RecB-dependent mutator phenotype in Neisseria meningitidis strains naturally defective in mismatch repair.
Several invasive serogroup B meningococcal strains phylogenetically related to the lineage III (ET-24) exhibited a mutator phenotype as shown by mutagenicity assay using rifampicin-resistance as a selection marker. Hypermutation was associated to the presence of defective mutL alleles that were genetically characterized. Interestingly, the mutator phenotype was suppressed when a non-functional recB(ET-37) allele, derived from ET-37 meningococcal strains, replaced the functional recB allele in a lineage III strain. In contrast, the same gene replacement did not affect mutation frequencies in a mismatch repair-proficient strain. These results suggested that in MutL-deficient strains spontaneous mutations mostly arise from post-replicative DNA synthesis associated to the activity of the RecBCD recombination pathway.
Colicchio
Roberta
R
Dipartimento di Biologia e Patologia Cellulare e Molecolare L. Califano, Università di Napoli Federico II, and Istituto di Endocrinologia ed Oncologia Sperimentale G. Salvatore of the CNR, Via S. Pansini 5, 80131 Napoli, Italy.
Pagliarulo
Caterina
C
Lamberti
Florentia
F
Vigliotta
Giovanni
G
Bruni
Carmelo Bruno
CB
Alifano
Pietro
P
Salvatore
Paola
P
D000251:Adenosine Triphosphatases / Q000502:physiology*; D053843:DNA Mismatch Repair; D004261:DNA Replication; D024881:Drug Resistance, Bacterial / Q000235:genetics; D043211:Exodeoxyribonuclease V / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D051719:MutS DNA Mismatch-Binding Protein / Q000235:genetics; D009154:Mutation; D009345:Neisseria meningitidis / Q000145:classification / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D012293:Rifampin; D012703:Serotyping; D014170:Transformation, Genetic
D043211:Exodeoxyribonuclease V; D000251:Adenosine Triphosphatases; D051719:MutS DNA Mismatch-Binding Protein; D012293:Rifampin