Nunoshiba T, Nishioka H
Mutat Res. 1987 Jan;183(1):39-44. doi: 10.1016/0167-8817(87)90043-5.
Introduction of the R-factor plasmid pKM101 increased resistance to UV-killing in uvr lexA(Ind-) recA+ strains of E. coli K12 as well as B, while their UV mutability was not affected. Similar effects were also observed in those strains when the 18-B plasmid (a pBR322 derivative carrying the region (about 5 kb) of the 35.4 kb pKM101 plasmid) was introduced. The muc genes which are considered to be involved in error-prone repair are contained in 18-B. These results suggest the possibility that the pKM101 effect requires the host recA gene and a common genetic region, including the muc genes, in both plasmids and is associated with some unmutable repair systems.
R 因子质粒 pKM101 的导入增加了大肠杆菌 K12 以及 B 的 uvr lexA(Ind-) recA+菌株对紫外线杀伤的抗性,而它们的紫外线诱变率未受影响。当导入 18 - B 质粒(一种携带 35.4 kb pKM101 质粒约 5 kb 区域的 pBR322 衍生物)时,在这些菌株中也观察到了类似的效果。被认为参与易错修复的 muc 基因包含在 18 - B 中。这些结果表明,pKM101 的作用可能需要宿主 recA 基因以及一个包括 muc 基因在内的共同遗传区域,该区域存在于两种质粒中,并且与某些不可变修复系统相关。