OsTOPBP1C orchestrates rice immunity through a transcription-dependent functional switching

Nuclear processes underpin host phenotypic plasticity and environmental adaptation, yet how distinct nuclear processes are coordinated in response to external biotic stimuli remains elusive. Here, we employed genome-wide association study (GWAS) to identify OsTOPBP1C, encoding a multifunctional protein that modulates rice resistance to bacterial blight (BB) caused by Xanthomonas oryzae pv. oryzae (Xoo). We discovered that the Xoo-secreted transcription activator-like effector TalDR22^GIV subverts host immunity by commandeering the transcriptional control of OsTOPBP1C. This effector antagonizes OsTOPBP1C transcription induced jointly by the avirulence protein TalAE73^GIV and the DNA damage response integrator OsSOG1, thereby sustaining DNA repair function and counteracting immune responses. Promoter activity assays and transcriptomic analyses support that OsTOPBP1C fine-tunes rice immunity via a transcription-dependent mechanism. Mechanistically, OsTOPBP1C exerts dual roles in rice immunity: under infection, reduced transcription shifts its function toward DNA repair, which promotes OsSOG1-mediated susceptibility; conversely, high transcription enables it to potentiate salicylic acid (SA)-mediated defense through suppressing OsSAH3 transcription activated by OsMYC2. Our findings reveal a pathogen strategy for rewiring host nuclear processes and demonstrate how host gene transcription shapes immune plasticity, offering insights into the molecular choreography of host-pathogen interactions.