Model for SUMO proteins function in DSB repair. Following DSB, end resection is required for HR or Alt-NHEJ repair; otherwise, DNA ends are protected from minimal processing and C-NHEJ is employed to repair the damage. A, in the HDR pathway, SUMO1 (S1) stimulates the repair process by a non-covalent binding to SIM of RAD51 or other repair proteins. We model that the SUMO1-SIM interaction regulates RAD51 accretion on resected DSB ends. B and C, when SSA or Alt-NHEJ is utilized in response to a DSB, SUMO1 interacts non-covalently with an unknown repair factor (X or Y) via the SIM of the protein at sites of DSB to promote the subsequent repair events. D, in C-NHEJ, in which DNA ends are protected, SUMO1 and SUMO2/3 (S2/3) conjugation to an unknown target repair mediator (Z) is essential for efficient repair.