Department of Microbiology and Cell Science, University of Florida, P.O. Box 110700, Gainesville, FL 32611, USA.
J Plant Physiol. 2010 Jan 15;167(2):144-8. doi: 10.1016/j.jplph.2009.08.002.
Plant systemic acquired resistance (SAR) is a broad-spectrum immune response in which pathogen infection in local tissue induces resistance in systemic leaves. Activation of SAR requires the signal molecule salicylic acid (SA), which is primarily synthesized from chorismate via isochorismate through the action of isochorismate synthase 1 (ICS1) and a putative isochorismate pyruvate lyase. The Arabidopsis transcription coactivator NPR1 is a key regulator of SAR, which functions at multiple nodes in the SA signaling network. NPR1 not only acts downstream of SA to activate SAR, but also upstream of SA to suppress the expression of ICS1, thus inhibiting SA biosynthesis. NPR1 also positively regulates SA tolerance and plays a role in SA-mediated negative regulation of jasmonic acid (JA) signaling. The NPR1 protein contains a functional bipartite nuclear localization signal (NLS). It has been shown that the NLS and nuclear localization of NPR1 are required for activation of pathogenesis-related gene expression, whereas modulation of the crosstalk between SA- and JA-dependent defense pathways is mediated by cytosolic NPR1. In this study we used two transgenic lines, one expressing a mutated npr1 with a dysfunctional NLS and the other in which NPR1 nuclear localization can be induced by dexamethasone treatment, to test whether nuclear localization is required for other functions of NPR1. We found that prevention of NPR1 nuclear localization renders transgenic seedlings sensitive to the toxicity of high levels of SA and causes over-accumulation of ICS1 transcripts and SA in response to pathogen infection. Induction of NPR1 nuclear localization restores SA tolerance and normal accumulation of ICS1 transcripts and SA. These results indicate that the NLS and nuclear localization of NPR1 are required for regulation of SA tolerance, ICS1 expression and SA accumulation.
植物系统获得性抗性 (SAR) 是一种广谱免疫反应，其中局部组织中的病原体感染诱导系统叶片的抗性。SAR 的激活需要信号分子水杨酸 (SA)，SA 主要通过异分支酸合酶 1 (ICS1) 和假定的异分支酸丙酮酸裂解酶从分支酸合成。拟南芥转录共激活因子 NPR1 是 SAR 的关键调节因子，它在 SA 信号网络的多个节点上发挥作用。NPR1 不仅在 SA 下游作用以激活 SAR，而且在 SA 上游作用以抑制 ICS1 的表达，从而抑制 SA 生物合成。NPR1 还正向调节 SA 耐受性，并在 SA 介导的茉莉酸 (JA) 信号负调控中发挥作用。NPR1 蛋白含有一个功能性的双功能核定位信号 (NLS)。已经表明，NLS 和 NPR1 的核定位对于激活与发病相关的基因表达是必需的，而 SA 和 JA 依赖的防御途径之间的串扰的调节是由细胞质 NPR1 介导的。在这项研究中，我们使用了两个转基因系，一个表达了一种具有功能失调的 NLS 的突变 npr1，另一个系中 NPR1 的核定位可以通过地塞米松处理诱导，以测试核定位是否是 NPR1 其他功能所必需的。我们发现，阻止 NPR1 的核定位使转基因幼苗对高水平 SA 的毒性敏感，并导致 ICS1 转录物和 SA 在受到病原体感染时过度积累。NPR1 核定位的诱导恢复了 SA 耐受性和 ICS1 转录物和 SA 的正常积累。这些结果表明，NLS 和 NPR1 的核定位对于调节 SA 耐受性、ICS1 表达和 SA 积累是必需的。
