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 bona fide SA receptors, but play opposite roles in transcriptional regulation of SA-induced defense gene expression.

中文翻译：

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水杨酸受体NPR1和NPR3 / NPR4在植物免疫转录调控中的相反作用。

水杨酸（SA）是免疫力所需的植物防御激素。以前显示拟南芥NPR1和NPR3 / NPR4结合SA，并且提出了所有三种蛋白质作为SA受体。NPR1起转录共激活因子的作用，而NPR3 / NPR4被认为起促进NPR1降解的E3连接酶的作用。在这里，我们报道NPR3 / NPR4充当转录共阻遏物，而SA抑制它们的活性以促进下游免疫调节剂的表达。npr4-4D是功能获得性npr4等位基因，它使NPR4无法结合SA，从而组成性抑制SA诱导的免疫反应。相反，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。进一步的分析表明，NPR3 / NPR4和NPR1独立发挥功能来调节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起相反的作用。