Suppression of the Jasmonate Signaling Pathway by EIN3-LIKE1 Increases Postharvest Susceptibility to Gray Mold in Ripening Tomato Fruits

Postharvest decay, primarily occurring after ripening, leads to substantial losses. Ripening increases tomato susceptibility to Botrytis cinerea, linked to desensitization of jasmonate (JA) biosynthesis and defense signaling. During ripening, key JA biosynthesis genes such as allene oxide synthase (AOS) and 12-oxophytodienoate reductase 3 (OPR3) were downregulated in response to wounding or fungal challenges. The Slmyc2 mutants with impaired JA responses showed heightened pathogen sensitivity. Conversely, EIN3-Like sleil1 mutants exhibited elevated SlMYC2 levels, which increased expression of JA biosynthesis genes such as lipoxygenase D (LOXD), OPR3, AOS, and allene oxide cyclase (AOC) alongside defense genes including proteinase inhibitor PI-6, PI-27, polyphenol oxidase, and pathogenesis-related proteins, thereby enhancing resistance. Treatment with DNA methyltransferase inhibitor 5-azacytidine increased JA content, suggesting epigenetic regulation of JA-mediated defense. Collectively, intensified ethylene signaling during ripening, mediated by SlEIL1, suppressed JA-dependent responses against B. cinerea, highlighting ethylene-JA antagonism as a key driver of postharvest decay.