Mammalian RAD51 paralogs protect nascent DNA at stalled forks and mediate replication restart

摘要: Mammalian RAD51 paralogs are implicated in the repair of collapsed replication forks by homologous recombination. However, their physiological roles fork maintenance prior to collapse remain obscure. Here, we report on role short-term replicative stress devoid DSBs. We show that localize nascent DNA and common fragile sites upon stalling. Strikingly, deficient cells exhibit elevated levels 53BP1 nuclear bodies increased DSB formation, latter being attributed extensive degradation at stalled forks. RAD51C XRCC3 promote restart an ATP hydrolysis dependent manner disengaging other from halted Notably, find Fanconi anemia (FA)-like disorder breast ovarian cancer patient derived mutations fails protect fork, under-replicated genomic regions micro-nucleation. Taken together, prevent avoid collapse, thereby maintaining integrity suppressing tumorigenesis.