recA⁺ lexA⁺基因型。2-氨基嘌呤诱导的突变频率不受ColIb-P9或ColV-K30的影响。ColIb-P9 的存在降低了携带ColE1的细胞因DNA损伤剂（紫外线、N-甲基-N'-硝基-N-亚硝基胍、丝裂霉素C）诱导大肠杆菌素E1合成的能力，而ColV-K30则增加了产生大肠杆菌素E1的细胞百分比。在由氯霉素诱导的情况下未观察到这些质粒对大肠杆菌素E1合成诱导水平的影响，氯霉素诱导不依赖于recA和lexA基因的产物。
