Methyl Jasmonate Primed Defense Responses Against Penicillium expansum in Sweet Cherry Fruit

The effect of methyl jasmonate (MeJA) treatment on controlling blue mold decay caused by Penicillium expansum in sweet cherry fruit and the possible mechanisms were investigated. The results indicated that fruit treated with MeJA had significantly lower disease incidence and smaller lesion diameter than the control fruit did. The in vitro experiment showed that MeJA transiently inhibited spore germination and germ tube elongation of P. expansum. It is clear that MeJA triggers a priming mechanism in sweet cherry fruit, since only in fruit that had been pretreated with MeJA and then challenged with P. expansum was an enhanced capacity to augment defense responses observed. These augmented responses included enhanced activities of chitinase (CHI) and beta-1,3-glucanase (GLU), and increased gene expression levels of catalase (CAT), calmodulin (CaM), GLU, phenylalanine ammonia-lyase (PAL), nonexpressor of pathogenesis-related genes 1 (NPR1-like), and thaumatin-like (THAU). Moreover, MeJA inhibited the increase of activities of polygalacturonase (PG) and pectinmethylesterase (PME). These results suggest that the efficacy of MeJA on controlling blue mold decay in sweet cherry fruit may be related to the transient direct inhibitory effect against the pathogens, suppressed activities of PG and PME, and the priming of defense responses.