Khmel' I A, Kopylov V M, Vorob'eva I P, Kurepina Nikitin A N
Genetika. 1980;16(12):2107-19.
The frequency of UV-induced arg+ and his+ reversions is found to be enhanced by the presence of colicinogenic plasmids Ib-P9 and Ia-CA53 and reduced by the presence of plasmid V-K30. The effect of Ib-P9 on the UV-induced mutagenesis depended on recA and lexA genes and was independent on uvrA and recB genes. Plasmids Ib-P9 and V-K30 proved to exert no influence on the frequency of 2-aminopurine-induced mutations. The presence of Ib-P9 reduced the ability of cells carrying the colicinogenic factor E1 to induce colicin E1 synthesis under the action of DNA-damaged agents (UV, nitrosoguanidine, mitomycin C), while plasmid V-K30 enhanced the induction of colicin E1 synthesis. However this effect of plasmids on the induction of colicin E1 synthesis was not observed when the induction occurred under the action of chloramphenicol. Possible mechanisms governing the participation of plasmid gene products in processes related to the repair of DNA are discussed.
发现携带产大肠杆菌素质粒Ib - P9和Ia - CA53可提高紫外线诱导的arg +和his +回复突变频率,而携带质粒V - K30则降低该频率。Ib - P9对紫外线诱导诱变的影响取决于recA和lexA基因,且独立于uvrA和recB基因。事实证明,质粒Ib - P9和V - K30对2 - 氨基嘌呤诱导的突变频率没有影响。Ib - P9的存在降低了携带产大肠杆菌素因子E1的细胞在DNA损伤剂(紫外线、亚硝基胍、丝裂霉素C)作用下诱导大肠杆菌素E1合成的能力,而质粒V - K30则增强了大肠杆菌素E1合成的诱导作用。然而,当在氯霉素作用下进行诱导时,未观察到质粒对大肠杆菌素E1合成诱导的这种影响。讨论了控制质粒基因产物参与DNA修复相关过程的可能机制。