Early Response of Five Wine Grape Cultivars to Agrobacterium vitis Infection Suggests a Role of STS in Plant Defense

Crown gall disease, caused by Agrobacterium vitis , is a global threat to viticulture that severely compromises vine vigor and berry quality. To elucidate the molecular mechanisms underlying grapevine resistance, five cultivars were inoculated with A. vitis strain A10 under controlled greenhouse conditions. Pathological assessments revealed divergent disease progression patterns among cultivars in which Yan73 (Y73) and Muscat Blanc (MB) exhibited higher resistance, whereas Y73 displayed mild disease development. Conversely, Merlot (ML), Cabernet Sauvignon, and Chardonnay showed rapid symptom development, and ML was identified as the most susceptible, characterized by the highest incidence and severity. Given that bacterial pathogens such as A. vitis are notoriously difficult to eradicate after infection, characterizing the early infection phase is critical for effective management. Comparative transcriptional analysis (RNA-seq) was conducted to capture the early molecular responses across these cultivars. Differentially expressed genes shared among cultivars were significantly enriched in pathways related to plant–pathogen interaction, stilbene biosynthesis, and responses to oxygen levels. Notably, ethylene signaling and response pathways were predominantly enriched in the relatively resistant cultivars Y73 and MB, suggesting their pivotal role in early defense. Further investigation into the stilbene synthase (STS) pathway revealed that its primary catalytic product, resveratrol (Res), serves as a key defensive metabolite. In vivo assays demonstrated that exogenous Res treatments significantly attenuated disease incidence and severity in a dose-dependent manner. Overall, this study outlines the early immune response of grapevine to A. vitis infection and highlights the importance of STS and ethylene pathways in resistance, providing potential targets for breeding crown gall–resistant grape cultivars.