Exogenous Phytosulfokine α (PSKα) Alleviates Chilling Injury of Kiwifruit by Regulating Ca2+ and Protein Kinase-Mediated Reactive Oxygen Species Metabolism

Abstract

Kiwifruit fruit stored at low temperatures are susceptible to chilling injury, leading to rapid softening, which therefore affects storage and marketing. The effect of 150 nM mL−1 of exogenous phytosulfokine α (PSKα) on reactive oxygen species (ROS) metabolism, Ca2+ signaling, and signal-transducing MAPK in kiwifruit, stored at 0 °C for 60 days, was investigated. The results demonstrated that PSKα treatment effectively alleviated chilling injury in kiwifruit, with a 15% reduction in damage compared to the control on day 60. In addition, PSKα enhanced the activities and gene expression levels of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR), Ca2+−ATPase, and mitogen−activated protein kinase (MAPK). In contrast, the activities and gene expression levels of NADPH oxidase (NOX) were inhibited, leading to a lower accumulation of O2− and H2O2, which were 47.2% and 42.2% lower than those in the control at the end of storage, respectively. Furthermore, PSKα treatment enhanced the calmodulin (CaM) content of kiwifruit, which was 1.41 times that of the control on day 50. These results indicate that PSKα can mitigate chilling injury and softening of kiwifruit by inhibiting the accumulation of ROS, increasing antioxidant capacity by inducing antioxidant enzymes, activating Ca2+ signaling, and responding to MAPK protein kinase. The present results provide evidence that exogenous PSKα may be taken for a hopeful treatment in alleviating chilling injury and maintaining the quality of kiwifruit.