Nerol triggers oxidative stress, inducing membrane disruption and mitochondrial dysfunction in Monilinia fructicola

Monilinia fructicola , an extremely destructive pathogen, induces the postharvest decay of stone fruits. Nerol completely inhibited the growth of M. fructicola at a minimum inhibitory concentration of 0.2 mL/L. It disrupted mycelial membranes and released intracellular substances, such as nucleic acid, protein, and K + . Excessive reactive oxygen species (ROS) resulted in lipid peroxidation, which is responsible for membrane disruption. For the scavenging of excessive ROS, the antioxidant enzyme activities of catalase, superoxide dismutase, and peroxidase increased. However, glutathione (GSH) and GSH peroxidase activities decreased. Lasting oxidative stress disrupted mitochondria, which exhibited cristae loss and matrix transparency. The activities of key enzymes in tricarboxylic acid (TCA) cycle and ATPase were reduced, thereby causing ATP depletion. RNA sequencing revealed that nerol down-regulated the genes for L-glutamate and GSH synthesis while up-regulating those for GSH metabolism, resulting in a net GSH depletion. Metabolic disruptions occurred in membrane lipids and cell wall integrity, primarily involving steroids, sphingolipids, glycerophospholipids, and trehalose. Nerol disrupted the expressions of most genes involved in the TCA cycle. In vivo, 0.4 mL/L nerol completely inhibited the growth of M. fructicola on peaches. These results highlight nerol’s multiple antifungal mechanisms, supporting its development as a bio-preservative against M. fructicola .