Bagg A, Kenyon C J, Walker G C
Proc Natl Acad Sci U S A. 1981 Sep;78(9):5749-53. doi: 10.1073/pnas.78.9.5749.
The product of the umuC gene is required for UV and chemical mutagenesis in Escherichia coli. By the use of the Mud(Ap, lac) bacteriophage, we have obtained an operon fusion of the lac structural genes to the promoter/regulatory region of the umuC gene. The strain containing the umuC::Mud(Ap, lac) fusion was identified on the basis of its UV nonmutability. Strains containing this putative null allele of umuC were (i) nonmutable by UV and other agents, (ii) slightly UV sensitive, and (iii) deficient in their ability to carry out Weigle reactivation of UV-irradiation bacteriophage lambda. The UV nonmutability of the strain could be suppressed by a derivative of the mutagenesis-enhancing plasmid pKM101. beta-Galactosidase synthesis in umuC::Mud(Ap, lac) fusion strains was inducible by UV and other DNA-damaging agents. Genetic analysis of the regulation of beta-galactosidase in umuC::Mud(Ap, lac) strains suggests that the lexA protein is the direct repressor of the umuC gene and that a function of the recA protein, probably its protease activity, is required for the removal of the lexA repressor at the time of umuC induction.
大肠杆菌中紫外线和化学诱变需要umuC基因的产物。通过使用Mud(Ap, lac)噬菌体,我们获得了lac结构基因与umuC基因启动子/调控区域的操纵子融合。含有umuC::Mud(Ap, lac)融合的菌株根据其紫外线不可诱变特性得以鉴定。含有这种假定的umuC无效等位基因的菌株:(i) 对紫外线和其他诱变剂不可诱变;(ii) 对紫外线轻度敏感;(iii) 进行紫外线照射噬菌体λ的韦格勒再活化的能力存在缺陷。该菌株的紫外线不可诱变特性可被诱变增强质粒pKM101的衍生物所抑制。在umuC::Mud(Ap, lac)融合菌株中,β-半乳糖苷酶的合成可被紫外线和其他DNA损伤剂诱导。对umuC::Mud(Ap, lac)菌株中β-半乳糖苷酶调控的遗传分析表明,lexA蛋白是umuC基因的直接阻遏物,并且在umuC诱导时,recA蛋白的功能,可能是其蛋白酶活性,是去除lexA阻遏物所必需的。