The function of inositol 1,4,5-trisphosphate (IP3) on nitric oxide (NO)-induced chilling tolerance and defense response in postharvest peach fruit was explored. The postharvest fruit were treated with sodium nitroprusside (SNP, exogenous NO donor), cPTIO (NO scavenger), and neomycin (IP3 inhibitor). It turned out that SNP treatment mitigated chilling injury (CI) and stimulated NO accumulation in postharvest peach fruit. Further, SNP enhanced phosphoinositide-specific phospholipase C (PI-PLC) activity and, thereby, stimulated IP3 prodution. SNP also upregulated the activity and expression of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), ascorbate peroxidase (APX), glutathione S-transferase (GST), and glutathione reductase (GR). In addition, SNP enhanced the expression of small ubiquitin-like modifier (SUMO) and methionine sulfoxide reductase (MSR) and weakened the activity and expression of lipoxygenase (LOX) and phospholipase D (PLD). These above impacts stimulated by SNP treatment were blocked by the addition of cPTIO and neomycin. Overall, IP3 was involved in NO-enhanced chilling tolerance and defense response in postharvest peach fruit.
Keywords: IP3; LOX and PLD; MSR and SUMO; NO; antioxidant system; peach fruit.