The Role of ABA in the Maturation and Postharvest Life of a Nonclimacteric Sweet Cherry Fruit

Abstract

The purpose of this study was to investigate the role of abscisic acid (ABA) in the pre- and postharvest maturation of the nonclimacteric sweet cherry. It was found that ABA content increased rapidly at the straw-colored stage and reached its highest level 4 days before commercial harvest time. The increase in ABA level was paralleled by an increase in the expression of a gene involved in ABA synthesis [9-cis-epoxycarotenoid dioxygenase (PacNCED1)]. Well before the ABA increase, the expression of a gene involved in ABA catabolism (PacCYP707A2) was downregulated. During the straw-colored stage, the application of exogenous ABA induced ABA accumulation, anthocyanin biosynthesis, and an increase in the maturity index (SSC/TA), thereby promoting fruit ripening. ABA treatment stimulated the expression of PacNCED1 and of genes involved in anthocyanin biosynthesis (PacCHS, PacF3H, PacCHI, PacDFR, and PacUFGT). The application of NiCl2 inhibited the release of ethylene and the expression of PacACO1 encoded 1-aminocyclopropane-1-carboxylic acid oxidase, of which the effect on fruit ripening was opposite that of ABA. Ethephon and nordihydroguaiaretic acid treatments, however, had no effect on fruit ripening. For postharvest fruit, the pedicel was a major route for water loss, and dehydration induced the transcription of PacNCED1 and the accumulation of ABA. Followed by ethylene release, the start of postharvest fruit senescence is triggered. In conclusion, endogenous ABA triggered the ripening of fruit via the modulation of ripening-related metabolism pathways such as anthocyanin accumulation. ABA also induced postharvest fruit senescence through stimulation of ethylene release in cherry fruit.