Phosphorylation and dephosphorylation reactions in stomatal guard cells of blue light signaling

蛋白质的磷酸化和去磷酸化参与了气孔保卫细胞的信号转导途径。由于保卫细胞可以同时对蓝光和植物激素脱落酸做出反应，我们使用保卫细胞原生质体研究了这些反应。蓝光受体对蓝光的反应是自动磷酸化的，并且发现14-3-3蛋白与促光激素中磷酸化的丝氨酸结合。该位点位于LOV1和LOV2之间。我们发现ABA抑制了气孔保卫细胞中的这种蓝光信号通路。ABA抑制质膜H^-ATPase的磷酸化，并抑制保卫细胞的H^泵。我们还发现ABA抑制了质膜H^-ATPase的ATP水解性。

Protein phosphorylation and dephosphoryaltion are involved in the signal transduction pathways of stomatal guard cells. Since the guard cells can respond to both blue light and phytohormone abscisic acid, we investigated these responses using guard cell protoplasts.The blue light receptor is autophosphorylated in response to blue light, and a 14-3-3 protein was found to bind to phosphorylated serine in phototropin. The site is identified to be localized between LOV1 and LOV2.We found that ABA inhibits this blue light signaling pathways in stomatal guard cells. ABA inhibited the phosphorylation of the plasma membrane H^+-ATPase and inhibited the H^+ pumping from guard cells. We also found that ABA inhibited the ATP hydrolytic activity of the plasma membrane H^+-ATPase.