Antifungal mechanism of selenium against Botrytis cinerea on grapes: Insights from metabolomic and transcriptomic analyses

• Se inhibits Botrytis cinerea growth in vitro and in vivo . • Se causes hyphal breakage, spore collapse, and membrane damage. • Se disrupts mitochondrial β-oxidation and cell wall biosynthesis. • Se downregulates pathogenicity factors and ABC transporters. • Se effectively controls gray mold in grape fruits in vivo . Gray mold, caused by Botrytis cinerea, is a serious postharvest disease of grapes resulting in significant economic losses. By combining multi-omics in vitro and in vivo assays, we evaluated the antifungal activity of 18 mg/L selenium (supplied as sodium selenite) against B. cinerea . Mechanistically, Se treatment caused severe morphological damage in B. cinerea , with scanning electron microscopy revealing broken hyphae and collapse. Metabolomics and transcriptomics analyses showed that Se disrupted mitochondrial β-oxidation and down-regulated genes involved in cell-wall precursor biosynthesis, compromising structural integrity. Se further perturbed cellular processes and energy metabolism by accumulating tricarboxylic acid cycle inhibitors and modulating amino acid turnover. Virulence-related genes ( Bcbrn2, Bcole1 ), ABC transporters ( ABCB1, PDR5 ) were down-regulated, reducing pathogenicity, efflux and carbohydrate transport. Overall, Se disrupted membrane structure, metabolic homeostasis and pathogenicity of B. cinerea through multiple pathways. The reliability of the transcriptomic data was confirmed by quantitative real-time PCR (qPCR) validation of key differentially expressed genes (R² = 0.9923). Importantly, in vivo trials confirmed that Se effectiveness suppressing B. cinerea infection in grape fruits.