大坝和错配修复系统对甲磺酸甲酯在大肠杆菌中的诱变及SOS诱导活性的影响。

Influence of dam and mismatch repair system on mutagenic and SOS-inducing activity of methyl methanesulfonate in Escherichia coli.

作者信息

Janion C, Plewako S, Bebenek K, Sledziewska-Gojska E

机构信息

Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw.

出版信息

Mutat Res. 1989 Jan;210(1):15-22. doi: 10.1016/0027-5107(89)90039-0.

DOI:10.1016/0027-5107(89)90039-0

PMID:2642600

Abstract

In contrast to earlier reports (Mohn et al., 1980; Glickman, 1982), we show that E. coli dam- cells are able to mutate following MMS treatment. Since the mutagenicity of MMS has been regarded as largely dependent on induction of the SOS functions, E. coli strains bearing the recA::lacZ or umuC::lacZ fusions were used to determine the ability of MMS to induce the SOS functions in the various dam+ and dam- strains. The mutagenicity of MMS was also tested in several of these strains. The results show that (i) there is no direct correlation between SOS-inducing ability and mutagenicity potency of MMS; and (ii) most of the premutagenic lesions induced by MMS are removed from DNA of dam+ or dam- cells by the mismatch repair system. The role of strand breaks in repair of mismatches induced by alkylating agents is discussed.

摘要

与早期报告（Mohn等人，1980年；Glickman，1982年）不同，我们发现大肠杆菌dam-细胞在MMS处理后能够发生突变。由于MMS的致突变性在很大程度上被认为依赖于SOS功能的诱导，因此使用携带recA::lacZ或umuC::lacZ融合基因的大肠杆菌菌株来确定MMS在各种dam+和dam-菌株中诱导SOS功能的能力。还在其中一些菌株中测试了MMS的致突变性。结果表明：（i）SOS诱导能力与MMS的致突变效力之间没有直接相关性；（ii）MMS诱导的大多数前突变损伤通过错配修复系统从dam+或dam-细胞的DNA中去除。讨论了链断裂在烷基化剂诱导的错配修复中的作用。