Abstract
• Knockout of SlNPR1 conferred disease resistance against B. cinerea to tomato fruit. • Knockout of SlNPR1 enhanced activities of defense enzymes including PAL, GLU, and CHI. • ROS homeostasis in slnpr1 was maintained by increased POD, SOD, GST and decreased CAT. • RNA-seq data showed that phenylpropanoid biosynthesis was induced in slnpr1 fruit. Tomato is the fourth most popular fresh-market fruit, whereas most commercial tomato cultivars are particularly susceptible to B. cinerea . Nonexpressor of pathogenesis-related gene 1 ( NPR1 ) is a critical regulator in plant resistance against various pathogens. However, the underlying mechanism of how SlNPR1 influences the defense against B. cinerea in tomato fruit remains unclear. In this study, two independent lines carrying homozygous mutation in SlNPR1 were used for studying its role in the interaction between tomato fruit and B. cinerea . Our results showed that knockout of SlNPR1 decreased the disease development of B. cinerea in tomato fruit. slnpr1 fruit exhibited smaller lesion sizes, higher activities of defense enzymes, and upregulated expressions of defense genes compared to wild type (WT). In addition, reactive oxygen species (ROS) homeostasis in slnpr1 fruit was balanced by increased activities of peroxidase (POD), superoxide dismutase (SOD) and glutathione S-transferase (GST), as well as decreased activity of catalase (CAT). Furthermore, SlNPR1 -mediated differential expression genes (DEGs) were significantly enriched in the secondary metabolic pathways, represented by phenylpropanoid biosynthesis. Taken together, these findings revealed that knockout of SlNPR1 resulted in increased activities of defense enzymes, changes in ROS homeostasis and activation of phenylpropanoid biosynthesis and some other signaling pathways, which contributes to resistance against B. cinerea in tomato fruit.
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