Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in Arabidopsis
Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in Arabidopsis
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DOI：
10.1105/tpc.12.11.2175
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发表时间：
2000-11-01
期刊：
影响因子：
11.6
通讯作者：
Dong, XN
中科院分区：
文献类型：
--
作者：
Clarke, JD;Volko, SM;Dong, XN
拟南芥抗病受多种信号转导途径调控，其中水杨酸（SA）、茉莉酸（JA）和乙烯（ET）是关键信号分子。在破坏这些途径的突变体（npr1、eds5、ein2和jar1）和组成性激活这些途径的突变体（cpr1、cpr5和cpr6）之间进行了互作分析，从而探索SA-和JA/ et介导的抗性反应之间的关系。有两个重要的发现。首先，cpr1、cpr5和cpr6所表现出的构成性抗病性被sa缺乏的eds5突变体完全抑制，但仅部分受到sa不敏感的npr1突变体的影响。此外，eds5抑制了cpr突变体的sa积累表型，而npr1则增强了这种表型。这些数据表明存在sa介导的、不依赖于npr1的耐药反应。其次，et不敏感突变ein2和ja不敏感突变jar1抑制了cpr5和cpr6表现出的不依赖于npr1的抗性反应。此外，ein2增强了cpr5和cpr5 npr1中SA的积累，而抑制了cpr6和cpr6 npr1中SA的积累。这些结果表明，cpr5和cpr6通过不同的途径调节抗性，并且sa介导的、不依赖npr1的抗性与JA/ et介导的应答途径的组分结合起作用。
Disease resistance in Arabidopsis is regulated by multiple signal transduction pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performed between mutants that disrupt these pathways (npr1, eds5, ein2, and jar1) and mutants that constitutively activate these pathways (cpr1, cpr5, and cpr6), allowing exploration of the relationship between the SA- and JA/ET-mediated resistance responses. Two important findings were made. First, the constitutive disease resistance exhibited by cpr1, cpr5, and cpr6 is completely suppressed by the SA-deficient eds5 mutant but is only partially affected by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accumulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance response. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutation jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6. Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 npr1 while dampening SA accumulation in cpr6 and cpr6 npr1. These latter results indicate that cpr5 and cpr6 regulate resistance through distinct pathways and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ET-mediated response pathways.