Abstract

The effect of methyl jasmonate (MeJA) on reducing anthracnose rot caused by Colletotrichum acutatum infection in postharvest loquat fruit ( Eriobotrya japonica L. cv. Jiefangzhong) and the possible mechanisms involved were investigated. Freshly harvested loquat fruit were treated with 10 μmol/L MeJA at 20 °C for 24 h. Both the treated and the untreated fruit were artificially wounded and inoculated with Colletotrichum acutatum spore suspension (1.0 × 10 5 spores/mL) 1 day after the treatment, and then incubated at 20 °C for 6 days. Treatment of loquat fruit with MeJA resulted in significantly lower disease incidence and smaller lesion diameters than in control fruit. MeJA treatment significantly inhibited activities of catalase (CAT) and ascorbate peroxidase (APX) while superoxide dismutase (SOD) activity was not significantly affected in early infection, thus resulting in a higher level of H 2O 2 in the earlier period of incubation. The enhanced H 2O 2 generation by MeJA treatment might serve as a signal to induce resistance against C. acutatum infection. However, MeJA treatment inhibited the increase in phenylalanine ammonia-lyase (PAL), polyphenoloxidase (PPO) and peroxidase (POD) activities and lignin content, indicating that lignification is not the major defense mechanism against anthracnose rot in loquat fruit. The in vitro experiment showed that MeJA significantly inhibited spore germination, germ tube elongation and mycelial growth of C. acutatum. These results suggest that MeJA treatment can effectively inhibit anthracnose rot caused by C. acutatum in postharvest loquat fruit. It is postulated that the control of the disease is directly because of the inhibitory effect of MeJA on pathogen growth, and indirectly because of the induced disease resistance triggered by enhanced H 2O 2 levels.

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