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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)

For most enzyme inducers, hyperplasia is transient and may require specific DNA labeling studies or immunohistochemical stains to clearly identify its occurrence

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doi: 10.1186/s12885-020-07447-3 69 WangQDaiXXiangXXuZSuSWeiDet al