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

First author:Yuli Ding;Affiliations:University of British Columbia(不列顛哥倫比亞大學):Vancouver,Canada

Corresponding author:Yuelin Zhang

Salicylic acid (SA) is a plant defense hormone required for immunity.ArabidopsisNPR1 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 (轉錄共抑制因子) and SA inhibits their activities to promote the expression of downstream immune regulators.npr4-4D, a gain-of-functionnpr4allele that renders (使) 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 arebona fideSA receptors, but play opposite roles in transcriptional regulation of SA-induced defense gene expression.

水楊酸SA是植物的防禦激素，對於植物免疫至關重要。擬南芥的NPR1和NPR3/NPR4被認為能夠結合SA，並且這三個蛋白都作為SA的受體。NPR1作為轉錄共激活子發揮功能，而NPR3/NPR4被認為起到E3連接酶的功能，促進NPR1的降解。本文報道了NPR3/NPR4作為轉錄共抑制因子發揮作用，SA會抑制這兩個蛋白的活性從而促進下游免疫基因的表達。一個npr4等位基因功能獲得性突變體npr4-4D會使得NPR4不能結合SA，組成型抑制了SA誘導的誘導的免疫響應。相反，NPR1的等效突變會廢除其與SA結合的能力，然而卻促進了SA誘導的誘導的免疫響應。進一步的分析顯示NPR1和NPR3/NPR4都是真實的SA受體，但在SA誘導防禦基因表達的轉錄調控中發揮相反的作用。

通訊：Yuelin Zhang(https://www.botany.ubc.ca/people/yuelin-zhang)

個人簡介：1989年，復旦大學，本科；1995年，美國俄克拉荷馬州立大學，生物化學與分子生物學博士；1995-1998年，北卡羅來納大學教堂山分校，化學系博士後；1998-1999年，杜克大學，細胞和分子生物學系博士後；2001-2005年，Michael Smith實驗室助理教授；2005-2011年，北京生命科學研究所，助理研究員；2011年，北京生命科學研究所，副研究員。

研究方向：植物免疫受體下游的信號轉導通路；植物系統獲得性抗性。

doi: https://doi.org/10.1016/j.cell.2018.03.044

Journal:Cell

Published online: 12 April, 2018

（P.S. 歡迎訪問個人博客：http://bbs.sciencenet.cn/u/TickingClock）

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