Cold antagonizes salt-induced jasmonate signaling to reconfigure the defense responses of pepper (Capsicum annuum L.).

Combined cold and salt stress antagonizes jasmonate signaling via MYC2 suppression, reallocating resources to flavonoid-based defense and revealing a strategic target for crop multi-stress resilience. Plants are frequently exposed to a combination of abiotic stresses, but the mechanisms governing their non-additive interactions remain largely unclear. In this study, we integrated phenomic, transcriptomic, and metabolomic analyses to elucidate the interplay between cold and salt stress in pepper (Capsicum annuum L.). Unlike individual stresses, which led to progressive damage, the combined stress elicited a pronounced antagonistic effect during a critical 6 ~ 9 h window, characterized by reduced electrolyte leakage (< 40%), a higher relative water content (25 ~ 30%), and attenuated oxidative injury. Transcriptomic profiling revealed that salt stress up-regulated FERL and the master regulator MYC2, involved in the jasmonate (JA) signaling pathway, by 40- and 20-fold, respectively, but these responses were significantly suppressed under combined stress. Further, targeted metabolomics revealed that pelargonidin-3-O-glucoside accumulated by a twofold increase to 1.2 μg g⁻1 under combined stress compared to salt stress alone. Functional validation using virus-induced gene silencing of CaMYC2 (78% efficiency) confirmed that MYC2 is essential for this antagonistic protection. Silenced plants exhibited exacerbated wilting, doubled hydrogen peroxide content, and reduced antioxidant enzyme activities. Collectively, these findings demonstrate that combined cold-salt stress reconfigures defense prioritization by antagonizing JA signaling through MYC2 suppression, thereby reallocating metabolic resources toward flavonoid-based protection. This study provides a mechanistic framework for understanding non-additive stress interactions and identifies strategic targets for enhancing crop multi-stress resilience.