Stress Hormone Signal Transduction in Arabidopsis

描述（由申请人提供）：脱落酸是植物中的中心应激激素，介导快速细胞反应，下调细胞增殖，导致细胞周期阻滞和抑制生长。下调细胞增殖的信号转导机制对于控制有丝分裂至关重要。拟南芥保护细胞是一个强大的分子遗传学、基因组学和时间分辨信号系统，用于定量分析早期信号级联反应中复杂的分子机制介导特异性，ABA信号转导将在拟南芥保护细胞中进行研究。我们将分析一个新发现的主要早期ABA信号转导通路的细胞机制。简而言之，我们发现ABA在保护细胞中引起活性氧（ROS）的快速产生，进而激活质膜钙（Ca2+）通道。这产生了ABA信号转导所需的Ca2+振荡参数的定义窗口。我们发现ABA信号突变体在新识别的ABA- ros - ca2 +的不同点上起作用。振荡信号通路，包括NADPH氧化酶基因AtrbohD和f、PP2C磷酸酶和mRNA帽结合蛋白ABH1的突变。

DESCRIPTION (provided by applicant): Abscisic acid is a central stress hormone in plants which mediates rapid cellular responses, down regulates cell proliferation, causes cell cycle arrest and inhibits growth. Signal transduction mechanisms that down regulate cell proliferation are of central importance for controlling mitogenesis. Abscisic acid (ABA) signal transduction will be investigated in Arabidopsis guard cells, which have been developed as a powerful molecular genetic, genomic and time-resolved signaling system for quantitatively dissecting the complex molecular machinery mediating specificity in early signaling cascades. We will analyze the cellular mechanisms of a newly revealed major early ABA signal transduction pathway. In brief, we showed that ABA causes rapid production of reactive oxygen species (ROS) in guard cells, which in turn activate plasma membrane calcium (Ca2+) channels. This produces a defined window of Ca2+ oscillation parameters that are required for ABA signal transduction. We identified ABA signaling mutants that function at distinct points in the newly recognized ABA-ROS-Ca2+. oscillation signaling pathway, including mutations in the NADPH oxidase genes AtrbohD &F, PP2C phosphatases and the mRNA cap binding protein ABH1. We will test the hypotheses: that ABA biochemically activates membrane NADPH oxidases causing ROS production; that negatively regulating Ca2+ sensors function in reading specific Ca2+ oscillations; and that abh1 amplifies ABA-induced Ca2+ oscillations due to mRNA processing of early ABA signal transducers. To address these hypotheses, we will pursue the following specific aims: (1) Characterize biochemical and molecular mechanisms mediating rapid ABA-induced ROS production and characterize proteins complexed with the abi1-1 PP2C. (2) Analyze mechanisms by which ROS activate Ca2+ channels and isolate the Ca2+ channel genes. (3) The mechanisms responsible for reading specific calcium oscillations remain largely unknown in eukaryotes. Characterize the roles of the TCH2 and CalcineurinB-AtCBL Ca2+ sensory proteins in reading Ca2+ oscillations. (4) Characterize the mechanisms by which the abh1 mRNA cap binding mutant amplifies ABA-induced Ca2+ oscillations. A new virus-induced gene silencing-based screen will be pursued for identifying novel redundant ABA signaling mutants. These studies will reveal important fundamental mechanisms by which a newly recognized early signaling pathway controls ABA stress signal transduction and will contribute to a general understanding of Ca2+ signaling specificity in eukaryotes.