title: Alternative pathways of methyl methanesulfonate-induced mutagenesis in Escherichia coli.
abstract: Methyl methanesulfonate (MMS) induced mutagenesis is known to be largely dependent on functional umuCD and recA genes. By phenotypic analysis of Arg+ (argE3, ochre) revertants according to their reversion of the mutations his-4 (ochre) and thr-1 (amber), we attempted to deduce the specificity and/or sites of MMS-induced mutations. It is shown that: (1) MMS-induced, umuC-dependent Arg+ revertants (which prevail in bacteria proficient in mismatch repair) result from a different mutational pathway from umuC-independent ones. UmuC-dependent Arg+ revertants belong to class 2 (Arg+His+Thr-), and umuC-independent ones to class 1 (Arg+His-Thr-). (2) The mismatch repair system very efficiently prevents mutations induced by MMS. We found that in the mutS strain, deficient in mismatch repair, class 1 Arg+ revertants are the most numerous, whereas class 2 Arg+ revertants occur at similar levels in MMS-treated mutS and mutS+ strains. Therefore the mismatch repair system very efficiently prevents formation of umuC-independent Arg+ revertants, but exerts negligible or no effect on umuC-dependent Arg+ revertants. (iii) Both mutS umuC and mutS recA strains, are highly mutable by MMS.
authors.affiliation: Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw.
authors.forename: E
authors.initials: E
authors.lastname: Sledziewska-Gójska
authors.forename: C
authors.initials: C
authors.lastname: Janion
mesh_terms: D001120:Arginine / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics; D004260:DNA Repair; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D005798:Genes, Bacterial; D008741:Methyl Methanesulfonate / Q000494:pharmacology*; D009153:Mutagens; D009154:Mutation; D011938:Rec A Recombinases / Q000235:genetics
chemical_list: D001426:Bacterial Proteins; D009153:Mutagens; D001120:Arginine; D008741:Methyl Methanesulfonate; D011938:Rec A Recombinases