2010年10月4日，北京生命科学研究所张跃林博士实验室在Proc. Natl. Acad. Sci. USA杂志在线发表题为“Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors”的文章。文章阐述了SARD1和CBP60g在转录水平调控ICS1的表达，影响水杨酸的合成和系统获得性抗性。
水杨酸是植物局部和系统获得性抗性所需的防御信号。ICS1在水杨酸合成途径中起了关键的作用，病原菌的侵染导致ICS1表达从而诱导SA的合成。
本文中我们发现在ICS1诱导和水杨酸合成途径中两个关键的调控因子SARD1和CBP60g。敲除SARD1减弱了局部抗性和系统获得性抗性, 过表达SARD1组成性激活防御反应。在sard1-1 cbp60g-1的双突变体中，在局部抗性和系统获得性抗性水平ICS1的上调和水杨酸的合成都被抑制，从而导致本底抗性的减弱和SAR的丧失。
电泳迁移实验表明SARD1和CBP60g是植物特有的DNA 结合蛋白，这两个蛋白在受到病原菌侵染时被募集到的ICS1的启动子上，表明他们在转录水平调控ICS1的表达从而影响水杨酸的合成。
张亚晰, 许少华和丁平涛为本文的共同第一作者，参与此工作的还有我所何静, 高明辉，李妍, 朱兆海，新疆农业科学院的王冬梅，University of British Columbia的Yuti Cheng, 徐芳和李昕教授。我所研究员张跃林博士是本文的通讯作者。此项研究为科技部863和北京市科委资助课题，在北京生命科学研究所完成。（生物谷Bioon.com）
生物谷推荐英文摘要：
PNAS doi: 10.1073/pnas.1005225107
Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors
Yaxi Zhanga,b,1, Shaohua Xua,c,1, Pingtao Dinga,b,1, Dongmei Wangd,2, Yu Ti Chengd, Jing Hea, Minghui Gaoa, Fang Xud, Yan Lia, Zhaohai Zhua, Xin Lid, and Yuelin Zhanga,3
aNational Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;
bCollege of Life Sciences, Beijing Normal University, Beijing 100875, China;
cGraduate Program, Chinese Academy of Medical Sciences and Peking union Medical College, Beijing 100730, China; and
dMichael Smith Laboratories, University of British Columbia, Vancouver, BC , Canada V6T 1Z4
Salicylic acid (SA) is a defense hormone required for both local and systemic acquired resistance (SAR) in plants. Pathogen infections induce SA synthesis through up-regulating the expression of Isochorismate Synthase 1 (ICS1), which encodes a key enzyme in SA production. Here we report that both SAR Deficient 1 (SARD1) and CBP60g are key regulators for ICS1 induction and SA synthesis. Whereas knocking out SARD1 compromises basal resistance and SAR, overexpression of SARD1 constitutively activates defense responses. In the sard1-1 cbp60g-1 double mutant, pathogen-induced ICS1 up-regulation and SA synthesis are blocked in both local and systemic leaves, resulting in compromised basal resistance and loss of SAR. Electrophoretic mobility shift assays showed that SARD1 and CBP60g represent a plant-specific family of DNA-binding proteins. Both proteins are recruited to the promoter of ICS1 in response to pathogen infections, suggesting that they control SA synthesis by regulating ICS1 at the transcriptional level.
