Ligation of newly replicated DNA controls the timing of DNA mismatch repair.

ABSTRACT: Mismatch repair (MMR) safeguards genome stability through recognition and excision of DNA replication errors.^1-4 How eukaryotic MMR targets the newly replicated strand in vivo has not been established. MMR reactions reconstituted in vitro are directed to the strand containing a preexisting nick or gap,^5-8 suggesting that strand discontinuities could act as discrimination signals. Another candidate is the proliferating cell nuclear antigen (PCNA) that is loaded at replication forks and is required for the activation of Mlh1-Pms1 endonuclease.^7-9 Here, we discovered that overexpression of DNA ligase I (Cdc9) in Saccharomyces cerevisiae causes elevated mutation rates and increased chromatin-bound PCNA levels and accumulation of Pms1 foci that are MMR intermedi

SUBMITTER: Reyes GX 

PROVIDER: S-EPMC8281387 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature