Nitric oxide-mediated PpRAP2.2 regulates the transcription of PpRbohA/D to enhance resistance to Monilinia fructicola in peach fruit

Abstract

Nitric oxide (NO), a critical signaling molecule, plays key roles in plant cell physiological processes, particularly in redox system. To investigate the resistance of exogenous NO to brown rot (Monilinia fructicola) in peach fruit during storage, postharvest peaches were treated with NO and c-PTIO (an NO scavenger), exploring the mechanism of NO enhancing disease resistance in peach fruit through reactive oxygen species (ROS) metabolism. The results indicated that NO significantly inhibited brown rot in postharvest peach fruit, evidenced by reduced disease incidence and smaller lesion diameters. Additionally, exogenous NO treatment decreased the expression of respiratory burst oxidase homologs (PpRbohs), which is a crucial factor in ROS metabolism. The transcription factor PpRAP2.2 was identified through yeast one-hybrid (Y1H) screening with the promoter of PpRbohD. The expression pattern of PpRAP2.2 was closely associated with superoxide anion (O2-) content and peach fruit disease resistance. PpRAP2.2, a nuclear-localized transcription factor, activated the expression of PpRbohA and PpRbohD by directly binding to their promoter. The virus-induced gene silencing (VIGS) assay showed that silencing of PpRAP2.2 facilitated peach disease resistance by reducing the transcription of PpRbohA and PpRbohD. Furthermore, the overexpression of PpRAP2.2 resulted in a significant reduction in disease incidence and conidiophores in transgenic tomatoes relative to control group under M. fructicola, suggesting that PpRAP2.2 effectively enhanced the resistance of tomatoes to M. fructicola. These results indicate that PpRAP2.2 enhances NO-mediated disease resistance in peach by regulating the expression of PpRbohA and PpRbohD. These finding provide a basis for further studies on function and regulatory mechanisms of peach fruit disease resistance.