Methyl jasmonate induces postharvest disease resistance to decay caused by Alternaria alternata in sweet cherry fruit

This research investigated the effect and mechanism of methyl jasmonate (MeJA) for decay caused by Alternaria alternata in postharvest sweet cherry. The results revealed MeJA at lower concentrations (0-0.05 mmol/L) had little effect on the mycelial growth of A. alternata in vitro. Furthermore, in vivo studies in fruits, applying optimal concentration 0.05 mmol/L MeJA significantly reduced the degree of decay, enhanced the activities of antioxidant enzymes and disease resistance-related enzymes (catalase, peroxidase, superoxide dismutase, polyphenol oxidase, phenylalanine ammonia lyase, chitinase, beta-1,3-glucanase), with membrane lipid peroxidation considerably reduced. Moreover, this MeJA treatment up-regulated the expression of antioxidant enzyme genes (PavPOD, PavPPO, PavSOD, PavCAT) and key genes related to jasmonic acid (JA) biosynthesis and signal transduction pathways (PavLOX, PavAOS, PavOPR3, PavMYC2). These results suggest their regulation by MeJA and a mechanism for how it could induce sweet cherry's resistance to A. alternata, rather than its fungitoxicity effect on pathogens.

Automated summary

The study found that methyl jasmonate (MeJA) had a minimal impact on the mycelial growth of Alternaria alternata in vitro at lower concentrations, but significantly reduced decay and enhanced antioxidant enzyme activities in sweet cherry fruits when applied at an optimal concentration. MeJA treatment also up-regulated the expression of key genes related to jasmonic acid biosynthesis and signal transduction pathways, suggesting a mechanism for inducing sweet cherry's resistance to A. alternata.