摘要
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 mutantjasmonic acid-hypersensitivel-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 thejah1-1 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. Thejah1-1 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.
基金
We gratefully acknowledge Dr Jianru Zuo （Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, China） for providing T-DNA mutagenized population of Arabidopsis, Dr Salome Prat （Institut de Biologia Molecular de Barcelona, Spain） for providing homozygous atmyc2-2 mutant （T-DNA insertion line SALK_083483） seeds and Dr Jane Glazebrook for assisting with camalexin measurements. This work was supported by grants from the Chinese Academy of Sciences （KSCX2- YW-N-045, KSCX2-YW-N-015）, the Ministry of Agriculture of China （2008ZX08009-003-001） and the Ministry of Science and Technology of China （2007CB948201, 2006AA10A116）. Work in the laboratory of Jerry D Cohen was supported by grants from the US National Science Foundation （MCB-0725149 and DBI- PGRP-0606666） and the USDA, National Research Initiative （2005-35318-16197）.
