Suppression of the Jasmonate Signaling Pathway by <i>EIN3-LIKE1</i> 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 <i>Botrytis cinerea</i>, linked to desensitization of jasmonate (JA) biosynthesis and defense signaling. During ripening, key JA biosynthesis genes such as <i>allene oxide synthase</i> (<i>AOS</i>) and <i>12-oxophytodienoate reductase 3</i> (<i>OPR3</i>) were downregulated in response to wounding or fungal challenges. The <i>Slmyc2</i> mutants with impaired JA responses showed heightened pathogen sensitivity. Conversely, <i>EIN3-Like sleil1</i> mutants exhibited elevated <i>SlMYC2</i> levels, which increased expression of JA biosynthesis genes such as <i>lipoxygenase D</i> (<i>LOXD</i>), <i>OPR3</i>, <i>AOS</i>, and <i>allene oxide cyclase</i> (<i>AOC</i>) alongside defense genes including <i>proteinase inhibitor PI-6</i>, <i>PI-27</i>, <i>polyphenol oxidase</i>, and <i>pathogenesis-related proteins</i>, 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 <i>SlEIL1</i>, suppressed JA-dependent responses against <i>B. cinerea</i>, highlighting ethylene-JA antagonism as a key driver of postharvest decay.