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.
Subject(s)
DNA Repair , Escherichia coli/genetics , Genes, Bacterial , Methyl Methanesulfonate/toxicity , Mutation/drug effects , SOS Response, Genetics , DNA, Bacterial/genetics , Mutagenicity TestsABSTRACT
It was shown that some base analogs, like n2Pur and n2oh6Ade (but not n2om6Ade or oh4Cyd) which strongly inhibit growth of dam- cells, mutagenize and preselect dam- populations. As a result dam- mut(-)--devoid of mismatch repair, dam+ revertants, or dam(-)--insensitive to a base analog are exclusively obtained after mutagenesis. The composition of these mutants depends on the base analog applied. By using reconstruction experiments, the frequency of these mutations induced by n2Pur was calculated.
