Low temperature conditioning (LTC) alleviates peach fruit chilling injury but the underlying molecular basis is poorly understood. Here, changes in transcriptome, ethylene production, flesh softening, internal browning and membrane lipids were compared in fruit maintained in constant 0 °C and LTC (pre-storage at 8 °C for 5 d before storage at 0 °C). Low temperature conditioning resulted in a higher rate of ethylene production and a more rapid flesh softening as a result of higher expression of ethylene biosynthetic genes and a series of cell wall hydrolases. Reduced internal browning of fruit was observed in LTC, with lower transcript levels of polyphenol oxidase and peroxidase, but higher lipoxygenase. Low temperature conditioning fruit also showed enhanced fatty acid content, increased desaturation, higher levels of phospholipids and a preferential biosynthesis of glucosylceramide. Genes encoding cell wall hydrolases and lipid metabolism enzymes were coexpressed with differentially expressed ethylene response factors (ERFs) and contained ERF binding elements in their promoters. In conclusion, LTC is a special case of cold acclimation which increases ethylene production and, operating through ERFs, promotes both softening and changes in lipid composition and desaturation, which may modulate membrane stability, reducing browning and contributing to alleviation of peach fruit chilling injury.
Peach is prone to postharvest chilling injury (CI). Here it was found that exogenous ethylene alleviated CI, accompanied by an increased endogenous ethylene production. Ethylene treatment resulted in a moderately more rapid flesh softening as a result of stronger expression of genes encoding expansin and cell wall hydrolases, especially xylosidase and galactosidase. Ethylene treatment alleviated internal browning, accompanied by changes in expression of polyphenol oxidase, peroxidase and lipoxygenases. An enhanced content of phospholipids and glycerolipids and a reduced content of ceramide were observed in ethylene-treated fruit, and these were associated with up-regulation of lipid phosphate phosphatase, fatty acid alpha-hydroxylase, and golgi-localized nucleotide sugar transporter, as well as down-regulation of aminoalcohol phosphotransferases. Expression of two ethylene response factors (ERFs), ESE3 and ABR1, was highly correlated with that of genes involved in cell wall metabolism and lipid metabolism, respectively. Furthermore, the expression of these two ERFs was strongly regulated by ethylene treatment and the temperature changes during transfer of fruit into or out of cold storage. It is proposed that ERFs fulfill roles as crucial integrators between cell wall modifications and lipid metabolism involved in CI processes ameliorated by exogenous ethylene.
Chilling injury (CI) is a physiological disorder induced by cold, which heavily limit crop production and postharvest preservation worldwide. Methyl jasmonate (MeJA) can alleviate CI in various fruit species, including peach; however, the underlying molecular mechanism is poorly understood. Here, changes in contents of phenolics, lipids, and jasmonic acid (JA) and gene expressions are compared between MeJA and control fruit. Exogenous MeJA inhibited expressions of PpPAL1, PpPPO1, and PpPOD1/2 but did not affect the phenolic content. Furthermore, MeJA fruit showed lower relative electrolyte leakage, indicating less membrane damage. Meanwhile, the enrichment of linoleic acid in the potential lipid biomarkers, especially phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol, coincided with lower expressions of PpFAD8.1 but higher PpLOX3.1 and JA content. In the JA signaling pathway, MeJA significantly upregulated expressions of PpMYC2.2 and PpCBF3 but downregulated PpMYC2.1. In conclusion, adjustments of fatty acids in phospholipids contribute to MeJA-induced alleviation of CI in peach fruit via induction of the JA-mediated C-repeat-binding factor pathway.
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