Opposite Roles of Salicylic Acid Receptors NPR1 and NPR3/NPR4 in Transcriptional Regulation of Plant Immunity
Opposite Roles of Salicylic Acid Receptors NPR1 and NPR3/NPR4 in Transcriptional Regulation of Plant Immunity
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DOI：
10.1016/j.cell.2018.03.044
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发表时间：
2018-05-31
期刊：
影响因子：
64.5
通讯作者：
Zhang, Yuelin
中科院分区：
文献类型：
--
作者：
Ding, Yuli;Sun, Tongjun;Zhang, Yuelin
水杨酸（SA）是免疫所需的植物防御激素。拟南芥 NPR1 和 NPR3/NPR4 先前已被证明可结合 SA，并且所有三种蛋白均被提议作为 SA 受体。 NPR1 充当转录共激活子，而 NPR3/NPR4 被认为充当促进 NPR1 降解的 E3 连接酶。在此，我们报道 NPR3/NPR4 作为转录辅阻遏物发挥作用，SA 抑制其活性以促进下游免疫调节因子的表达。 npr4-4D 是一种功能获得性 npr4 等位基因，使 NPR4 无法结合 SA，组成性抑制 SA 诱导的免疫反应。相比之下，NPR1 中的等效突变消除了其结合 SA 并促进 SA 诱导的防御基因表达的能力。进一步分析表明，NPR3/NPR4 和 NPR1 独立发挥作用，调节 SA 诱导的免疫反应。我们的研究表明，NPR1 和 NPR3/NPR4 都是真正的 SA 受体，但在 SA 诱导的防御基因表达的转录调控中发挥相反的作用。
Salicylic acid (SA) is a plant defense hormone required for immunity. Arabidopsis NPR1 and NPR3/NPR4 were previously shown to bind SA and all three proteins were proposed as SA receptors. NPR1 functions as a transcriptional co-activator, whereas NPR3/NPR4 were suggested to function as E3 ligases that promote NPR1 degradation. Here we report that NPR3/NPR4 function as transcriptional co-repressors and SA inhibits their activities to promote the expression of downstream immune regulators. npr4-4D, a gain-of-function npr4 allele that renders NPR4 unable to bind SA, constitutively represses SA-induced immune responses. In contrast, the equivalent mutation in NPR1 abolishes its ability to bind SA and promote SA-induced defense gene expression. Further analysis revealed that NPR3/NPR4 and NPR1 function independently to regulate SA-induced immune responses. Our study indicates that both NPR1 and NPR3/NPR4 are bonafide SA receptors, but play opposite roles in transcriptional regulation of SA-induced defense gene expression.