The Control Of Postharvest Black Rot Of Sweet Potato By Application Of Perillaldehyde And Mechanisms Of Action On Pathogenic Fungi

Black root rot caused by Ceratocystis fimbriata is the most damaging postharvest disease of sweet potatoes,causing notable losses of this crop.Black root rot can be controlled by synthetic fungicides,but these synthetic fungicides also have several negative effects on human being.Perillaldehyde?PAE?,a major component of herb perilla,is effective and eco-friendly of controlling this disease.The experiment showed that the mycelial growth of C.fimbriata was inhibited by PAE with a dose-dependent manner.Both in vitro and in vivo assays demonstrated that 25?l/l,50?l/l,and 100?l/l PAE doses,could inhibit the mycelial growth of C.fimbriata and remarkable lower lesion diameter compared to the control group.Even though the storage time was prolonged,PAE vapor treatment still drastically inhibited sweet potato decay in storage at 28°C.These PAE vapor treatments also enhanced the activities of superoxide dismutase?SOD?,catalase?CAT?,ascorbate peroxidase?APX?,peroxidase?POD?,polyphenol oxidase?PPO?,and phenylalanine ammonialyase?PAL?.These treatments also remarkably decreased weight loss rate and had minor effects on other fruit quality parameters,such as anthocyanin content and vitamin C?Vc?content.The study suggested that the effects of PAE on postharvest sweet potatoes may be attributed to the maintenance of enzymatic activity and fruit quality.In sum,PAE might be a promising approach to controlling C.fimbriata in sweet potato roots.I examined PAE's antifungal effects on mycelial growth and spore germination and further investigated the effects of PAE on cell wall integrity and cell membrane permeability.To elucidate the possible mechanisms of cell death triggered by PAE in C.fimbriata further,susceptibility of C.fimbriata to PAE toxicity was determined by cytoplasmic and mitochondrial calcium ion concentrations([Ca²⁺]c and[Ca²⁺]m),reactive oxygen species?ROS?,mitochondrial membrane potential?MMP?,cytochrome c?cyt c?release,metacaspase activation,phosphatidylserine?PS?externalization,and DNA fragmentation.Our results suggested that mycelial growth and spore germination were inhibited by the PAE in a dose-dependent manner.C.fimbriata cells treated with PAE can experience dramatic Ca²⁺overload and elevated ROS production,which were the major causes of apoptosis in C.fimbriata.On ROS assays,compared with the controls,at PAE concentrations of 0.0625,0.125,0.25,and0.5?l/ml,the proportion of fluorescent cells increased to 2.9±0.79%,17.4±0.53%,22.4±0.64%,and 27.1±0.38%,respectively.Ca²⁺overload and ROS accumulation induced depolarization of the MMP,contributing to mitochondrial dysfunction.Cyt c was also released from the mitochondria to the cytosol,triggering metacaspase activation,which mediates apoptotic processes in C.fimbriata.Our study has provided evidences of a novel mechanism for exploring possible antifungal agents for the postharvest management of food crops.