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Furthermore, the mutator phenotype associated with defective MutL activity was suppressed when a non-functional recB allele, derived from ET-37 meningococcal strains, replaced the functional recB allele, suggesting that in MutL-deficient strains, hypermutation mostly arises during post-replicative DNA synthesis associated with the activity of the RecBCD recombination pathway (Colicchio et al., 2006a)