BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage

SummaryBRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.

Graphical AbstractFigure optionsDownload high-quality image (185 K)Download as PowerPoint slideHighlights
► BRCA1 promotes resistance to UV damage and concentrates at UV-stalled forks
► BRCA1-dependent localization of RFC at UV-stalled forks contributes to their repair
► BRCA1/RFC/9-1-1 interactions contribute to post-UV G2/M checkpoint activation
► BRCA1 suppresses translesional synthesis in UV-damaged cells