Methyl jasmonate induces the resistance of postharvest blueberry to gray mold caused by Botrytis cinerea.

Abstract

The effects of postharvest methyl jasmonate (MeJA) treatment (50 μmol L-1 ) on the control of gray mold caused by Botrytis cinerea in blueberry fruit were evaluated by analyzing (i) the levels of disease resistance signals; (ii) the activity of enzymes involved in antioxidant system, disease resistance and phenylpropanoid pathway, and (iii) the secondary metabolite content. The results indicated that MeJA treatment significantly restrained the development of gray mold decay in blueberries. The treatment induced a nitric oxide (NO) burst and increased the endogenous hydrogen peroxide (H2 O2 ) content in the earlier period of storage. The enhanced NO and H2 O2 generation by MeJA treatment might serve as a signal to induce resistance against B. cinerea infection. Furthermore, in inoculated fruit, MeJA treatment significantly promoted antioxidant enzymes and defense-related enzyme activity, which included superoxide dismutase, catalase, ascorbate peroxidase, chitinase, and β-1,3-glucanase, and the degree of membrane lipid peroxidation was reduced. The MeJA treatment enhanced the phenylpropanoid pathway by provoking phenylalanine ammonialyase, cinnamate 4-hydroxylase, and 4-coumarate CoA ligase activity, which was accompanied by elevated levels of phenolics and flavonoids in blueberry fruit. These results suggested that MeJA could induce the disease resistance of blueberries against B. cinerea by regulating the antioxidant enzymes, defense-related enzymes, and the phenylpropanoid pathway through the activation of signaling molecules.