|Zheng, Y. H.|
|Tang, S. S.|
|Rui, H. J.|
Submitted to: Journal of the Science of Food and Agriculture
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/26/2008
Publication Date: 1/5/2009
Citation: Jin, P., Zheng, Y., Tang, S., Rui, H., Wang, C.Y. 2009. Ehancing disease resistance in peach fruit with methyl jasmonate. Journal of the Science of Food and Agriculture. 89:802-808. Interpretive Summary: Peaches are highly susceptible to physiological deterioration and pathological infection during ambient temperature storage and ripening. In an effort to reduce the use of fungicides, we looked into alternative methods for retarding decay and spoilage during the postharvest period. We found that a naturally occurring substance, methyl jasmonate, was able to enhance the resistance of peach fruit to fungal diseases. We further determined that methyl jasmonate may exert its effect on reducing postharvest decay in peaches by enhancing the activities of several defense enzymes and by increasing the content of phenolic substances. This research should be of interest to other scientists and information obtained from this study could be useful to peach industry.
Technical Abstract: The effect of methyl jasmonate (MeJA) on postharvest diseases caused by P. expansum, B. cinerea and R. stolonifer in peach fruit (Prunus persica Batsch cv Dahebai) and the possible mechanisms involved were investigated. Peaches were harvested at the firm-mature stage and treated with 1 or 500 µmol/L MeJA vapor at 20 °C for 24 h. At 0, 12, 24 and 36 h after treatment, both treated and nontreated fruit were artificially wounded and inoculated with P. expansum, B. cinerea or R. stolonifer spore suspensions (1.0×10(5) spores/ml), and then incubated at 20 °C for 6 days. MeJA at 1 µmol/L significantly prevented the postharvest diseases (e.g. blue mold, gray mold and soft rot), while 500 µmol/L MeJA had little effect on peach fruit decay. Incubation for 12 h was the optimal length of time after MeJA treatment with the lowest disease incidence and lesion diameter for all pathogens. The activities of defense enzymes including chitinase (CHI), ß-1,3-glucanase (GLU), phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO) and peroxidase (POD) were enhanced by 1 µmol/L MeJA treatment, and the level of total phenolic content in 1 µmol/L MeJA treated fruit was also higher than that in control fruit. However, there were little changes in the 500 µmol/L MeJA treated fruit. In addition, 1 µmol/L MeJA affected H2O2-metabolizing enzymes such as superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX), and induced a higher level of H2O2 during incubation, which might serve as a signal to induce resistance against P. expansum infection. In contrast, the levels of SOD and H2O2 in 500 µmol/L MeJA treated fruit were lower than that in control fruit during the incubation period. These results suggest that the effect of MeJA treatment on postharvest diseases in peach fruit is dependent on the concentration applied. The concentration (1 µmol/L) which was effective in reducing decay also promoted the activities of defense enzymes and increased total phenolic content. MeJA might have enhanced disease resistance of fruit tissue by increasing anti-pathogenic proteins and antimicrobial phenolic compounds.