Stonesifer J, Baltz R H
Proc Natl Acad Sci U S A. 1985 Feb;82(4):1180-3. doi: 10.1073/pnas.82.4.1180.
Streptomyces fradiae JS6 (mcr-6) is defective in the repair of potentially lethal damage to DNA induced by mitomycin C (MC), hydroxylamine (NH2OH), methyl methanesulfonate (MMS), 4-nitroquinoline 1-oxide (NQO), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and ultraviolet light (UV), but it exhibits nearly normal sensitivity to ethyl methanesulfonate (EMS)-induced lethality. JS6 is substantially less mutable by MNNG, MMS, NQO, UV, NH2OH, and also EMS than is the parental strain. A spontaneous revertant of JS6 showed wild-type levels of resistance to all of these agents and wild-type levels of induced mutagenesis, indicating that a single mutation caused the multiple traits displayed by JS6. The mcr-6 gene product thus appears to control an error-prone (mutagenic) DNA repair system. Mediation of EMS mutagenesis by an error-prone repair pathway in S. fradiae, rather than by direct mispairing as in Escherichia coli, suggests that the streptomycetes have evolved more efficient error-avoidance mechanisms than those commonly observed in the single-celled eubacteria.
弗氏链霉菌JS6（mcr - 6）在修复由丝裂霉素C（MC）、羟胺（NH2OH）、甲磺酸甲酯（MMS）、4 - 硝基喹啉1 - 氧化物（NQO）、N - 甲基 - N' - 硝基 - N - 亚硝基胍（MNNG）和紫外线（UV）诱导的对DNA的潜在致死性损伤方面存在缺陷，但它对甲磺酸乙酯（EMS）诱导的致死性表现出近乎正常的敏感性。与亲本菌株相比，JS6对MNNG、MMS、NQO、UV、NH2OH以及EMS的诱变作用明显更低。JS6的一个自发回复突变体对所有这些试剂表现出野生型水平的抗性以及野生型水平的诱导诱变，表明单个突变导致了JS6所表现出的多种性状。因此，mcr - 6基因产物似乎控制着一个易错（诱变）的DNA修复系统。弗氏链霉菌中EMS诱变是通过易错修复途径介导的，而不是像大肠杆菌那样通过直接错配，这表明链霉菌已经进化出比单细胞真细菌中常见的更有效的错误避免机制。
