Receptor-like kinase RLK15 binds a fungal RNase effector to enhance autophosphorylation and activate host defense

Fungal pathogens secrete diverse effectors to suppress host immunity, yet the plant receptors that perceive these virulence factors often remain elusive. Here, we identify Ss1624, a secreted RNase from the sugarcane smut pathogen Sporisorium scitamineum, and show that it is recognized by the plasma-membrane-localized CrRLK1L-family receptor kinase RLK15. This recognition triggers canonical immune outputs, including reactive oxygen species burst, callose deposition, defense gene activation, and induces hypersensitive cell death. Mechanistically, Ss1624 physically interacts with the receptor-like kinase RLK15, which is required for Ss1624-triggered cell death. Functional assays indicate that this interaction enhances RLK15 autophosphorylation in a kinase activity-dependent manner, suggesting that Ss1624 can act as an elicitor. Transcript profiling further reveals coordinated expression patterns of Ss1624 and RLK15 during infection, and perturbation of Ss1624 expression alters RLK15 transcript levels and pathogenic outcomes. Extending these findings to rice, the ortholog OsRLK15 contributes positively to resistance to bacterial and fungal diseases without yield penalty in rice. Our results support a model in which a secreted RNase effector is directly sensed by a receptor kinase to initiate broad-spectrum immune responses, providing insights into host-pathogen interactions and identifying RLK15 as a candidate for crop improvement.