2010年10月4日，北京生命科學研究所張躍林博士實驗室在Proc. Natl. Acad. Sci. USA雜志在線發(fā)表題為“Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors”的文章,。文章闡述了SARD1和CBP60g在轉(zhuǎn)錄水平調(diào)控ICS1的表達，影響水楊酸的合成和系統(tǒng)獲得性抗性。
水楊酸是植物局部和系統(tǒng)獲得性抗性所需的防御信號,。ICS1在水楊酸合成途徑中起了關(guān)鍵的作用,，病原菌的侵染導致ICS1表達從而誘導SA的合成。
本文中我們發(fā)現(xiàn)在ICS1誘導和水楊酸合成途徑中兩個關(guān)鍵的調(diào)控因子SARD1和CBP60g,。敲除SARD1減弱了局部抗性和系統(tǒng)獲得性抗性, 過表達SARD1組成性激活防御反應,。在sard1-1 cbp60g-1的雙突變體中，在局部抗性和系統(tǒng)獲得性抗性水平ICS1的上調(diào)和水楊酸的合成都被抑制,，從而導致本底抗性的減弱和SAR的喪失,。
電泳遷移實驗表明SARD1和CBP60g是植物特有的DNA 結(jié)合蛋白，這兩個蛋白在受到病原菌侵染時被募集到的ICS1的啟動子上,，表明他們在轉(zhuǎn)錄水平調(diào)控ICS1的表達從而影響水楊酸的合成,。
張亞晰, 許少華和丁平濤為本文的共同第一作者，參與此工作的還有我所何靜, 高明輝,，李妍, 朱兆海,，新疆農(nóng)業(yè)科學院的王冬梅，University of British Columbia的Yuti Cheng, 徐芳和李昕教授,。我所研究員張躍林博士是本文的通訊作者,。此項研究為科技部863和北京市科委資助課題，在北京生命科學研究所完成,。（生物谷Bioon.com）
生物谷推薦英文摘要：
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.
