SNAC4/9 negatively regulate the resistance of tomatoes to B. cinerea by suppressing phenylpropanoid metabolic pathway

B. cinerea causes severe postharvest gray mold in tomato. SNAC4/9 are NAC transcription factors that regulate ripening and stress responses, but their role in phenylpropanoid-mediated disease resistance remains unclear. This study used Micro-Tom tomato fruits to investigate this mechanism. We demonstrate that SNAC4/9 act as key negative regulators of gray mold resistance in tomato, with SNAC9 exhibiting stronger inhibitory effects than SNAC4. They directly bind promoters of PAL, C4H, CHS, and HQT, downregulating key enzymatic activities in the phenylpropanoid pathway, reducing phenolic/flavonoid accumulation, and redirecting metabolic flux. Exogenous chlorogenic acid (CGA) demonstrates a tripartite synergistic mechanism: directly inhibiting pathogen growth, downregulating SNAC4/9 expression, and reactivating phenylpropanoid biosynthetic genes and enzymatic (phenylalanine ammonia-lyase (PAL), cinnamate 4-hydroxylase (C4H), and chalcone synthase (CHS)) activities via feedback loops to promote defense metabolite accumulation, ultimately delaying fruit disease onset. This study deciphers the cascade regulatory network of the SNAC4/9-phenylpropanoid pathway, revealing novel dimensions of SNAC4/9-mediated defense in fruit. It establishes both a theoretical foundation for disease-resistant breeding and sustainable postharvest management, and an actionable solution for implementing green preservation technologies that replace chemical fungicides.