Verticillium dahliae CAP-containing effectors hijack the β-subunit of the SnRK1 complex to suppress plant immunity

Abstract The soil-borne fungus Verticillium dahliae causes Verticillium wilt, a devastating disease threatening global cotton production. Like many pathogens, V. dahliae delivers effectors into plant cells to facilitate infection. The CAP (Cysteine-rich secretory protein, Antigen 5 and Pathogenesis-related protein 1) superfamily represents a typical group of secretory proteins that function as virulence factors and modulate plant immunity. Although V. dahliae utilizes CAP proteins to disrupt plant immune responses, the underlying mechanisms remain unclear. In this study, we initially screened the targets of VdCAP1 in cotton and demonstrated that it interacts with the β-subunit of SnRK1 complex both in vivo and in vitro. Silencing GhSnRK1β1 significantly enhanced susceptibility to V. dahliae infection, indicating its positive role in cotton defense against the pathogen. Further investigation revealed that VdCAP1 disrupts the interaction between SnRK1β1 and the core α-subunit of the SnRK1 complex and reduces the nuclear accumulation of GhSnRK1β1. Notably, GhSnRK1β1 exhibits opposing roles depending on its subcellular localization. Nuclear-localized GhSnRK1β1 promotes flg22-triggered ROS accumulation, whereas cytoplasmic-localized GhSnRK1β1 suppresses ROS accumulation. Furthermore, co-expression of VdCAP1 also promotes GhSnRK1β1-mediated ROS scavenging. Another secretory protein, VdCAP3, which functions as a plant immunity suppressor, interacts with GhSnRK1β1 and similarly restricts its nuclear accumulation to suppress plant immunity. Collectively, these findings indicated that VdCAP1/3 suppresses plant immunity by targeting SnRK1β1, thereby increasing V. dahliae pathogenicity.