Molecular Mechanisms of CO2 Signal Transduction

气孔是由叶片表皮上的保卫细胞对形成的。气孔调节CO2向叶片的扩散，进行光合固碳，控制植物蒸腾水分的流失。保护细胞的信号转导机制网络感知和转导二氧化碳、水分状态、光和其他环境刺激，调节气孔开度，以优化不同条件下的二氧化碳流入、水分流失和植物生长。叶片中CO2浓度升高导致气孔关闭，CO2浓度降低导致气孔开放。光合作用和呼吸作用引起叶片中二氧化碳浓度的变化。此外，预计在本世纪内大气[CO2]将翻一番，这些环境CO2的增加使不同植物物种的气孔开度减少高达40%。然而，对保护细胞中介导二氧化碳诱导的气孔运动的分子信号转导机制知之甚少。一项研究表明，胞质钙（[Ca2+]cyt）升高有助于二氧化碳诱导的气孔运动。P.I.的新发现的实验室研究表明，[CO2]的变化调节了拟南芥保护细胞中胞质[Ca2+]cyt的升高。保护细胞对二氧化碳的反应提供了一个合适的系统来分析细胞质Ca2+模式对植物信号转导的贡献。本研究的长期目标是了解保护细胞中介导二氧化碳信号转导的分子机制。该研究将探讨保护细胞中[Ca2+]cyt升高模式的CO2调节有助于气孔关闭和/或打开过程中CO2诱导的信号转导的假设。为了验证这一假设，将进行以下具体目标的研究：描述野生型保护细胞对二氧化碳的反应。检查已知突变体对二氧化碳信号转导的影响，这些突变体在保护细胞信号网络的不同点上影响Ca2+和/或脱落酸信号，表征影响二氧化碳信号传导的遗传机制，并确定哪些成分特定于定义的信号传导途径。深入了解[Ca2+]cyt是如何被转导的，并明确定义了保护细胞表达的CDPKs在气孔反应中的作用。表征新的CO2信号突变体。私家侦探将通过公共论坛、研究和职业培训以及本科生和高中生的准备，进一步开展外联工作。了解二氧化碳调节气孔开度的分子机制是理解植物与大气之间气体交换调控的基础，有助于预测大气CO2升高对气孔的影响，也可能有助于未来作物植物工程和植物碳汇面对不断变化的环境条件。

Stomatal pores are formed by guard cell pairs in the epidermis of leaves. Stomata regulate the diffusion of CO2 into leaves for photosynthetic carbon fixation and control transpirational water loss of plants. A network of signal transduction mechanisms in guard cells sense and transduce CO2, water status, light and other environmental stimuli to regulate stomatal apertures for optimization of CO2 influx, water loss and plant growth under diverse conditions. Elevated CO2 concentrations in leaves cause stomatal closure, whereas reduced CO2 concentrations result in stomatal opening. Photosynthesis and respiration cause CO2 concentration changes in leaves. Moreover, atmospheric [CO2] is predicted to double within the present century and these ambient CO2 increases reduce stomatal apertures of different plant species by up to 40 %. However, relatively little is known about the molecular signal transduction mechanisms in guard cells that mediate CO2-induced stomatal movements. A study suggests that cytosolic calcium ([Ca2+]cyt) elevations contribute to CO2-induced stomatal movements. New findings in the P.I.'s laboratory show that changes in [CO2] modulate cytosolic [Ca2+]cyt elevations in Arabidopsis guard cells. The guard cell CO2 response provides an opportune system to analyze hypotheses that cytosolic Ca2+ patterns contribute to signal transduction in plants. The long term goal of this research is to achieve an understanding of the molecular mechanisms that mediate CO2 signal transduction in guard cells. The research will investigate the hypothesis that CO2 modulation of the [Ca2+]cyt elevation pattern in guard cells contributes to CO2-induced signal transduction during stomatal closing and/or opening. To test this hypothesis, studies with the following specific aims will be pursued: Characterize CO2 responses of wildtype guard cells. Examine the effects on CO2 signal transduction of known mutants that affect Ca2+ and/or abscisic acid signaling at distinct points within the guard cell signaling network, to characterize genetic mechanisms that affect CO2 signaling and to determine which components are specific to defined signaling pathways. Gain insight into how [Ca2+]cyt is transduced and specifically define the roles of selected guard cell-expressed CDPKs in stomatal responses. Characterize new CO2 signaling mutants. The P.I. will further pursue outreach efforts through public forums and through research and career training and preparation of undergraduate and high school students. Understanding the molecular mechanisms by which CO2 modulates stomatal apertures is fundamental to understanding the regulation of gas exchange between plants and the atmosphere, will help to predict effects of atmospheric CO2 elevation on stomata and may also contribute to future engineering of crop plants and plant carbon sinks in the face of changing environmental conditions.