STRESS HORMONE SIGNAL TRANSDUCTION IN ARABIDOPSIS

拟南芥应激激素信号转导

• 批准号: 6351328
• 负责人: JULIAN I SCHROEDER
• 金额: $ 23.94万
• 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 2004-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6351328
• 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 (adapted from the applicant's description): Abscisic acid is a central stress hormone in plants which mediates rapid cellular responses and down regulates cell proliferation, causes cell cycle arrest and inhibits growth. Early signal transduction mechanisms that down regulate cell proliferation are of central importance for controlling mitogenesis. The long-term goal of this research is to achieve a detailed quantitative understanding of the network of events that mediate early abscisic acid signal transduction in the easily manipulated genetic model system, Arabidopsis thaliana. Abscisic acid (ABA) signal transduction will be analyzed in Arabidopsis guard cells, which provide a powerful system for quantitatively dissecting the complex molecular machinery mediating specificity in early signaling cascades. The hypothesis that the ABI1 and ABI2 phosphatases and ERA1 negatively regulate ABA signaling at different points in the early ABA signaling network will be tested. Using a combination of quantitative cell biological and molecular genetic the specific aims if this proposal include: (1) Determine whether era1F'Tase deletion enhances ABA-induced early cytosolic Ca2+ ([Ca2+]cyt) increases. (2) Determine whether the abi1and abi2 mutants impair Ca2+ entry via the plasma membrane and/or second messenger regulated Ca2+ release from intracellular stores. (3) Determine the cellular locations of the wild-type and mutant ABI protein phosphatases in wildtype and in era1 FTase deletion backgrounds. (4) Identify genes encoding farnesylated targets of ERAl in guard cells. (5) Clone and characterize the function of a new recessive ABA hypersensitive mutant gene, abh1.

描述（根据申请人的描述改编）：脱甲酸是一个 中央应激激素中介导快速细胞反应的植物和 下调调节细胞增殖，引起细胞周期停滞并抑制 生长。降低调节细胞的早期信号转导机制 增殖对于控制有丝分裂而言至关重要。这 这项研究的长期目标是实现详细的定量 理解介导早期脱节酸信号的事件网络 易于操纵的遗传模型系统的转导拟南芥 塔利亚娜。脱节酸（ABA）信号转导将在 拟南芥守卫细胞，为定量提供了强大的系统 剖析早期的复合分子机械介导的特异性 信号级联。 ABI1和ABI2磷酸酶和ERA1的假设1 在ABA早期的不同点处负调节ABA信号 信号网络将进行测试。结合定量细胞 生物学和分子遗传的特定目的是否包括： （1）确定ERA1F'Tase缺失是否增强了ABA诱导的早期胞质 Ca2+（[Ca2+] Cyt）增加。 （2）确定ABI1和ABI2突变体是否 通过质膜和/或第二使者调节，CA2+进入CA2+进入 Ca2+从细胞内存储中释放。 （3）确定细胞位置 野生型和ERA1 FTase中的野生型和突变体ABI蛋白磷酸酶 删除背景。 （4）识别编码ERAL的法尼化靶标的基因 在后卫细胞中。 （5）克隆并表征新隐性ABA的功能 超敏突变基因，ABH1。