15 NSFBIO SAUR regulation of stomatal aperture

保卫细胞通过调节气孔的开闭来控制光合作用和蒸腾作用。我们知道很多关于保卫细胞如何响应干旱胁迫激素阿坝而收缩，导致气孔关闭。与此相反，我们有稀疏的知识的生化事件，保卫细胞膨胀，导致气孔开放响应光和昼夜节律。我们发现拟南芥SAUR（Small Auxin Up RNA）蛋白能够促进气孔开放。这项提议将揭示它们在什么条件下以及通过什么机制这样做。SAUR基因是所有陆地植物中的一大类。几种拟南芥SAUR蛋白定位于质膜并促进细胞扩增。这些蛋白质通常是短寿命的，但可以稳定在质膜中。我们知道，密切相关的SAUR蛋白通过抑制膜相关蛋白磷酸酶促进生长，否则在一个关键的调节位点去磷酸化质膜H+-ATP酶，并增加H+-ATP酶质子泵。相同的SAURs也促进气孔开放时，在保卫细胞中表达和这些的一个子集优先表达在保卫细胞中的条件下，气孔是开放的，但被抑制干旱或阿坝。相反，阿坝激活保卫细胞中的其他SAUR基因，这可能对气孔功能产生相反的影响。因此，我们不知道这些相反的作用是否是独特的，它们是否重叠，或者SAUR介导的信号传导是否影响保卫细胞中的其他转运和稳态过程。质膜和液泡膜中的多种转运蛋白影响保卫细胞的收缩和膨胀，它们的活性往往直接或间接地依赖于其他转运蛋白的激活状态。因此，了解气孔动态，这是至关重要的，以获得一个全球性的，系统的观点保卫细胞运输和稳态。该项目的一个主要组成部分将利用计算模型，使用基于实验测量的参数来模拟这些耦合。目前的建模起点将借鉴过去的预测，H+-ATP酶活性的变化将有显着的影响气孔开度。例如，H+-ATP酶活性增加的模型导致气孔在黄昏关闭较慢，也改变了其他几种离子的细胞质浓度。这些知识将有助于实验设计，也将形成后续验证的基础。合作研究人员在保卫细胞生理学（Blatt），计算建模（Blatt），生物化学（Gray），遗传学（Reed，Nagpal）和生长素反应（Gray，Nagpal，Reed）方面具有互补的专业知识。合作将汇集三个实验室开发的资源和专业知识，使多管齐下的方法成为可能。

Guard cells control photosynthesis and transpiration by regulating opening and closing of stomatal pores. We know much about how guard cells shrink in response to the drought stress hormone ABA, leading to stomatal closure. In contrast, we have sparse knowledge of the biochemical events by which guard cells swell to cause stomatal opening in response to light and diurnal rhythms. We have found that Arabidopsis SAUR (Small Auxin Up RNA) proteins can promote stomatal opening. This proposal will be to unravel under what conditions and by what mechanisms they do so.SAUR genes are a large class in all land plants. Several Arabidopsis SAUR proteins localize to the plasma membrane and promote cell expansion. These proteins are normally short-lived, but can be stabilized in the plasma membrane. We know that closely related SAUR proteins promote growth by inhibiting membrane-associated protein phosphatases that otherwise dephosphorylate plasma membrane H+-ATPases at a key regulatory site and increase H+-ATPase proton pumping. The same SAURs also promote stomatal opening when expressed in guard cells and a subset of these are preferentially expressed in guard cells under conditions in which stomata are open, but are repressed by drought or ABA. By contrast, ABA activates other SAUR genes in guard cells which may have opposing effects on stomatal function. Thus, what we do not know is whether these opposing actions are unique, whether they overlap, or whether SAUR-mediated signalling affects other transport and homeostatic processes in guard cells. Multiple transporters in both the plasma membrane and the tonoplast influence guard cell shrinking and swelling, and their activities often depend either directly or indirectly on the activation status of the others. Thus, to understand stomatal dynamics, it is essential to gain a global, systems view of guard cell transport and homeostasis. A major component of this project will exploit computational models that simulate these couplings using parameters based on experimental measurements. Starting points for current modelling will draw on past predictions that changes in H+-ATPase activity will have significant effects on stomatal aperture. For example, increased H+-ATPase activity in the model leads to slower stomatal closing at dusk and also to changed cytoplasmic concentrations of several other ions. Such knowledge will aid in experimental design and will also form a basis for subsequent validation.The collaborating researchers have complementary expertise in guard cell physiology (Blatt), computational modeling (Blatt), biochemistry (Gray), genetics (Reed, Nagpal), and auxin response (Gray, Nagpal, Reed). The collaboration will pool resources and expertise developed in the three labs to make possible the multipronged approach.