Double strand breaks (DSBs) can initiate mitotic catastrophe, a complex oncosuppressive phenomenon characterized by cell death during or after cell division. Through single-cell analysis of extended live imaging, we unveiled how cell cycle-regulated DSB repair in human cells guides disparate cell death outcomes during mitotic catastrophe. Following DSB induction in G2, passage of unresolved homologous recombination (HR) intermediates into mitosis promotes mitotic death in the immediate attempt at cell division. These HR intermediates are dependent upon ATR, BRCA2, PALB2, and RAD51, and counteracted by RTEL1, BTR and SLX4, but not GEN1. HR-driven mitotic death requires spindle assemble checkpoint-dependent mitotic arrest, is propagated by WAPL-dependent cohesion fatigue, and is executed through intrinsic BAX and BAK apoptosis. Conversely, the non-homologous end joining factors DNA-PKcs and LIG4, the microhomology mediated end joining factor POLθ, and the single strand annealing (SSA) factor RAD52, cooperate to enable damaged G1 cells to complete the first cell cycle with chromosome segregation errors. This occurs at the cost of delayed cGAS, MAVS, and Casepase-8 driven extrinsic lethality and corresponding interferon production. Targeting SSA promotes non-immunogenic and HR-dependent mitotic death, while inhibiting mitotic death enhances interferon production. Together the data indicate that a temporal repair hierarchy, coupled with cumulative DSB load, serves as a reliable predictor of mitotic catastrophe outcomes. In this pathway, HR suppresses interferon production by promoting mitotic lethality.