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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.
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Li et al. (2026) studied this question.
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