BRCA1 is required for postreplication repair after UV-induced DNA damage

Shailja Pathania; Jenna Nguyen; Sarah J. Hill; Ralph Scully; Guillaume O. Adelmant; Jarrod A. Marto; Jean Feunteun; David M. Livingston

doi:10.1016/j.molcel.2011.09.002

BRCA1 is required for postreplication repair after UV-induced DNA damage

Shailja Pathania
, Jenna Nguyen
, Sarah J. Hill
, Ralph Scully
, Guillaume O. Adelmant
, Jarrod A. Marto
, Jean Feunteun
, David M. Livingston

Biology

Harvard University
Dana-Farber Cancer Institute
Beth Israel Deaconess Medical Center
UMR8200 Institut Gustave-Roussy

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English
Pages (from-to)	235-251
Number of pages	17
Journal	Molecular Cell
Volume	44
Issue number	2
DOIs	https://doi.org/10.1016/j.molcel.2011.09.002
State	Published - Oct 21 2011

ASJC Scopus Subject Areas

Molecular Biology
Cell Biology

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10.1016/j.molcel.2011.09.002

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title = "BRCA1 is required for postreplication repair after UV-induced DNA damage",

abstract = "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.",

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doi = "10.1016/j.molcel.2011.09.002",

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AU - Pathania, Shailja

AU - Nguyen, Jenna

AU - Hill, Sarah J.

AU - Scully, Ralph

AU - Adelmant, Guillaume O.

AU - Marto, Jarrod A.

AU - Feunteun, Jean

AU - Livingston, David M.

PY - 2011/10/21

Y1 - 2011/10/21

N2 - 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.

AB - 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.

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AN - SCOPUS:82455218968

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SP - 235

EP - 251

JO - Molecular Cell

JF - Molecular Cell

IS - 2

ER -

BRCA1 is required for postreplication repair after UV-induced DNA damage

Abstract

ASJC Scopus Subject Areas

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