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XB-ART-50453
Mol Cell October 2, 2014; 56 (1): 174-85.
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BRCA1 promotes unloading of the CMG helicase from a stalled DNA replication fork.

Long DT , Joukov V , Budzowska M , Walter JC .


Abstract
The tumor suppressor protein BRCA1 promotes homologous recombination (HR), a high-fidelity mechanism to repair DNA double-strand breaks (DSBs) that arise during normal replication and in response to DNA-damaging agents. Recent genetic experiments indicate that BRCA1 also performs an HR-independent function during the repair of DNA interstrand crosslinks (ICLs). Here we show that BRCA1 is required to unload the CMG helicase complex from chromatin after replication forks collide with an ICL. Eviction of the stalled helicase allows leading strands to be extended toward the ICL, followed by endonucleolytic processing of the crosslink, lesion bypass, and DSB repair. Our results identify BRCA1-dependent helicase unloading as a critical, early event in ICL repair.

PubMed ID: 25219499
PMC ID: PMC4185004
Article link: Mol Cell
Grant support: [+]

Species referenced: Xenopus laevis
Genes referenced: brca1

References [+] :
Bekker-Jensen, Assembly and function of DNA double-strand break repair foci in mammalian cells. 2010, Pubmed