Figure 5.

Model describing possible mechanism of RAD52-DSS1 activity in the DSB repair. DSBs or stalled replication forks are resected to produce ssDNA required for homology-directed repairs, alternatively blocked resection allows repair by c-NHEJ. While initial small resection makes DNA ends available for a-NHEJ, extensive resection generates long ssDNA stretches occupied by RPA. BRCA2 in the complex with DSS1 helps to alleviate RPA inhibitory effect and load RAD51 presynaptic filament to promote HR. RAD52-mediated SSA/BIR represents an alternative repair pathway, where DSS1 may facilitate this process via stimulation of RAD52 binding and strand invasion activities. Therefore, in the absence of BRCA2, RAD52/DSS1 becomes essential to process breaks/forks via SSA/BIR pathways.