Chromosome-wide Rad51 Spreading and SUMO-H2A.Z-Dependent Chromosome Fixation in Response to a Persistent DNA Double-Strand Break

摘要: DNA double-strand breaks (DSBs) are acutely hazardous for cells, as they can cause genome instability. DSB repair involves the sequential recruitment of factors to DSBs, followed by Rad51-mediated homology probing, synthesis, and ligation. However, little is known about how cells react if no found DSBs persist. Here, monitoring a single persistent break, we show that, following resection RPA recruitment, Rad51 spreads chromosome-wide bidirectionally from but selectively only on broken chromosome. Remarkably, later fixed nuclear periphery in process that requires Rad51, histone variant H2A.Z, its SUMO modification, DNA-damage checkpoint. Indeed, H2A.Z deposited close break early transiently directs resection, DSB-induced checkpoint activation, anchoring. Thus, induces multifaceted response, which linked specific chromatin mark.