<scp>VqLecRKV.4</scp> and <scp>VqBAK1</scp> Modulate Grapevine Resistance to Powdery Mildew by Regulating Dynamic Balance of <scp>ROS</scp>

Grapevine powdery mildew, caused by the fungal pathogen Erysiphe necator, severely impacts plant growth and berry quality. However, the grapevine receptors and molecular mechanisms underlying grapevine resistance to E. necator remain poorly understood. In this study, we identify a G-type Lectin receptor-like kinase (LecRK), VqLecRKV.4, identified from the wild Chinese grapevine Vitis quinquangularis, whose expression is significantly upregulated in response to E. necator infection. Overexpression of VqLecRKV.4 in the susceptible cultivar V. vinifera 'Thompson Seedless' confers enhanced resistance against the pathogen, as evidenced by significantly reduced fungal colonisation and sporulation. Through TurboID-mediated proximity labelling, we demonstrate that VqLecRKV.4 interacts with VqCu/ZnSOD1. Further analysis reveals that VqLecRKV.4 promotes ROS accumulation and cell death by upregulating VqCu/ZnSOD1 expression, thereby inhibiting E. necator colonisation. A critical challenge in plant immunity is balancing immune responses to avoid overactivation. Here, we discover that VqBAK1 interacts with VqLecRKV.4 and attenuates its overreaction. Collectively, our findings reveal that the VqLecRKV.4-VqBAK1 module fine-tunes grapevine resistance to powdery mildew by maintaining ROS homeostasis, providing novel insights into the molecular mechanisms of grapevine immunity and its regulation to prevent detrimental overreaction.