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