BRCA2 controls DNA:RNA hybrid level at DSBs by mediating RNase H2 recruitment
RNase H
DOI:
10.1038/s41467-018-07799-2
Publication Date:
2018-12-12T17:20:45Z
AUTHORS (16)
ABSTRACT
DNA double-strand breaks (DSBs) are toxic lesions, which, if not properly repaired, may lead to genomic instability, cell death and senescence. Damage-induced long non-coding RNAs (dilncRNAs) transcribed from broken ends contribute damage response (DDR) signaling. Here we show that dilncRNAs play a role in DSB repair by homologous recombination (HR) contributing the recruitment of HR proteins BRCA1, BRCA2, RAD51, without affecting DNA-end resection. In S/G2-phase cells, pair resected form DNA:RNA hybrids, which recognized BRCA1. We also BRCA2 directly interacts with RNase H2, mediates its localization DSBs S/G2 cell-cycle phase, controls hybrid levels at DSBs. These results demonstrate regulated HR-mediated repair.
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