VlNAC29 confers resistance to white rot in grapevine via integrating SA and redox signaling.
White rot, caused by the Coniella diplodiella (Cd), is a devastating disease of grapevine that drives severe losses in yield and quality worldwide. NAC transcription factors are important regulators of plant immune responses. However, the functional roles and regulatory mechanisms of NAC in grapevine defense against Cd remain largely unclear. Here, we demonstrated that VlNAC29 acts as a key positive regulator of grapevine white rot resistance. We showed that NAC29 expression is significantly induced by the chitin, salicylic acid (SA), and Cd infection in both the white rot-resistant grape cultivar ('Zhuosexiang') and susceptible cultivars ('Thompson Seedless' or 'Red Globe'). Subcellular localization and transcriptional activity assays confirmed that VlNAC29 encodes a nuclear-localized protein with transactivation activity. Promoter reporter assays further revealed that the VlNAC29 promoter is strongly activated by SA and chitin. The overexpression of VlNAC29 in grapevine significantly enhanced resistance to Cd infection, as evidenced by enhancing antioxidant enzyme activity and markedly upregulating the expression of defense related genes. Integrative analysis of RNA-seq and qRT-PCR revealed that VlNAC29 modulates the expression of core genes involved in PTI, SA-mediated resistant pathway, and ROS metabolism. Collectively, our findings reveal that VlNAC29 orchestrates SA mediated defense and ROS homeostasis to enhance grapevine resistance against white rot. This research not only advances the mechanistic understanding of NAC mediated grapevine resistance response, but also provides a promising genetic target for molecular breeding of disease resistant grapevines.