PMID:2192282

Citation	Fix, DF, Koehler, DR and Glickman, BW (1990) Uracil-DNA glycosylase activity affects the mutagenicity of ethyl methanesulfonate: evidence for an alternative pathway of alkylation mutagenesis. Mutat. Res. 244:115-21
Abstract	Mutagenesis induced by the alkylating agent ethyl methanesulfonate (EMS) is thought to occur primarily via mechanisms that involve direct mispairing at alkylated guanines, in particular, O6-ethyl guanine. Recent evidence indicates that alkylation of guanine at the O-6 position might enhance the deamination of cytosine residues in the complementary strand. To determine whether such deamination of cytosine could play a role in the production of mutations by EMS, the efficacy of this agent was tested in uracil-DNA glycosylase deficient (Ung) strains of Escherichia coli. The Ung- strains showed a linear response with increasing doses of EMS. This response was independent of the umuC gene product. In contrast, the Ung+ strains yielded a dose-squared response that became linear at higher doses of EMS when the cells were defective for the umuC gene product. These results support a model for mutagenesis involving the deamination of cytosines opposite O6-alkylated guanines followed by an error-prone repair event.
Links	PubMed
Keywords	DNA Glycosylases; DNA Replication; DNA, Bacterial/biosynthesis; Dose-Response Relationship, Drug; Escherichia coli/enzymology; Escherichia coli/genetics; Ethyl Methanesulfonate/toxicity; Kinetics; Methylation; Mutagenicity Tests; N-Glycosyl Hydrolases/deficiency; Species Specificity; Uracil-DNA Glycosidase
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