Trichoderma elicitor CP3 induces phosphorylation and nuclear export of SRP to enhance tomato resistance to gray mold

Beneficial Trichoderma fungi enhance plant immunity, but the molecular mechanisms of elicitor-mediated immune priming are still not well defined. Here, we identified a cerato-platanin (CP) family elicitor, CP3, from T. asperellum that enhances tomato resistance to Botrytis cinerea. CP3 is secreted and localizes to the host nucleus, where it interacts with the tomato protein SRP. This interaction recruits casein kinase 1 to phosphorylate SRP at Ser-185, thereby triggering its nuclear export to the plasma membrane. Subsequently, SRP binds the ubiquinone biosynthesis protein COQ9, forming a signaling module that activates reactive oxygen species production and jasmonate/ethylene defense pathways to establish induced systemic resistance. Genetic disruption of CP3, SRP, or COQ9 abolishes CP3-induced resistance, confirming their essential roles. Our findings reveal a complete CP3–SRP–COQ9 signaling axis through which a beneficial fungal elicitor reprograms host nucleocytoplasmic trafficking to activate tailored immunity, offering new molecular targets for engineering disease-resistant crops.