A plant viral effector subverts FER‐RALF1 module‐mediated intracellular immunity

Summary The receptor‐like kinase FERONIA (FER) is a prominent member of the Catharanthus roseus RLK1 (CrRLK1L) family, functioning as a modulator of immune receptor kinase complex formation in response to rapid alkalinization factors (RALFs). Typically, FER recognizes mature extracellular RALFs to combat bacterial and fungal infections. However, any role of the FER‐RALF signalling cascade in plant viral infections remains unexplored. Here, we used turnip mosaic virus (TuMV), an important member of the genus Potyvirus , and the host Nicotiana benthamiana as a model system to explore the role of the FER‐RALF cascade in plant–virus interactions. RALF1 from N. benthamiana (NbRALF1) positively regulated host resistance to inhibit TuMV infection. Co‐expression studies showed that this process does not involve the conserved RRXL and YISY motifs typically associated with RALF function. Instead, NbRALF1 induced cell death and significantly inhibited TuMV infection in a manner that depends on the entire RALF1 sequence and also NbFER. These results suggest a novel mechanism where NbRALF1 may inhibit viral infection through intracellular interactions with NbFER, differing from the previously reported extracellular FER‐RALF interactions that induce resistance to fungi and bacteria. Furthermore, we discovered that TuMV 6K2 interacts with NbRALF1 and promotes its degradation through the 26S proteasome pathway, thereby counteracting the host resistance induced by the NbFER‐NbRALF1 cascade. Our findings imply the existence of an uncharacterized intracellular immunity signalling pathway mediated by the NbFER‐NbRALF1 cascade and reveal a mechanism by which plant viruses counteract RALF1‐FER module‐mediated immunity.