In this study, to investigate the physiological and molecular mechanisms of melatonin inhibiting the postharvest rot of blueberry fruits, blueberry fruits were dipped in 0.3 mmol L−1 melatonin solution for 3 min and stored at 0°C for 80 days. The results indicated that melatonin did not significantly (p > 0.05) inhibit the mycelial growth or spore germination of Alternaria alternata, Botrytis cinerea, and Colletotrichum gloeosporioides. In addition, an in vivo study revealed that melatonin treatment increased the enzymatic activities of phenylalanine ammonia lyase (PAL), cinnamate 4-hydroxylase (C4H), 4-coumarate-CoA ligase (4CL), cinnamyl alcohol dehydrogenase (CAD), polyphenol oxidase (PPO), and peroxidase (POD) in fruits. Furthermore, genes related to jasmonic acid synthesis were upregulated (VaLOX, VaAOS, and VaAOC), as were those related to pathogenesis-related proteins (VaGLU and VaCHT) and phenylpropane metabolism (VaPAL, VaC4H, Va4CL, VaCAD, VaPPO, and VaPOD), which promoted the accumulation of total phenols, flavonoids, anthocyanins, and lignin in the fruits. These results suggest that melatonin enhances the postharvest disease resistance of blueberry fruits by mediating the jasmonic acid signaling pathway and the phenylpropane pathway.

We investigated the effects of melatonin (MT) treatment on the physiological quality and cell wall metabolism of kiwifruit during a 12-day shelf life period (20 ± 1 °C, 90 ± 5% RH), after 90 days of cold storage (0 ± 0.5 °C, 90 ± 5% RH). Our results showed that MT treatment delayed kiwifruit softening, as evidence by the enhanced endurance of a healthy appearance, quality, color difference L* value, and firmness of the fruit flesh. MT treatment reduced fruit decay rate, respiration rate, and malondialdehyde content; furthermore, MT-treated kiwifruit maintained high levels of total soluble solids, titratable acid, and ascorbic acid. Additionally, MT inhibited the decrease in fruit pectin, cellulose, and hemicellulose contents; it delayed the increase in watersoluble pectin content and kept pectin methyl esterase, polygalacturonase, cellulase, and β-galactosidase activities low. These results indicated that melatonin may have reduced the speed of softening of kiwifruit and preserved fruit quality by inhibiting enzymatic degradation of the cell wall, and by delaying pro-pectin, cellulose, and hemicellulose degradation, as well as the increase of water-soluble pectin content. These findings indicate that MT treatment may be an effective measure to delay kiwifruit postharvest cell-wall metabolism and preserve fruit quality.

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