EBR-induced metabolic reprogramming contributes to kiwifruit resistance against gray mold

Gray mold caused by Botrytis cinerea is a devastating postharvest disease of kiwifruit. Although 24-Epibrassinolide (EBR) has shown promise in enhancing disease resistance, its metabolic mechanisms in kiwifruit remain unclear. Here, we employed an integrated physiological and metabolomic approach to investigate EBR-induced resistance against B. cinerea in postharvest kiwifruit. EBR treatment significantly reduced lesion development compared to controls. Metabolomic profiling at 24, 48, and 72 h identified 35, 64, and 57 differentially accumulated metabolites, respectively. KEGG pathway enrichment revealed four core pathways: phenylpropanoid/flavonoid biosynthesis, amino acid metabolism, purine/cytokinin signaling, and cuticular/lipid metabolism. Temporal analysis uncovered a triphasic metabolic trajectory: early chemical defense priming (24 h), mid-stage defense amplification with signaling activation (48 h), and late-stage metabolic recovery (72 h). These findings indicate that EBR treatment is associated with time-dependent changes in defense-related metabolites and physiological responses in kiwifruit during B. cinerea infection, suggesting a potential coordinated defense response involving chemical and physical barriers, signaling, and metabolic reallocation. This study provides a comprehensive metabolomic framework for understanding EBR-mediated resistance and offers potential candidate metabolites for postharvest disease management in kiwifruit.