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- W2763248055 abstract "Abstract Besides its role in homologous recombination, the tumor suppressor BRCA2 protects stalled replication forks from nucleolytic degradation. Defective fork stability contributes to chemotherapeutic sensitivity of BRCA2 -defective tumors by yet-elusive mechanisms. Using DNA fiber spreading and direct visualization of replication intermediates, we report that reversed replication forks are entry points for fork degradation in BRCA2 -defective cells. Besides MRE11 and PTIP, we show that RAD52 promotes stalled fork degradation and chromosomal breakage in BRCA2 -defective cells. Inactivation of these factors restores reversed fork frequency and chromosome integrity in BRCA2 -defective cells. Conversely, impairing fork reversal prevents fork degradation, but increases chromosomal breakage, uncoupling fork protection, and chromosome stability. We propose that BRCA2 is dispensable for RAD51-mediated fork reversal, but assembles stable RAD51 nucleofilaments on regressed arms, to protect them from degradation. Our data uncover the physiopathological relevance of fork reversal and illuminate a complex interplay of homologous recombination factors in fork remodeling and stability." @default.
- W2763248055 created "2017-10-20" @default.
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- W2763248055 date "2017-10-16" @default.
- W2763248055 modified "2023-10-14" @default.
- W2763248055 title "Replication fork reversal triggers fork degradation in BRCA2-defective cells" @default.
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- W2763248055 doi "https://doi.org/10.1038/s41467-017-01164-5" @default.
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