Control of wounding-triggered postharvest physiological deterioration by metal ions in crops

Postharvest physiological deterioration (PPD), characterized by rapid tissue discoloration, is a pervasive challenge that inflicts substantial economic losses on a broad range of crops, with cassava being one of the most susceptible species. Wounding-induced reactive oxygen species (ROS) accumulation exerts a central regulatory role in crop PPD. However, the regulatory mechanisms underlying how plants accumulate ROS to initiate PPD in response to wounding remain elusive. Herein, we found that the superoxide anion (O 2 •- , a ROS) burst after wounding constitutes a primary event spatially correlated with cassava PPD, and identified numerous genes encoding ferrous (Fe 2+ )-/copper (Cu 2+ )-core enzymes in O 2 •- -accumulated tissues. Application of Fe 2+ -competitor (cobalt/Co 2+ , nickel/Ni 2+ ), Fe 2+ -chelator (ferrozine), or high concentration of Cu 2+ , significantly suppressed tissue discoloration and O 2 •- accumulation. Additionally, Co 2+ disrupted the biosynthesis of secondary metabolites associated with PPD in cassava, and its robust effect on inhibiting O 2 •- burst and tissue discoloration was conserved across multiple crop species. These results suggest that metal ion-dependent enzymatic pathways might be essential for the regulation of wounding-triggered O 2 •- burst and PPD onset in plants, which provides a promising theoretical basis for developing targeted postharvest preservation strategies applicable to a wide spectrum of crops.