Abstract
Okra fruit have short postharvest potential and are susceptible to chilling injury (CI). To increase our understanding of the metabolism of okra fruit we have analyzed the transcriptomic and metabolomic changes of the fruit stored at 4, 10, and 22 ℃ for six days. Compared with 0 d, storage at 22 °C for 6 days, senescence and lignification of fruit were associated with upregulation of genes related to abscisic acid (ABA) synthesis and signal transduction (ZEP, NCED, AAO, PYR/PYL, PP2C), lignin synthesis (HCT, 4CL, CCR, CAD, F5H, COMT), and cellulose synthesis (CesA). Chilling injury of okra at 4 ℃ may be caused by the activation of the α-linolenic acid metabolic pathway and flavonoid synthesis pathway, compromised membrane integrity, and higher reactive oxygen species levels. Storage at 10 ℃ resulted in the downregulation of ABA synthesis, signal transduction, and lignin synthesis genes, inhibition of α-linolenic acid pathway metabolites, and the expression of membrane lipid degradation genes (PLD, PLA, lipase, DGK, LOX). Conversely, there was an upregulation of antioxidant enzymes (APX, AO, POD, Grx, MDHAR) and genes involved in the flavonoid synthesis pathway (C4H, CHS, CHI, F3H, ANS), and with their corresponding metabolites (pinocembrin, butin, epiafzelechin, catechin). These changes were associated with slower fruit senescence, indicating that 10 ℃ better maintained the physiological quality of okra fruit after harvest. Based on these findings, a network model was established to control the postharvest quality of okra fruit under different temperature treatments. This study explored the regulatory mechanism of okra at different temperatures at the molecular level and laid a theoretical foundation for improving the quality of postharvest okra and extending its shelf life.
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