RecB-dependent mutator phenotype in Neisseria meningitidis strains naturally defective in mismatch repair

Several invasive serogroup B meningococcal strains phylogenetically related to the lineageIII (ET-24) exhibited amutator phenotype as shown bymutagenicity assay using rifampicinresistanceas a selection marker. Hypermutationwas associated to the presence of defectivemutL alleles that were genetically characterized. Interestingly, the mutator phenotype wassuppressedwhena non-functional recBET-37 allele, derived fromET-37 meningococcal strains,replaced the functional recB allele in a lineage III strain. In contrast, the same gene replacementdid not affect mutation frequencies in a mismatch repair-proficient strain. Theseresults suggested that in MutL-deficient strains spontaneous mutations mostly arise frompost-replicative DNA synthesis associated to the activity of the RecBCD recombination pathway.