Similarly, dual-luciferase reporter (DLR) analysis revealed that SlMsrB5–SlMYC2 interaction significantly increased the ability of SlMYC2-mediated transcriptional activation of SlATG13a, SlATG13b, SlATG18a, and SlATG18h. On the other hand, silencing SlMsrB5 inhibited the transcript levels of SlMYC2-targeted genes ( SlATG13a, SlATG13b, SlATG18a, and SlATG18h). SlMsrB5 partially repaired oxidized SlMYC2 and restored its DNA-binding ability. 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. Moreover, SlMsrB5, a methionine sulfoxide reductase, could interact with SlMYC2.

SlMYC2 could also bind to the promoters of several SlATGs, including SlATG13a, SlATG13b, SlATG18a, and SlATG18h, and activate their transcript levels. In this study, we noticed that silencing SlMYC2 significantly reduced the increase in autophagy-related genes ( SlATGs) expression induced by MeJA. MYC2 is involved in MeJA-mediated postharvest fruit biological metabolism, but it is unclear how it affects MeJA-induced fruit autophagy. Methyl jasmonate (MeJA) has been shown to induce autophagy in various plant stress responses and metabolic pathways.

Yt transcript