Journal
CELL REPORTS
Volume 34, Issue 4, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.108669
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Funding
- National Institutes of Health (NIH) [1R35GM137800]
- Department of Cell Biology, Microbiology and Molecular Biology (CMMB)
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DCAF14, a substrate receptor for the CRL4 complex, plays a crucial role in stabilizing stalled replication forks and preventing double-strand breaks, thereby promoting genome integrity. This study demonstrates the replication stress response functions of DCAF14 in ensuring genome maintenance.
Replication stress response ensures impediments to DNA replication do not compromise replication fork stability and genome integrity. In a process termed replication fork protection, newly synthesized DNA at stalled replication forks is stabilized and protected from nuclease-mediated degradation. We report the identification of DDB1- and CUL4-associated factor 14 (DCAF14), a substrate receptor for Cullin4-RING E3 ligase (CRL4) complex, integral in stabilizing stalled replication forks. DCAF14 localizes rapidly to stalled forks and promotes genome integrity by preventing fork collapse into double-strand breaks (DSBs). Importantly, CRL4(DCAF14) mediates stalled fork protection in a RAD51-dependent manner to protect nascent DNA from MRE11 and DNA2 nucleases. Thus, our study shows replication stress response functions of DCAF14 in genome maintenance.
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