The Arabidopsis P450 protein CYP82C2 modulates jasmonate-induced root growth inhibition, defense gene expression and indole glucosinolate biosynthesis

• Published in: Cell research Vol. 20; no. 5; pp. 539 - 552
• Main Authors: Liu, Fang, Jiang, Hongling, Ye, Songqing, Chen, Wen-Ping, Liang, Wenxing, Xu, Yingxiu, Sun, Bo, Sun, Jiaqiang, Wang, Qiaomei, Cohen, Jerry D, Li, Chuanyou
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.05.2010; Nature Publishing Group
• Subjects: 631/136/334/2244/710; 631/449/2661; 631/449/2667; 631/80/86/2365; Accumulation; Arabidopsis; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis - microbiology; Arabidopsis Proteins - metabolism; Biomedical and Life Sciences; Biosynthesis; Botrytis - pathogenicity; Cell Biology; Cloning; Cyclopentanes - metabolism; Cytochrome; Cytochrome P-450 Enzyme System - metabolism; Cytochrome P450; Environmental changes; Fatty acids; Gene Expression Regulation, Plant; Genes, Plant; Glucosinolates - metabolism; Herbivores; Indoles - metabolism; Life Sciences; Metabolites; Mutants; Mutation; original-article; Oxylipins - metabolism; Pathogens; Plant Diseases; Plant growth; Plant Roots - growth & development; Secondary metabolites; root growth inhibition; defense response; jasmonic acid; tryptophan; indole glucosinolates
• ISSN: 1001-0602; 1748-7838
• DOI: 10.1038/cr.2010.36

Jasmonic acid (JA) is a fatty acid-derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens. Molecular genetic studies have established that JA also performs a critical role in several aspects of plant development. Here, we describe the characterization of the Arabidopsis mutant jasmonic acid-hypersensitive1-1 ( jah1-1 ), which is defective in several aspects of JA responses. Although the mutant exhibits increased sensitivity to JA in root growth inhibition, it shows decreased expression of JA-inducible defense genes and reduced resistance to the necrotrophic fungus Botrytis cinerea . Gene cloning studies indicate that these defects are caused by a mutation in the cytochrome P450 protein CYP82C2. We provide evidence showing that the compromised resistance of the jah1-1 mutant to B . cinerea is accompanied by decreased expression of JA-induced defense genes and reduced accumulation of JA-induced indole glucosinolates (IGs). Conversely, the enhanced resistance to B. cinerea in CYP82C2 -overexpressing plants is accompanied by increased expression of JA-induced defense genes and elevated levels of JA-induced IGs. We demonstrate that CYP82C2 affects JA-induced accumulation of the IG biosynthetic precursor tryptophan (Trp), but not the JA-induced IAA or pathogen-induced camalexin. Together, our results support a hypothesis that CYP82C2 may act in the metabolism of Trp-derived secondary metabolites under conditions in which JA levels are elevated. The jah1-1 mutant should thus be important in future studies toward understanding the mechanisms underlying the complexity of JA-mediated differential responses, which are important for plants to adapt their growth to the ever-changing environments.