Concentration-dependent impacts of exogenous methyl jasmonate (MeJA) on chlorophyll degradation of apple fruit during ripening

Although jasmonates (JAs) have been proved to regulate degreening of apple fruit, the relevant molecular mechanisms have not yet been clarified. Previous reports revealed that the effects of JAs on degreening of harvested horticultural crops might be dependent on concentration applied. Whether a similar result can be obtained from apple fruit is still unclear. This research explored the impacts of different concentrations of methyl jasmonate (MeJA) treatment on chlorophyll (Chl) degradation of postharvest apple fruit. Apples (Malus × domestica Borkh.) of commercial maturity were treated with 10 or 1500 µM MeJA and then stored at 20 ± 0.5 °C. The results indicated that exogenous 10 µM MeJA delayed degreening and ripening of apple fruit, whereas 1500 µM MeJA treatment had the opposite effects. Treatment with 10 µM MeJA alleviated Chl-oxidation by reducing Chl-peroxidase (POX) activity and reactive oxygen species (ROS) levels in chloroplast of apple peel during ripening, whereas 1500 µM MeJA treatment had the opposite effects. Activities of Magnesium-dechelatase (MDcase) and pheophytinase (PPH) in apple peel were differentially suppressed by 10 µM MeJA treatment while promoted by 1500 µM MeJA treatment during ripening. Application of 10 µM MeJA delayed the peak of endogenous jasmonic acid (JA) content, reduced jasmonate resistant 1 (JAR1) content and allene oxide synthase (AOS) activity, and differentially down-regulated expression of MdNYC3, MdNYE1a, MdPPH1, MdPAO6, MdPAO8, MdRCCR2 and MdMYC2a in apple peel during ripening, whereas opposite results were obtained from the 1500 µM MeJA-treated apple fruit. At the late ripening stage, MdHCAR expression in apple peel was promoted by 10 µM MeJA treatment while reduced by 1500 µM MeJA treatment. Transcript levels of MdNYC1 and MdNOL2 were generally reduced by both treatments at the late ripening stage. Transient overexpression of MdMYC2a accelerated Chl degradation of apple peel by promoting PPH and MDcase activities and enhancing expression of the above Chl catabolic genes (CCGs), except MdHCAR whose expression was down-regulated by it during ripening. The AOS activity, JA and JAR1 contents in apple peel were increased after transient overexpression of MdMYC2a during ripening. These data indicated that the PAO pathway and Chl-oxidation were regulated by JA signal in apple peel during ripening, and exogenous MeJA regulated Chl degradation of apple fruit in a concentration-dependent manner.