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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。

Opposite Roles of Salicylic Acid Receptors NPR1 and NPR3/NPR4 in Transcriptional Regulation of Plant Immunity.

机构信息

Department of Botany, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.

Department of Botany, University of British Columbia, Vancouver, BC V6T 1Z4, Canada; Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.

出版信息

Cell. 2018 May 31;173(6):1454-1467.e15. doi: 10.1016/j.cell.2018.03.044. Epub 2018 Apr 12.

Abstract

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.

摘要

水杨酸(SA)是植物免疫所需的防御激素。先前已经表明拟南芥 NPR1 和 NPR3/NPR4 结合 SA,并且这三种蛋白都被提议作为 SA 受体。NPR1 作为转录共激活因子发挥作用,而 NPR3/NPR4 被认为作为 E3 连接酶起作用,促进 NPR1 的降解。在这里,我们报告 NPR3/NPR4 作为转录共抑制子发挥作用,并且 SA 抑制它们的活性以促进下游免疫调节剂的表达。npr4-4D 是一个 NPR4 的功能获得突变体,使 NPR4 不能结合 SA,持续抑制 SA 诱导的免疫反应。相比之下,NPR1 中的等效突变会使其丧失与 SA 结合并促进 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 独立地发挥作用以调节 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。

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