Grzesiuk E, Janion C
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warszawa, Poland.
Mutagenesis. 1998 Mar;13(2):127-32. doi: 10.1093/mutage/13.2.127.
It has been shown that the decline in mutant frequency (MFD) (argE3(ochre)-->Arg+) which occurs in MMS-treated and then transiently starved AB1157 Escherichia coli K-12 cells concerns revertants which arose by supL suppressor formation in a process which is umuDC dependent. Here we have examined whether MMS-induced Arg+ revertants are susceptible to decline when bacteria are deficient in mismatch repair. We show that there is an absence of MFD in MMS-treated M1 (mutS) and in EC2416 (mutS delta umuDC) cells defective in mismatch repair which is associated with a change in the spectrum of MMS-induced mutations formed. In contrast to AB1157, transformation of M1 (mutS) bacteria with plasmids harbouring various combinations of umuD(D')C genes does not enhance the level of MMS-induced mutations but may influence the proportion of supL mutations. These supL mutations show MFD. Repair processes under MFD conditions were confirmed by analysis of plasmid DNA isolated from MMS-treated bacteria at different stages of their starvation and digestion with Fpg protein.
研究表明，在经甲磺酸甲酯（MMS）处理后再短暂饥饿的AB1157大肠杆菌K-12细胞中出现的突变频率下降（MFD）（argE3（赭石型）→Arg+）涉及在一个umuDC依赖性过程中通过supL抑制子形成而产生的回复突变体。在此，我们研究了当细菌错配修复缺陷时，MMS诱导的Arg+回复突变体是否易出现频率下降。我们发现，在错配修复缺陷的经MMS处理的M1（mutS）细胞和EC2416（mutSΔumuDC）细胞中不存在MFD，这与所形成的MMS诱导突变的谱变化有关。与AB1157不同，用携带各种umuD（D'）C基因组合的质粒转化M1（mutS）细菌不会提高MMS诱导的突变水平，但可能会影响supL突变的比例。这些supL突变表现出MFD。通过分析在饥饿和用Fpg蛋白消化的不同阶段从经MMS处理的细菌中分离的质粒DNA，证实了MFD条件下的修复过程。
