Effects of postharvest deastringency and 1-methylcyclopropene treatments on membrane permeability, membrane-degrading enzymes and their encoding genes in persimmon (Diospyros kaki, cv Mopanshi) fruit

Abstract

Astringent persimmon fruit softens rapidly after harvest deastringency treatment. The purpose of this study was to understand the characteristics of membrane deterioration and its mechanism during rapid softening. The experiment included three treatments: (1) control, (2) CO2 treatment (≈100% CO2, 24 h), and (3) CO2 plus 1-methylcyclopropene (1-MCP, 1.5 μL∙L-1) treatment. CO2 treatment can effectively remove the astringency of persimmon fruit and cause a sharp drop in fruit firmness. The addition of 1-MCP was beneficial for firmness maintenance, but the process of astringency removal was delayed by one day. The fruit respiration rate and ethylene evolution rate were significantly increased by CO2 treatment, regardless of the presence or absence of 1-MCP, but the addition of 1-MCP could reduce the peak value and delay the occurrence of ethylene peaks by one day. The deastringency treatment resulted in a significant increase in membrane permeability and malondialdehyde content, and 1-MCP could significantly reduce membrane damage. CO2 treatment induced an enormous increase in LOX activity and the transcription of DkLOX3; however, 1-MCP significantly inhibited these increases. The PLD activity and DkPLDα1 expression level of the CO2-treated fruit were significantly promoted, and the addition of 1-MCP had less inhibition effect on the PLD activity and no significant inhibition on the DkPLDα1 expression. These results demonstrate that CO2 deastringency treatment could cause severe damage to the membrane integrity by promoting LOX and PLD activities and related gene expression. 1-MCP may ameliorate membrane damage mainly by inhibiting LOX activity and DkLOX3 gene expression and partly by suppressing PLDα1 expression.