Calcium-dependent protein kinase PpCDPK29-mediated Ca2+-ROS signal and PpHSFA2a phosphorylation regulate postharvest chilling tolerance of peach fruit

Abstract

Green and chemical-free hot water (HW) treatment can effectively reduce the chilling injury of peach fruit; however, the mechanism of inducing chilling resistance by heat treatment is still unclear. This study found that HW treatment could activate reactive oxygen species (ROS) signalling, forming ROS-Ca²⁺ signalling. Furthermore, we identified a peach Ca²⁺ sensor, calcium-dependent protein kinase 29 (PpCDPK29), as a positive regulator of postharvest chilling resistance. PpCDPK29 interacted with ROS-generating proteins (PpRBOHC/D) and antioxidant enzymes (PpSOD and PpCAT1) to jointly maintain ROS homeostasis. Meanwhile, we found that PpHSFA2a was phosphorylated by PpCDPK29 and transferred to the nucleus, which enhanced the binding ability of PpHSFA2a to the target genes. Here, PpHSFA2a activated the transcription of target genes PpHSP18.5, PpHSP70, PpGSTU7, PpGSTU19, PpGolS1 and PpBAM1, acted as molecular chaperones, improved ROS scavenging and enhanced osmoregulation to alleviate postharvest chilling injury of peach fruit. In summary, HW treatment could alleviate postharvest chilling injury in peach fruit by activating the PpCDPK29-mediated Ca²⁺-ROS and HSF-HSP signalling pathways, providing a novel signalling network for postharvest quality control of peach fruit.