知名女教授董欣年《Cell》文章

　　

生物通报的，杜克大学生物系，法国植物生物研究所，英国爱丁堡大学植物分子科学研究所等处的研究者在最近一期的《Cell》上，Proteasome-Mediated Turnover of the Transcription Coactivator NPR1 Plays Dual Roles in Regulating Plant Immunity，领衔的通讯作者是来自杜克大学的董欣年教授。

 

董欣年教授毕业于武汉大学学士, 在哈佛大学完成博士后研究，其主要研究方向为水杨酸和茉莉酸介导的信号转导途径及其相互作用(Cross-talk)机制。

 

系统获得性抗性（systemic acquired resistance， SAR），系统获得性抗性是植物防卫反应基因被系统诱导表达的结果，特别是NPR1基因的共激活作用。

 

NPR1的核易位作用是共激活作用中的关键步骤，但是NPR1蛋白如何调节核结构的机制一直不明确。在本研究中，董欣年等人展示了NPR1蛋白在靶基因的转录调节上的重要作用。当不存在有外源病原刺激时，NPR1蛋白不断地被蛋白酶体清除掉，防止其激活不恰当的SAR作用。当出现外源病原时，蛋白酶体又发挥促进NPR1磷酸化的作用，促进SAR发生。

 

这些数据表明，NPR1蛋白在SAR的作用过程中发挥双重作用，调节植物的免疫应答反应。

（生物通 小茜）

生物通推荐原文检索：

Proteasome-Mediated Turnover of the Transcription Coactivator NPR1 Plays Dual Roles in Regulating Plant Immunity

Steven H. Spoel1,3,4,Zhonglin Mou1,3,5,Yasuomi Tada1,6,Natalie W. Spivey1,Pascal Genschik2andXinnian Dong1,,

 

1 Department of Biology, Duke University, Durham, NC 27708, USA

2 Institut de Biologie Moléculaire des Plantes du CNRS, 12, rue du Général Zimmer, 67084 Strasbourg, France

Corresponding author

3 These authors contributed equally to this work

4 Present address: Institute of Molecular Plant Sciences, University of Edinburgh, Edinburgh, EH9 3JR, UK

5 Present address: Department of Microbiology and Cell Science, University of Florida, P.O. Box 110700, Gainesville, FL 32611, USA

6 Present address: Life Science Research Center, Kagawa University, Kagawa, 761-0795, Japan

 

【Summary】

Systemic acquired resistance (SAR) is a broad-spectrum plant immune response involving profound transcriptional changes that are regulated by the coactivator NPR1. Nuclear translocation of NPR1 is a critical regulatory step, but how the protein is regulated in the nucleus is unknown. Here, we show that turnover of nuclear NPR1 protein plays an important role in modulating transcription of its target genes. In the absence of pathogen challenge, NPR1 is continuously cleared from the nucleus by the proteasome, which restricts its coactivator activity to prevent untimely activation of SAR. Surprisingly, inducers of SAR promote NPR1 phosphorylation at residues Ser11/Ser15, and then facilitate its recruitment to a Cullin3-based ubiquitin ligase. Turnover of phosphorylated NPR1 is required for full induction of target genes and establishment of SAR. These invivo data demonstrate dual roles for coactivator turnover in both preventing and stimulating gene transcription to regulate plant immunity.