Stress Hormone Signal Transduction in Arabidopsis

拟南芥中的应激激素信号转导

• 批准号: 7010367
• 负责人: JULIAN I SCHROEDER
• 金额: $ 27.9万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-02-01 至 2008-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7010367
• 关键词: Arabidopsis; alkyltransferase; biological signal transduction; calcium channel; calcium flux; calcium indicator; cell growth regulation; cell membrane; cell proliferation; cytoplasm; eukaryote; gene deletion mutation; genetic library; hormone regulation /control mechanism; intracellular transport; molecular cloning; molecular dynamics; mutant; phosphomonoesterases; phytohormones; plant growth /development; protein structure function; second messengers; stress proteins; water channel

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.

描述（由申请人提供）：脱甲酸是植物中的一种中央应激激素，介导了快速的细胞反应，下调调节细胞增殖，导致细胞周期停滞并抑制生长。降低细胞增殖的信号转导机制对于控制有丝分裂而言至关重要。拟南芥保护细胞中将研究脱甲酸（ABA）信号转导，该细胞已开发为一种强大的分子遗传，基因组和时间分辨信号系统，用于定量地剖析早期信号级联中介导的复杂分子机械介导的特异性。我们将分析新揭示的主要早期ABA信号转导途径的细胞机制。简而言之，我们表明ABA导致后卫细胞中的活性氧（ROS）的快速产生，后者又激活了质膜钙（Ca2+）通道。这会产生ABA信号转导所需的Ca2+振荡参数的定义窗口。我们确定了在新认识的ABA-ROS-CA2+中在不同点起作用的ABA信号突变体。振荡信号通路，包括NADPH氧化酶基因ATRBOHD＆F，PP2C磷酸酶和mRNA CAP结合蛋白ABH1的突变。 我们将检验这些假设：ABA生化会激活膜NADPH氧化酶，从而导致ROS产生；负调控Ca2+传感器在读取特定CA2+振荡中起作用；并且ABH1由于早期ABA信号传感器的mRNA处理而放大ABA诱导的Ca2+振荡。为了解决这些假设，我们将追求以下特定目的：（1）表征介导ABA诱导的ROS产生的生化和分子机制，并表征与ABI1-1 PP2C复杂化的蛋白质。 （2）分析ROS激活Ca2+通道并分离Ca2+通道基因的机制。 （3）负责读取特定钙振荡的机制在真核生物中基本上未知。表征TCH2和钙调蛋白B-ATCBL Ca2+感觉蛋白在读取Ca2+振荡中的作用。 （4）表征ABH1 mRNA帽结合突变体扩增ABA诱导的Ca2+振荡的机制。将追求一种新的基于病毒诱导的基因沉默筛选，以识别新型的冗余ABA信号突变体。这些研究将揭示重要的基本机制，通过这些机制，新认识的早期信号通路控制ABA应力信号转导，并有助于对真核生物中Ca2+信号特异性的一般理解。