OsTOPBP1C orchestrates rice immunity through transcription-dependent functional switching

Nuclear processes underpin host phenotypic plasticity and environmental adaptation, but how distinct nuclear processes are coordinated in response to external biotic stimuli remains poorly understood. Here, we performed a genome-wide association study and identified OsTOPBP1C, which encodes a multifunctional protein that modulates rice resistance to bacterial blight caused by Xanthomonas oryzae pv. oryzae. We demonstrated that the Xoo-secreted transcription activator-like effector TalDR22^GIV subverts host immunity by commandeering the transcriptional control of OsTOPBP1C. TalDR22^GIV antagonizes OsTOPBP1C transcription induced by the avirulence protein TalAE73^GIV and the DNA damage response integrator OsSOG1, thereby sustaining the DNA repair function of OsTOPBP1C and counteracting immune responses. Promoter activity assays and transcriptomic analyses revealed that OsTOPBP1C fine-tunes rice immunity through a transcription-dependent mechanism. Mechanistically, OsTOPBP1C plays two roles in rice immunity: during infection, reduced transcription shifts its function toward DNA repair, thereby promoting OsSOG1-mediated susceptibility; conversely, high levels of OsTOPBP1C transcription enable it to potentiate salicylic acid-mediated defenses by suppressing the transcription of OsSAH3 activated by OsMYC2. Our findings reveal a pathogen strategy for rewiring host nuclear processes and demonstrate how host gene transcription shapes immune plasticity, providing insight into the molecular choreography of host-pathogen interactions.