Zhestianikov V D, Savel'eva G E, Zherebtsov S V, Khanbekian L M, Korol'ko O F
Tsitologiia. 1987 Jun;29(6):695-705.
The presence of pKM101 or ColIb-P9 plasmids in E. coli leads to the increase in the survival of UV-irradiated cells of wild type and of polAI, recB21 recC22 and dnaGts mutants; it does not change the survival of recA13 and lex3 mutants and does not influence kinetics and efficiency of postreplication repair (PRR) of DNA in cells of all the strains examined (with the exception of PG3 dnaGts mutant whose PRR of DNA in the presence of pKM101 plasmid is somewhat lower). The survival of both plasmid-containing and plasmid-free bacteria treated with chloramphenicol decreases in the same degree, but the survival of chloramphenicol-treated recA13, lex3 recB21 rec C22 mutants does not change. The pKM101 plasmid does not lend the dnaGts mutant a new capacity of repairing postreplication gaps with the participation of inducible component of PRR; the chloramphenicol-sensitive component of PRR is absent in this mutant. Plasmid and plasmid-free E. coli strains of wild type and of the polA1 mutant do not differ by the kinetics and level of inducible chloramphenicol-sensitive component of PRR of DNA.
大肠杆菌中pKM101或ColIb - P9质粒的存在会导致野生型以及polA1、recB21 recC22和dnaGts突变体的紫外线照射细胞存活率增加；它不会改变recA13和lex3突变体的存活率，并且不影响所检测的所有菌株细胞中DNA复制后修复（PRR）的动力学和效率（除了PG3 dnaGts突变体，其在pKM101质粒存在下的DNA PRR略低）。用氯霉素处理的含质粒和不含质粒的细菌存活率以相同程度降低，但氯霉素处理的recA13、lex3 recB21 recC22突变体的存活率不变。pKM101质粒不会使dnaGts突变体获得在PRR诱导成分参与下修复复制后缺口的新能力；该突变体中不存在PRR的氯霉素敏感成分。野生型和polA1突变体的含质粒和不含质粒的大肠杆菌菌株在DNA PRR诱导性氯霉素敏感成分的动力学和水平上没有差异。
