Molecular Mechanisms of CO2 Signal Transduction

气孔孔是由叶表皮中的保卫细胞对形成的。气孔调节CO2向叶片扩散，起到光合作用固碳和控制植物蒸腾失水的作用。保卫细胞中的一系列信号转导机制感知和转导CO2、水分状况、光和其他环境刺激，以调节气孔开度，从而优化不同条件下的CO2内流、水分损失和植物生长。叶片中CO2浓度升高会导致气孔关闭，而CO2浓度降低会导致气孔张开。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，大气[二氧化碳]预计在本世纪内将翻一番，这些环境二氧化碳的增加使不同植物的气孔开度减少了高达40%。然而，对保卫细胞中介导CO2诱导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([Ca~(2+)]Cyt)升高有助于CO2诱导的气孔运动。P.I.S实验室的新发现表明，[CO_2]的变化调节了拟南芥保卫细胞胞浆[Ca~(2+)]的升高。保卫细胞的二氧化碳响应提供了一个合适的系统来分析细胞内钙离子模式对植物信号转导有贡献的假说。这项研究的长期目标是了解保卫细胞中介导二氧化碳信号转导的分子机制。本研究将探讨在气孔关闭和/或开放过程中，CO2对保卫细胞[Ca~(2+)]Cyt升高模式的调节参与了CO_2诱导的信号转导。为了验证这一假设，将进行以下特定目标的研究：表征野生型保卫细胞的二氧化碳反应。研究在保卫细胞信号网络中的不同点上影响钙和/或脱落酸信号的已知突变体对二氧化碳信号转导的影响，以表征影响二氧化碳信号的遗传机制，并确定哪些成分是特定于已定义的信号通路的。深入了解[Ca~(2+)]Cyt是如何被转导的，并明确特定的保卫细胞表达的CDPKs在气孔反应中的作用。描述新的二氧化碳信号突变体。P.I.将通过公共论坛，通过研究和职业培训，以及为本科生和高中生做好准备，进一步开展外联工作。了解CO2调节气孔开度的分子机制是了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和植物碳汇的工程研究。

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.