Abstract
Here it is reported that the incidence of mutators among isolates of pathogenic Escherichia coli and Salmonella enterica is high (over 1 percent). These findings counter the theory, founded on studies with laboratory-attenuated strains, that suggests mutators are rare among bacterial populations. Defects in methyl-directed mismatch repair underlie all mutator phenotypes described here. Of nine independently derived hypermutable strains, seven contained a defective mutS allele. Because these mutant alleles increase the mutation rate and enhance recombination among diverse species, these studies may help explain both the rapid emergence of antibiotic resistance and the penetrance of virulence genes within the prokaryotic community.
MeSH terms
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Adenosine Triphosphatases*
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Bacterial Proteins / genetics
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Biological Evolution
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Cloning, Molecular
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DNA Repair / genetics
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DNA-Binding Proteins*
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Disease Outbreaks
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Drug Resistance, Microbial / genetics
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Escherichia coli / genetics*
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Escherichia coli / pathogenicity*
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Escherichia coli Infections / epidemiology
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Escherichia coli Infections / microbiology
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Escherichia coli O157 / genetics
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Escherichia coli O157 / pathogenicity
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Escherichia coli Proteins*
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Food Microbiology
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Genetic Complementation Test
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Humans
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Molecular Sequence Data
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MutS DNA Mismatch-Binding Protein
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Mutation*
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Phenotype
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Polymerase Chain Reaction
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Recombination, Genetic
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Salmonella / genetics*
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Salmonella / pathogenicity*
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Salmonella Food Poisoning / epidemiology
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Salmonella Food Poisoning / microbiology
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Selection, Genetic
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Sequence Deletion
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Sigma Factor / genetics
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Virulence / genetics
Substances
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Bacterial Proteins
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DNA-Binding Proteins
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Escherichia coli Proteins
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Sigma Factor
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sigma factor KatF protein, Bacteria
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Adenosine Triphosphatases
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MutS DNA Mismatch-Binding Protein
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MutS protein, E coli
Associated data
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GENBANK/U29579
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GENBANK/U69873