Abstract
Saccharin is generated from probenazole (PBZ) in plants and acts as a plant defense activator. Our study of the mechanism underlying saccharin-induced systemic acquired resistance in Arabidopsis thaliana suggests an antagonistic interaction between salicylic acid (SA)- and jasmonic acid (JA)-signaling as revealed through gene expression analyses. In wild-type plants (Col-0) exposed to saccharin, there was a consistent increase in callose deposition and in expression of SA-marker genes, PR1 and PR2, which coincided with a decrease in expression of JA-marker genes such as VSP2, LOX2 and PDF1.2. Actually, pretreatment of Col-0 with saccharin or PBZ conferred resistance to Pseudomonas syringae pv. tomato DC3000, but not to Pectobacterium carotovorum subsp. carotovorum, Botrytis cinerea, or Colletotrichum higginsianum. Enhanced expression of SA- and JA-marker genes and the augmented deposition of callose were evident after a challenge with virulent DC3000 in saccharin-pretreated plants. Consistently, pretreatment of saccharin and PBZ with SA- and JA-defective mutants led to diminished resistance in NahG-transgenic and npr1 mutant plants, but not in jar1 mutant plants, suggesting that saccharin and PBZ induce resistance in A. thaliana against Pto DC3000 mainly via activation of SA-signaling, leading to suppression of JA/ET-signaling and vice versa. Collectively, an antagonism between SA- and JA-signaling conditioned by saccharin renders resistance to a specific pathogen in Arabidopsis.
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