Alternative pathways of methyl methanesulfonate-induced mutagenesis in Escherichia coli

• Published in: Molecular & general genetics Vol. 216; no. 1; p. 126
• Main Authors: Sledziewska-Gójska, E, Janion, C
• Format: Journal Article
• Language: English
• Published: Germany 01.03.1989
• Subjects: Arginine - metabolism; Bacterial Proteins - genetics; DNA Repair; Escherichia coli - drug effects; Escherichia coli - genetics; Escherichia coli - metabolism; Genes, Bacterial; Methyl Methanesulfonate - pharmacology; Mutagens; Mutation; Rec A Recombinases - genetics
• ISSN: 0026-8925
• DOI: 10.1007/BF00332240

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.