Rac-GR24-Induced Defense Responses Against Gray Mold in Postharvest Cherry Fruit Revealed by Physiological and Omics Analyses

Strigolactones (SLs) are carotenoid-derived phytohormones that regulate plant growth, development, and stress adaptation. Although SL-related regulation of plant immunity has been increasingly recognized, its role in postharvest disease resistance remains largely unexplored. In this study, postharvest cherries were treated with different concentrations (0, 0.01, 0.1, 0.5, 1, 1.5, and 2 μM) of rac-GR24, a synthetic SL analogue, or with Tis-108, a chemical inhibitor of SL biosynthesis that targets the cytochrome P450 MAX1 (CYP711A), prior to inoculation with Botrytis cinerea. Among the tested concentrations, 0.1 μM rac-GR24 most effectively suppressed gray mold development, as reflected by reduced disease incidence, lesion diameter, and fungal biomass compared with the control, together with enhanced activities of defense-related enzymes, including CHI and GLU, whereas Tis-108 treatment aggravated disease development. Integrated transcriptomic and metabolomic analyses revealed significant changes in pathways related to phenylalanine, tyrosine, and tryptophan biosynthesis, as well as phenylpropanoid and flavonoid biosynthesis. Notably, rac-GR24 treatment markedly increased the expression and activities of key enzymes involved in the phenylpropanoid pathway, including PAL, C4H, and 4CL. Consistent with these molecular responses, rac-GR24 treatment significantly increased the accumulation of total phenolics, flavonoids, and representative compounds such as catechin, epicatechin, rutin, and chlorogenic acid. Overall, these findings suggest that rac-GR24 treatment is associated with defense responses and changes in phenylpropanoid metabolism in postharvest sweet cherry. This study provides new insights into the molecular basis of defense responses induced by rac-GR24 and highlights its potential as an effective strategy to reduce postharvest losses.