Phosphatase Regulation of Plant K+ Channels

小行星9316319 Ca ~（++）对植物的施用阻止气孔开放。 Ca ~（++）的作用之一是阻断介导K ~（++）吸收的内向K ~（++）通道。 最近已经获得的证据表明，这种激活是由类似于动物蛋白磷酸酶2B的磷酸酶的Ca++激活引起的。 所提出的全细胞膜片钳实验将测试蛋白磷酸酶2B是否在信号转导途径中在脱落酸和/或活化的G蛋白和/或肌醇三磷酸的“下游”起作用。 利用保卫细胞原生质体和保卫细胞蛋白质提取物的平行生物化学研究将确定脱落酸、Ca++和蛋白磷酸酶2B是否引起相同蛋白质的去磷酸化，如果蛋白磷酸酶2B是脱落酸应答的第二介导物，则可以预测。 完整的保卫细胞的显微注射实验将解决蛋白磷酸酶2B的可能性，替代或另外，其他环境信号，防止气孔开放的第二信使。 气孔保卫细胞是植物光合CO2吸收和蒸腾失水的重要调控点。 气孔开度受保卫细胞的渗透性膨胀和收缩的调节，而渗透性膨胀和收缩是由保卫细胞质膜上的离子流驱动的。 一些报道暗示Ca++作为脱落酸的第二信使之一，脱落酸是一种阻止气孔开放并降低内向K+电流的植物激素。 在这个建议中，补充电生理，细胞生物学和生化实验概述了测试的假设，调节气孔开放的环境信号作用于内向的K+通道通过磷酸酶2B同源。 这些研究的结果将提供深入了解植物利用的第二信使系统，将环境信号转化为离子通道活性的改变。 结果也将是感兴趣的环境生理学家谁想要了解外部和内部环境如何影响气孔孔径，从而影响植物生产力。 ***

9316319 Assmann Application of Ca++ to plants prevents stomatal opening. One effect of Ca++ is to inactivate the inward K+ channels that mediate K+ uptake. Evidence has recently been obtained that this activation results from Ca++ activation of a phosphatase analogous to animal protein phosphatase 2B. The proposed whole-cell patch clamp experiments will test whether the protein phosphatase 2B acts " downstream" of abscisic acid and/or activated G-protein and/or inositoltriphosphate in a signal transduction pathway. Parallel biochemical studies utilizing guard cell protoplasts and guard cell protein extracts will determine whether abscisic acid, Ca++ and protein phosphatase 2B cause dephosphorylation of the same protein, as would be predicted if protein phosphatase 2B is a second mesenger for the abscisic acid response. Microinjection experiments on intact guard cells will address the possibility that protein phosphatase 2B is, alternatively or in addition, a second messenger for other environmental signals that prevent stomatal opening. %%% Stomatal guard cells are vital control points in the regulation of photosynthetic CO2 uptake and transpirational water loss. Stomatal appertures are regulated by osmotic swelling and shrinking of guard cells, driven by ion fluxes across the guard-cell plasma membrane. Several reports implicate Ca++ as one of the second messengers for abscisic acid, a plant hormone that prevents stomatal opening and also reduces inward K+ current. In this proposal complementary electrophysiological, cell biological and biochemical experiments are outlined to test the hypothesis that environmental signals which regulate stomatal opening act on inward K+ channels via a phosphatase 2B homologue. Results from these studies will provide insight into the second messenger systems utilized by plants to translate environmental signals into alterations of ion channel activity. Results will also be of interest to environmental physiologis ts who would like to understand how the external and internal environments affects stomatal apertures and thereby impacts plant productivity. ***