Calcium Channel Regulation in Arabidopsis Guard Cells

拟南芥保卫细胞中的钙通道调节

• 批准号: 0132894
• 负责人: Zhen-Ming Pei
• 金额: $ 28.58万
• 依托单位: Duke University
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-04-01 至 2005-03-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0132894&HistoricalAwards=false
• 关键词: Calcium; Channel; Regulation; Arabidopsis; Guard

Drought stress is a major limitation for agricultural production. More than 95% of water loss from plants occurs via stomatal pores, which are formed by pairs of guard cells in the leaf epidermis. Stomata open and close in response to various environmental signals, such as light, CO2 and water status. A signaling network in guard cells integrates these signals to regulate stomatal movements, which control water loss and CO2 uptake. The long-term goal of the project is to dissect this signaling network by studying Ca2+ channels, which have been proposed to play a key role. Elevation of cytosolic free Ca2+ concentrations in guard cells is an early event during abscisic acid-triggered stomatal closing. Ion channel-mediated Ca2+ influx gives rise to the cytosolic Ca2+ increase. It has been shown previously that hydrogen peroxide activates Ca2+ channels in the plasma membrane of guard cells. Inhibition of NADPH oxidase prevents H2O2 production and reduces abscisic acid-induced stomatal closing. Additionally, preliminary studies have revealed that nitric oxide also triggers stomatal closure. This project will further study H2O2 and nitric oxide regulation of the Ca2+ channels via a combined cell biological, biophysical, and molecular genetic approach. The effects of biologically active oxidants and antioxidants on the Ca2+ channels will be analyzed. Furthermore, the role of NADPH oxidase in guard cell abscisic acid signaling will be determined. The effects of nitric oxide on stomatal movements will also be examined.The information gained in the project will provide insight into the guard cell signaling network and contribute to the identification of potential molecular and genetic targets for engineering drought-resistant plants. Furthermore, the project may also impact on the understanding of how nitric oxide, a major air pollutant, affects the global ecosystem via plants.

干旱胁迫是农业生产的主要限制因素。植物95%以上的水分流失是通过气孔进行的，气孔是由叶表皮上成对的保卫细胞形成的。气孔的开闭响应于各种环境信号，如光、CO2和水分状况。保卫细胞中的信号网络整合这些信号来调节气孔运动，从而控制水分损失和CO2吸收。该项目的长期目标是通过研究Ca 2+通道来剖析这个信号网络，Ca 2+通道被认为起着关键作用。保卫细胞胞质游离Ca ~（2+）浓度升高是脱落酸诱导气孔关闭的早期事件。离子通道介导的Ca ~（2+）内流引起胞浆Ca ~（2+）增加。先前已经显示过氧化氢激活保卫细胞质膜中的Ca 2+通道。NADPH氧化酶的抑制阻止H2 O2的产生，并减少脱落酸诱导的气孔关闭。此外，初步研究表明，一氧化氮也触发气孔关闭。该项目将通过细胞生物学、生物物理学和分子遗传学相结合的方法进一步研究H2 O2和一氧化氮对Ca 2+通道的调节。将分析生物活性氧化剂和抗氧化剂对Ca 2+通道的影响。此外，NADPH氧化酶在保卫细胞脱落酸信号传导中的作用将被确定。此外，研究人员还将研究一氧化氮对气孔运动的影响，并将利用该项目获得的信息深入了解保卫细胞信号网络，为抗旱植物的基因工程改造提供潜在的分子和遗传靶点。此外，该项目还可能影响对一氧化氮（一种主要空气污染物）如何通过植物影响全球生态系统的理解。