Autophagy is involved in methyl jasmonate-mediated resistance against Botrytis cinerea in postharvest tomato fruit by regulating jasmonate signaling and reactive oxygen species homeostasis

Postharvest fruit decay is one of the most important limitations for the fruit industry, which results in tremendous economic losses. Methyl jasmonate (MeJA), a critical hormone that participates in postharvest fruit disease control, could activate the autophagy pathway in plants, which plays an important role in stress response. To reveal the role of autophagy in MeJA-induced postharvest fruit resistance against Botrytis cinerea, green-mature tomato fruit was treated with 0.05 mmol L−1 MeJA for 12 h after immersing 50 mmol L−1 lithium chloride (LiCl, an activator of autophagy) or 5 mmol L−1 hydroxychloroquine (HCQ, an inhibitor of autophagy), respectively, for 10 min and stored at 25 ± 1 °C for 12 d The results indicated that MeJA treatment induced transcript levels of autophagy-related genes (SlATGs), promoted autophagosome formation, as well as inhibited disease incidence and lesion diameter of postharvest tomato by activating the transcript levels of genes related jasmonic acid (JA) signaling pathway (SlLOX, SlAOC, SlMYC2, and SlCOI1) and regulating reactive oxygen species (ROS) metabolism, including the increased activities of superoxide dismutase, catalase, peroxidase, ascorbate peroxidase, glutathione reductase, monodehydroascorbate reductase, and dehydroascorbate reductase and the decreased contents of superoxide anion radical and hydrogen peroxide. However, the above impacts regulated by MeJA were weakened by HCQ pretreatment and boosted by LiCl pretreatment. Moreover, correlation analysis suggested that disease development was negatively correlated with the transcript levels of genes related to autophagy and JA signaling pathway, especially SlATG13a, SlATG18a, and SlMYC2. The principal component analysis also showed that autophagy was involved in MeJA-induced postharvest fruit quality regulation. Overall, these findings indicated that MeJA treatment enhanced postharvest fruit disease resistance, at least in part, via the JA and autophagy pathway.