A Virus-Inducible E3-RLCK-MADS Module Coordinates Suppression of Plant Immunity and Fertility in Rice.

Viruses often hijack host developmental programs to promote infection, but the mechanistic links between reproductive regulation and antiviral immunity remain incompletely understood. Here, we identify a virus-triggered hierarchical degradation cascade that links antiviral immunity and fertility regulation in rice. We show that the rice grassy stunt virus (RGSV) effector P3 transcriptionally activates P3IP1, a RING-type E3 ubiquitin ligase. P3IP1 ubiquitinates and destabilizes the receptor-like cytoplasmic kinase RLCK22, which functions as a scaffold to stabilize the floral MADS-box transcription factors MADS1 and MADS15. The loss of RLCK22 results in decreased MADS1/15 protein levels, accompanied by reduced pollen viability and increased susceptibility to viral infection. Genetic and biochemical analyses support the existence of a regulatory module involving P3IP1, RLCK22, and MADS1/15. Mutants of mads1, mads15, or rlck22 exhibit overlapping molecular and antiviral phenotypes, including altered pollen viability and impaired transcriptional responses to RGSV. Our findings uncover a virus-inducible E3-RLCK-MADS axis linking post-translational regulation of development and defense, providing new insight into how pathogens manipulate plant fitness through targeted protein degradation.