STRESS HORMONE SIGNAL TRANSDUCTION IN ARABIDOPSIS

描述（改编自申请人的描述）：脱落酸是一种抗氧化剂。 植物中的中枢应激激素，其介导快速细胞反应， 下调细胞增殖，导致细胞周期停滞并抑制 增长下调细胞增殖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。的 本研究的长期目标是实现一个详细的定量 了解早期脱落酸信号介导的事件网络 在易于操作的遗传模型系统中，拟南芥 thaliana.脱落酸（ABA）信号转导将在 拟南芥保卫细胞，这提供了一个强大的系统，定量 解剖在早期癌症中介导特异性的复杂分子机制， 信号级联。假设ABI1和ABI2磷酸酶和ERA1 在ABA早期的不同点负调控ABA信号 将测试信令网络。使用定量细胞 生物学和分子遗传学-这项建议的具体目标包括： (1)确定era1F 'Tase缺失是否增强ABA诱导的早期胞浆 Ca2+（[Ca2 +] cyt）增加。(2)确定abi1和abi2突变体是否 通过质膜和/或第二信使调节的Ca2+内流受损 Ca2+从细胞内储存释放。(3)确定以下设备的蜂窝位置 野生型和突变型ABI蛋白磷酸酶 删除背景。(4)鉴定编码ERAl的法尼基化靶标的基因 在警卫室里(5)一个新的隐性ABA基因的克隆及其功能研究 过敏突变基因abh 1。

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.