Escherichia coli mutator mutants deficient in methylation-instructed DNA mismatch correction.
Our approach to the isolation of DNA mismatch-correction-deficient mutants was based upon the isolation of 2-aminopurine-resistant second-site revertants of Escherichia coli dam- mutants. We isolated such second-site revertants which, when separated from the dam- mutation, have a mutator character of their own. These new mutators all mapped at three known mutator loci, mutH, mutL, and mutS, which exhibit the same mutagenic spectrum as the dam- mutator: increased levels of base substitution and frameshift mutations. The mutator potencies of double and triple mut- mutants suggest that these mutators are involved in the same general mismatch-repair pathway. All these mutations result in a hyper-recombination phenotype, but in four-factor crosses among lambda phages, a specific loss of intragenic recombination (Pam3 X Pam80) was found in mutL and mutS mutants, as would be predicted from the postulated role of mismatch correction in gene conversion and high negative interference phenomena.
D015075:2-Aminopurine / Q000494:pharmacology; D004260:DNA Repair; D004261:DNA Replication; D004269:DNA, Bacterial / Q000235:genetics*; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics*; D005796:Genes; D008745:Methylation; D009154:Mutation; D011995:Recombination, Genetic
D004269:DNA, Bacterial; D015075:2-Aminopurine