2009年8月29日，北京生命科学研究所周俭民实验室在The Plant Cell杂志上发表题为“ETHYLENE INSENSITIVE3 and ETHYLENE INSENSITIVE3-LIKE1 Repress SALICYLIC ACID INDUCTION DEFICIENT2 Expression to Negatively Regulate Plant Innate Immunity in Arabidopsis”的文章。
水杨酸(SA)是植物抗病中的重要激素，它的合成受到精密调控。该文章报道了转录因子EIN3和EIL1直接结合在水杨酸合成基因SID2的启动子区，抑制水杨酸的合成, 从而负调控植物免疫反应。结果还揭示了乙烯信号途径和水杨酸信号途径间新的交叉调控。
该文章的共同第一作者是北京生命科学研究所博士陈华民，博士生薛丽还有堪萨斯大学的Satya Chintamanani；参与这项工作的还有林惠琼，崔海涛，加拿大英属哥伦比亚大学的Hugo Germain，上海交通大学的柴瑞博士，中科院遗传与发育所的左建儒教授，堪萨斯大学的唐晓艳博士，英属哥伦比亚大学的李昕博士以及北京大学的郭红卫教授；周俭民博士为本文的通讯作者。该研究由科技部和北京市科委资助。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
