植物激素脱落酸（ABA）调节植物生长发育过程和植物对逆境的适应。ABA信号首先通过细胞受体被识别，然后引起一系列细胞内下游信号转导事件，最终导致生物学效应。研究证明，ABA信号受体有多种，包括细胞表面受体和细胞内受体。张大鹏研究组以前鉴定了一种细胞内叶绿体中的ABA受体，命名为ABAR（Nature, 2006, 443: 823-826）。之后他们提供了ABAR是ABA受体的进一步的生物化学和遗传学证据；而且，发现ABAR分子的C-端是结合ABA和介导ABA信号的核心区（Plant Physiology, 2009, 150: 1940-1954）。但是，ABAR介导的下游信号通路一直是悬而未决的问题。
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张大鹏研究组发现，ABAR是一个跨越叶绿体被膜的蛋白质，其C-端和N-端曝露在细胞质中；ABAR在细胞质一侧的C-端部分与一组WRKY转录因子（AD1A/WRKY40、AD1B/WRKY18、AD1C/WRKY60）互相作用。他们提供的遗传学和生物化学证据表明，AD1A/B/C是一组转录抑制因子，负调节ABA信号通路；AD1A是其中的核心调节子。ABAR与ABA信号分子结合后，可以刺激AD1A从细胞核到细胞质的转移，促进ABAR与AD1A的互相作用；进而激发一种未知因子（或信号系统），阻遏AD1A的表达，从而解除AD1A对ABA响应基因（比如ABI5等）转录的抑制，最终实现ABA的生理效应。
这些发现描述了一个从信号原初识别到下游基因表达的新的ABA信号通路（即ABA-ABAR-AD1A-ABI5信号级联通路，参见图1）。研究论文于6月11日在线发表于国际著名植物学期刊Plant Cell。(生物谷Bioon.net)
生物谷推荐原文出处：
Plant Cell doi:10.1105/tpc.110.073874
The Mg-Chelatase H Subunit of Arabidopsis Antagonizes a Group of Transcription Repressors to Relieve ABA-Responsive Genes of Inhibition
Yi Shanga,1, Lu Yana,b,1, Zhi-Qiang Liua,b,1, Zheng Caoa,b,1, Chao Meia,1, Qi Xina,b, Fu-Qing Wua,b, Xiao-Fang Wanga,b, Shu-Yuan Dua, Tao Jianga,b, Xiao-Feng Zhanga, Rui Zhaoa,b, Hai-Li Suna,b, Rui Liua,b, Yong-Tao Yua and Da-Peng Zhanga,2
a Protein Science Laboratory of the Ministry of Education, School of Life Sciences, Tsinghua University, Beijing 100084, China
b College of Biological Sciences, China Agricultural University, Beijing 100094, China
The phytohormone abscisic acid (ABA) plays a vital role in plant development and response to environmental challenges, but the complex networks of ABA signaling pathways are poorly understood. We previously reported that a chloroplast protein, the magnesium-protoporphyrin IX chelatase H subunit (CHLH/ABAR), functions as a receptor for ABA in Arabidopsis thaliana. Here, we report that ABAR spans the chloroplast envelope and that the cytosolic C terminus of ABAR interacts with a group of WRKY transcription factors (AD1A/WRKY40, AD1B/WRKY18, and AD1C/WRKY60) that function as negative regulators of ABA signaling in seed germination and postgermination growth. AD1A, a central negative regulator, inhibits expression of ABA-responsive genes, such as ABI5. In response to a high level of ABA signal that recruits AD1A from the nucleus to the cytosol and promotes ABAR–AD1A interaction, ABAR relieves the ABI5 gene of inhibition by repressing AD1A expression. These findings describe a unique ABA signaling pathway from the early signaling events to downstream gene expression.
