Shanabruch W G, Rein R P, Behlau I, Walker G C
J Bacteriol. 1983 Jan;153(1):33-44. doi: 10.1128/jb.153.1.33-44.1983.
Salmonella typhimurium LT2 mutH, mutL, mutS, and uvrD mutants were especially sensitive to mutagenesis by both the recA+-dependent mutagen methyl methane sulfonate and the recA+-independent mutagen ethyl methane sulfonate, but not to mutagenesis by agents such as 4-nitroquinoline-1-oxide and UV irradiation. Similarly, these mutator strains were very sensitive to mutagenesis by the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea. The increased susceptibility to mutagenesis by small alkylating agents due to mutH, mutL, mutS, and uvrD mutations was not accompanied by an increased sensitivity to killing by these agents. Various models are discussed in an effort to explain why strains thought to be deficient in methyl-instructed mismatch repair are sensitive to mutagenesis by methylating and ethylating agents.
鼠伤寒沙门氏菌LT2的mutH、mutL、mutS和uvrD突变体对依赖recA +的诱变剂甲磺酸甲酯和不依赖recA +的诱变剂乙磺酸乙酯的诱变作用特别敏感,但对4-硝基喹啉-1-氧化物和紫外线照射等诱变剂的诱变作用不敏感。同样,这些突变体菌株对甲基化剂N-甲基-N'-硝基-N-亚硝基胍和N-甲基-N-亚硝基脲的诱变作用也非常敏感。由于mutH、mutL、mutS和uvrD突变导致对小烷基化剂诱变作用的敏感性增加,并未伴随着对这些试剂杀伤作用的敏感性增加。文中讨论了各种模型,试图解释为什么被认为在甲基指导的错配修复方面存在缺陷的菌株对甲基化和乙基化试剂的诱变作用敏感。