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

BRCA1 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 excisio...

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Bibliographic Details
Published in:Molecular cell 2011-10, Vol.44 (2), p.235-251
Main Authors: Pathania, Shailja, Nguyen, Jenna, Hill, Sarah J., Scully, Ralph, Adelmant, Guillaume O., Marto, Jarrod A., Feunteun, Jean, Livingston, David M.
Format: Article
Language:English
Subjects:
BRCA1 Protein - genetics
BRCA1 Protein - metabolism
Cell Line
DNA
DNA Breaks, Double-Stranded
DNA Damage
DNA repair
DNA Repair - physiology
DNA Replication
Humans
replication
Replication Protein C - genetics
Replication Protein C - metabolism
tumor suppressor proteins
ultraviolet radiation
Ultraviolet Rays
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Summary:BRCA1 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. [Display omitted] ► 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
ISSN:1097-2765
1097-4164
DOI:10.1016/j.molcel.2011.09.002