Abstract
Black spot caused by Alternaria alternata is one of the most common postharvest diseases in fruit and vegetables. A comprehensive investigation into its pathogenicity mechanism is imperative in order to propose a targeted and effective control strategy. The effect of nitric oxide (NO) on the pathogenicity of A. alternata and its underlying mechanism was studied. The results showed that treatment with 0.5 mM L-1 of sodium nitroprusside (SNP) (NO donor) increased the lesion diameter of A. alternata in vivo and in vitro, which was 22.8% and 13.2% higher than that of the control, respectively. Exogenous NO treatment also induced endogenous NO accumulation by activating nitric oxide synthase (NOS). In addition, NO triggered an increase in reactive oxygen species (ROS) levels. NO enhanced activities and gene expression levels of NADPH oxidase (NOX), superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR). Moreover, NO stimulated cell wall degrading enzymes by activating the corresponding gene expression in vivo and in vitro. These results suggested that exogenous NO promoted the pathogenicity of A. alternata by inducing ROS accumulation and activating antioxidants and cell wall degrading enzymes. The present results could establish a theoretical foundation for the targeted control of the black spot disease in pear fruit.