STRESS HORMONE SIGNAL TRANSDUCTION IN ARABIDOPSIS

描述(改编自申请人的描述)：脱落酸是一种 植物中的中枢应激激素，它介导快速的细胞反应和 下调细胞增殖，导致细胞周期停滞并抑制 成长。下调细胞的早期信号转导机制 增殖对于控制有丝分裂是至关重要的。这个 本研究的长期目标是实现详细的量化 对调节早期脱落酸信号的事件网络的理解 易于操作的拟南芥遗传模型系统中的转导 塔里安娜。脱落酸(ABA)的信号转导将在 拟南芥保卫细胞，它提供了一个强大的系统 早期对介导特异性的复杂分子机制的剖析 信号级联。ABI1和ABI2磷酸酶与ERA1的假说 ABA早期不同时间点对ABA信号的负调控 信令网络将进行测试。使用定量单元格组合 生物学和分子遗传学如果这项提议包括： (1)确定era1F‘Tase缺失是否增强ABA诱导的早期胞质 Ca~(2+)([Ca~(2+)]细胞)增加。(2)确定abi1和abi2突变体 通过质膜和/或第二信使调节的钙离子内流受损 钙离子从细胞内储藏中释放出来。(3)确定蜂窝位置 野生型和突变ABI蛋白磷酸酶在野生型和ERA1 FTase中的表达 删除背景。(4)筛选编码外周血法呢化靶基因 在看守牢房里。(5)一个新的隐性脱落酸基因的克隆和功能鉴定 超敏突变基因abh1。

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.