S-Nitrosylation of AtSABP3 Antagonizes the Expression of Plant Immunity*
S-Nitrosylation of AtSABP3 Antagonizes the Expression of Plant Immunity*
复制标题
DOI：
10.1074/jbc.m806782200
复制
发表时间：
2009-01
影响因子：
4.8
通讯作者：
Yiqin Wang;A. Feechan;B. Yun;R. Shafiei;A. Hofmann;P. Taylor;Peng Xue;Fuquan Yang;Zhen-Sheng Xie;J. Pallas;C. Chu;G. Loake
中科院分区：
文献类型：
--
作者：
Yiqin Wang;A. Feechan;B. Yun;R. Shafiei;A. Hofmann;P. Taylor;Peng Xue;Fuquan Yang;Zhen-Sheng Xie;J. Pallas;C. Chu;G. Loake
细胞氧化还原状态的变化是病原体攻击后跨门的公认反应。在这种情况下，一氧化氮（NO）的合成是一个显着的特点，植物响应企图微生物感染和这种氧化还原为基础的调节器的发展，植物免疫。然而，相关的分子机制尚未确定。在这里，我们表明，NO的积累过程中的亚硝化爆发促进增加的S-亚硝基化的拟南芥水杨酸结合蛋白3（AtSABP 3）在半胱氨酸（Cys）280，抑制结合的免疫激活剂，水杨酸（SA），和碳酸酐酶（CA）的这种蛋白质的活性。AtSABP 3的CA功能是宿主表达对病原体感染的抗性所必需的。因此，通过S-亚硝基化抑制AtSBAP 3 CA功能可能有助于调节植物防御反应的负反馈回路。因此，AtSABP 3是植物中S-亚硝基化的第一个靶标之一，其中这种基于氧化还原的翻译后修饰的生物学功能已经被发现。这些数据提供了由病原体感染引发的NO水平变化与抗病性表达之间的分子联系。
Changes in cellular redox status are a well established response across phyla following pathogen challenge. In this context, the synthesis of nitric oxide (NO) is a conspicuous feature of plants responding to attempted microbial infection and this redox-based regulator underpins the development of plant immunity. However, the associated molecular mechanism(s) have not been defined. Here we show that NO accretion during the nitrosative burst promotes increasing S-nitrosylation of the Arabidopsis thaliana salicylic acid-binding protein 3 (AtSABP3) at cysteine (Cys) 280, suppressing both binding of the immune activator, salicylic acid (SA), and the carbonic anhydrase (CA) activity of this protein. The CA function of AtSABP3 is required for the expression of resistance in the host against attempted pathogen infection. Therefore, inhibition of AtSBAP3 CA function by S-nitrosylation could contribute to a negative feedback loop that modulates the plant defense response. Thus, AtSABP3 is one of the first targets for S-nitrosylation in plants for which the biological function of this redox-based post-translational modification has been uncovered. These data provide a molecular connection between the changes in NO levels triggered by attempted pathogen infection and the expression of disease resistance.