2009年8月29日，北京生命科學研究所周儉民實驗室在The Plant Cell雜誌上發表題為「ETHYLENE INSENSITIVE3 and ETHYLENE INSENSITIVE3-LIKE1 Repress SALICYLIC ACID INDUCTION DEFICIENT2 Expression to Negatively Regulate Plant Innate Immunity in Arabidopsis」的文章。
水楊酸(SA)是植物抗病中的重要激素，它的合成受到精密調控。該文章報導了轉錄因子EIN3和EIL1直接結合在水楊酸合成基因SID2的啟動子區，抑制水楊酸的合成, 從而負調控植物免疫反應。結果還揭示了乙烯信號途徑和水楊酸信號途徑間新的交叉調控。
該文章的共同第一作者是北京生命科學研究所博士陳華民，博士生薛麗還有堪薩斯大學的Satya Chintamanani；參與這項工作的還有林惠瓊，崔海濤，加拿大英屬哥倫比亞大學的Hugo Germain，上海交通大學的柴瑞博士，中科院遺傳與發育所的左建儒教授，堪薩斯大學的唐曉豔博士，英屬哥倫比亞大學的李昕博士以及北京大學的郭紅衛教授；周儉民博士為本文的通訊作者。該研究由科技部和北京市科委資助。（生物谷Bioon.com）
生物谷推薦原始出處：
Plant Cell August 28, 2009; 10.1105/tpc.108.065193
ETHYLENE INSENSITIVE3 and ETHYLENE INSENSITIVE3-LIKE1 Repress SALICYLIC ACID INDUCTION DEFICIENT2 Expression to Negatively Regulate Plant Innate Immunity in Arabidopsis
Huamin Chen 1, Li Xue 2, Satya Chintamanani 3, Hugo Germain 4, Huiqiong Lin 5, Haitao Cui 2, Run Cai 6, Jianru Zuo 7, Xiaoyan Tang 3, Xin Li 4, Hongwei Guo 8, and Jian-Min Zhou 5*
1 School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China; National Institute of Biological Sciences, Beijing 102206, China
2 National Institute of Biological Sciences, Beijing 102206, China; State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
3 Department of Plant Pathology, Kansas State University, Manhattan, Kansas 66506
4 Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada
5 National Institute of Biological Sciences, Beijing 102206, China
6 School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China
7 State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
8 National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing 100871, China
Pathogen/microbe-associated molecular patterns (PAMPs/MAMPs) trigger plant immunity that forms the first line inducible defenses in plants. The regulatory mechanism of MAMP-triggered immunity, however, is poorly understood. Here, we show that Arabidopsis thaliana transcription factors ETHYLENE INSENSITIVE3 (EIN3) and ETHYLENE INSENSITIVE3-LIKE1 (EIL1), previously known to mediate ethylene signaling, also negatively regulate PAMP-triggered immunity. Plants lacking EIN3 and EIL1 display enhanced PAMP defenses and heightened resistance to Pseudomonas syringae bacteria. Conversely, plants overaccumulating EIN3 are compromised in PAMP defenses and exhibit enhanced disease susceptibility to Pseudomonas syringae. Microarray analysis revealed that EIN3 and EIL1 negatively control PAMP response genes. Further analyses indicated that SALICYLIC ACID INDUCTION DEFICIENT2 (SID2), which encodes isochorismate synthase required for pathogen-induced biosynthesis of salicylic acid (SA), is a key target of EIN3 and EIL1. Consistent with this, the ein3-1 eil1-1 double mutant constitutively accumulates SA in the absence of pathogen attack, and a mutation in SID2 restores normal susceptibility in the ein3 eil1 double mutant. EIN3 can specifically bind SID2 promoter sequence in vitro and in vivo. Taken together, our data provide evidence that EIN3/EIL1 directly target SID2 to downregulate PAMP defenses.