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Chitosan Controls Postharvest Decay on Cherry Tomato Fruit Possibly via the Mitogen-Activated Protein Kinase Signaling Pathway

Zhang, Danfeng, Wang, Hongtao, Hu, Yi, Liu, Youngsheng
Journal of agricultural and food chemistry 2015 v.63 no.33 pp. 7399-7404
Botrytis cinerea, cherry tomatoes, chitosan, genes, gray mold, hydrogen peroxide, malondialdehyde, mitogen-activated protein kinase, peroxidase, postharvest diseases, signal transduction
The inhibitive effects of chitosan on gray mold caused by Botrytis cinerea on cherry tomato fruit were evaluated. Decay incidence was tested on tomato stored at 22 °C. Hydrogen peroxide accumulation, malondialdehyde (MDA) production, peroxidase (POD) activity, and several related gene expressions (including MPK3, MPK6, PR1a1, and PR5) were determined. Results showed that 0.2% of chitosan solution significantly inhibited the tomato gray mold 3 days after inoculation. Hydrogen peroxide accumulated in the fruit epidermal peel along with chitosan treatment, while MDA production was not increased. POD activity was remarkably enhanced by the application of chitosan. The relative expressions of MPK3, MPK6, and PR1a1 were significantly induced in 10 min after chitosan treatment, while PR5 was induced in 20 min. These findings suggested that the effects of chitosan on inhibiting gray mold in cherry tomato fruit were probably associated with the mitogen-activated protein kinase (MAPK) signaling pathway.