Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.

ABSTRACT: The Fanconi anemia (FA) repair pathway governs repair of highly genotoxic DNA interstrand crosslinks (ICLs) and relies on translesion synthesis (TLS). TLS is facilitated by REV1 or site-specific monoubiquitination of proliferating cell nuclear antigen (PCNA) (PCNA-Ub) at lysine 164 (K164). A Pcna^K164R/K164R but not Rev1^-/- mutation renders mammals hypersensitive to ICLs. Besides the FA pathway, alternative pathways have been associated with ICL repair (1, 2), though the decision making between those remains elusive. To study the dependence and relevance of PCNA-Ub in FA repair, we intercrossed Pcna^K164R/+; Fancg^-/+ mice. A combined mutation (Pcna^K164R/K164R; Fancg^-/- ) was found embryonically leth

SUBMITTER: Shah R 

PROVIDER: S-EPMC11217772 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature