Jasmonate Modulates Strawberry Susceptibility to Anthracnose by Activating SnRK2.1 to Regulate the WRKY50‐JAZ5 Module

ABSTRACT Colletotrichum spp., hemibiotrophic fungal pathogens, threaten global strawberry production. Jasmonate (JA) regulates plant‐ Colletotrichum interactions, but its mechanisms remain unclear. Here we demonstrate that both exogenous methyl jasmonate (MeJA) treatment and elevated endogenous MeJA levels increase strawberry susceptibility to anthracnose. Two key JA biosynthesis genes, FveAOS2 and FveAOC3 , were identified as contributors to Colletotrichum ‐induced susceptibility. Further analysis revealed that the FveSnRK2.1–FveWRKY50 phosphorylation module functions as an important molecular switch in regulating disease susceptibility. Specifically, Colletotrichum infection or MeJA application activates FveSnRK2.1, which phosphorylates FveWRKY50 at serine residue 88 (S88). This phosphorylation enhances the stability and transcriptional activity of FveWRKY50, leading to increased expression of FveAOS2 and FveAOC3 , higher MeJA accumulation and enhanced susceptibility. Notably, the strawberry JASMONATE‐ZIM DOMAIN (JAZ) protein FveJAZ5 suppresses susceptibility by directly interacting with FveWRKY50, thereby preventing its interaction with FveSnRK2.1 and inhibiting the activation of FveAOS2 and FveAOC3 . Upon pathogen attack or MeJA signalling, FveJAZ5 is degraded, thereby releasing FveWRKY50 from suppression. The study elucidates a Colletotrichum ‐induced ‘JA signaling – JA biosynthesis’ positive feedback loop that drives strawberry susceptibility. Knocking out FveWRKY50 and overexpressing FveJAZ5 generated anthracnose‐resistant germplasms. These findings deepen understanding of plant‐ Colletotrichum interactions and provide genes for resistant strawberry breeding.