Probenazole treatment inhibits anthocyanins biosynthesis via salicylic acid and AtNPR1 signal pathway in Arabidopsis
It has been found that anthocyanins were accumulated in Arabidopsis under drought or salt stress. In this study, such accumulation was found to be inhibited by external applied probenazole (3-allyloxy-1, 2-benzisothiazole-1,1-dioxide, PBZ), which is the active ingredient in oryzemate used for the protection of rice from Magnaporthe grisea (blast fungus). Microarray analysis indicated that expression of nine key genes in anthocyanins synthesis pathway was significantly repressed to about 4 folds lower by PBZ treatment. In transgenic Arabidopsis plants with a β-glucuronidase (GUS) reporter gene driven by a CaMV35S mini promoter combined with four salicylic acid-responsive elements, PBZ treatment resulted in increased expression of the GUS gene. When a salicylic acid (SA) synthesis mutant, sid2-2, and a SA signal transduction pathway mutant, npr-1, were treated with PBZ under the same drought condition, inhibition of anthocyanin accumulation was not observed. In addition, over-expression of NPR1 by CaMV35S promoter resulted in more inhibition on anthocyanins accumulation. Taken together, these results indicated that inhibition of anthocyanins accumulation by PBZ treatment is through SA and NPR1 signaling pathway in Arabidopsis.
Key words: Probenazole, anthocyanins biosynthesis, isochorismate synthase 1, nonexpressor of pathogenesis-related genes 1.