Interaction of methionine sulfoxide reductase B5 with SlMYC2 stimulates the transcription of MeJA-mediated autophagy-related genes in tomato fruit.

Methyl jasmonate (MeJA) has been shown to induce autophagy in various plant stress responses and metabolic pathways. MYC2 is involved in MeJA-mediated postharvest fruit biological metabolism, but it is unclear how it affects MeJA-induced fruit autophagy. In this study, we noticed that silencing significantly reduced the increase in () expression induced by MeJA. SlMYC2 could also bind to the promoters of several , including , , , and , and activate their transcript levels. Moreover, SlMsrB5, a methionine sulfoxide reductase, could interact with SlMYC2. Methionine oxidation in SlMYC2 and mimicking sulfoxidation in SlMYC2 by mutation of methionine-542 to glutamine reduced the DNA-binding ability and transcriptional activity of SlMYC2, respectively. SlMsrB5 partially repaired oxidized SlMYC2 and restored its DNA-binding ability. On the other hand, silencing inhibited the transcript levels of -targeted genes (, , and ). Similarly, dual-luciferase reporter (DLR) analysis revealed that SlMsrB5-SlMYC2 interaction significantly increased the ability of SlMYC2-mediated transcriptional activation of , , and . These findings demonstrate that SlMsrB5-mediated cyclic oxidation/reduction of methionine in SlMYC2 influences expression. Collectively, these findings reveal the mechanism of SlMYC2 in transcriptional regulation, providing insight into the mechanism of MeJA-mediated postharvest fruit quality regulation.