Metabolomics analysis reveals that MeJA treatment induces postharvest blueberry resistance to Botrytis cinerea

Abstract

Blueberry (Vaccinium spp.) is a berry with high nutritional and economic value, but it can easily be infected by Botrytis cinerea during postharvest storage. Our previous research has demonstrated that methyl jasmonate (MeJA) treatment can restrain the development of gray mold decay in blueberries. However, the crucial metabolic-product response to MeJA treatment has not yet been elucidated definitely. In this study, metabolomics was used to study the effect of MeJA on the metabolism level of blueberry fruit infected by B. cinerea. A total of 782 differential metabolites were screened, and results of principal component analysis showed that MeJA treatment induced obvious changes in the metabolic profile of blueberry fruit. MeJA treatment activated the phenylpropane metabolic pathway and promoted the accumulation of rutin, quercetin, ferulic acid, protocatechuic acid, gallic acid, sinapic acid, and hyperin in blueberry fruits. MeJA also enhanced the metabolism of unsaturated fatty acids and induced the synthesis of aspartate, phenylalanine, oleic acid, linolenic acid, and γ-linolenic acid. This enhancement may be related to MeJA inducing the glycolysis pathway and TCA cycle in blueberry fruit to provide sufficient energy and carbon skeleton. Overall, this study highlighted the differential metabolites after MeJA treatment during blueberry infection by B. cinerea and provided a basis for the formulation of new control strategies.