Effect of p-coumarate esters resistant against postharvest Botrytis cinerea infection in apple fruit

•Methyl and ethyl p-coumarates inhibited infection of Botrytis cinerea on apples.•Treatments with MpCA and EpCA acted via destroying plasma membrane of the pathogen.•MpCA and EpCA enhanced apple phenylalanine ammonia-lyase and peroxidase activities.•Exogenous MpCA and EpCA stimulated great accumulation of chlorogenic acid in apples.•MpCA and EpCA would provide a promising approach for control of postharvest decays. Gray mold rot caused by Botrytis cinerea is one of the most common diseases resulted in considerable postharvest losses of fruits. The antifungal activity of esterified p-coumarates on Botrytis rot in apple fruit were investigated. Results showed that the mycelial growth and spore germination of B. cinerea were effectively inhibited by the application of methyl p-coumarate (MpCA) and ethyl p-coumarate (EpCA). Treatments with MpCA and EpCA resulted in a large leakage of intercellular electrolytes, soluble proteins and sugars, and ultrastructural distortion of the pathogen during growth, suggesting that p-coumarate esters may act via destroying the plasma membrane of the pathogen. In addition, treatments with MpCA and EpCA significantly inhibited the infection on apple fruit by B. cinerea. MpCA and EpCA up-regulated expression of genes encoding a pathogenesis-related protein (PR1), phenylalanine ammonia-lyase (PAL) and peroxidase (POD), enhanced activities of PAL and POD, and stimulated the accumulation of chlorogenic acid and catechin in the fruit. MpCA and EpCA thereby activated the disease-resistance system and the metabolism of polyphenols and flavonoids against the infection by B. cinerea. Collectively, two p-coumarate esters could not only exert their directly antifungal activity, but also induce the defense mechanism of host apple fruit. Application of MpCA and EpCA would provide a promising approach for the control of postharvest diseases of fruits.