The telomere‐binding protein KU is required for DSB repair in rice mitosis but not in meiosis

Non-homologous end joining (NHEJ) is an error-prone but efficient primary repair pathway for DNA double-strand breaks (DSBs) during mitosis. A critical unresolved question is whether NHEJ acts as a backup when homologous recombination (HR) is impaired during meiosis. Here, we integrated biochemical, cytological, and genetic approaches to dissect the biological role of KU70/KU80, the core component of the NHEJ machinery, in both mitotic and meiotic DSB repair in rice (Oryza sativa). Biochemical analysis confirmed that KU70 and KU80 form a stable heterodimer. KU deficiency caused hypersensitivity to bleomycin in somatic cells, underscoring its essential function in mitotic DSB repair. KU70 localized to meiotic telomeres but was dispensable for normal meiotic progression and DSB repair efficiency. Moreover, KU deficiency neither altered the aberrant chromosome associations in HR-defective mutants (com1, rec8, meica1, hus1, and rad1) nor genetically interacted with key HR factors (ZIP4 and MER3). Taken together, our findings establish rice meiosis operates under an HR-dominant DSB repair regime independent of KU-mediated NHEJ. This stands in striking contrast to the critical role of NHEJ in mitotic DSB repair and clearly demonstrates that KU-mediated NHEJ does not serve as a backup repair pathway for impaired HR during plant meiosis.