Nitric oxide regulates K+ and Cl- channels in guard cells through a subset of abscisic acid-evoked signaling pathways
Nitric oxide regulates K+ and Cl- channels in guard cells through a subset of abscisic acid-evoked signaling pathways
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DOI：
10.1073/pnas.1434381100
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发表时间：
2003-09-16
影响因子：
11.1
通讯作者：
Blatt, MR
中科院分区：
文献类型：
--
作者：
Garcia-Mata, C;Gay, R;Blatt, MR
脱落酸(ABA)触发了一系列复杂的信号事件，导致保卫细胞质膜离子通道和溶质外流的协同调节，从而驱动植物叶片的气孔关闭。最近的工作表明，在拟南芥和蚕豆保卫细胞中，一氧化氮(NO)及其合成是ABA信号转导的先决条件。它的作用机制(S)在保卫细胞中并不是很清楚，通常在高等植物中也是如此。在这里，我们直接证明，NO通过促进细胞内钙离子释放，提高胞内游离钙离子浓度，选择性地调节蚕豆保卫细胞的钙敏感离子通道。NO敏感的钙释放可被鸟苷环化酶拮抗剂和环状ADP核糖依赖的膜内钙通道拮抗剂阻断，这意味着这一作用是通过cGMP依赖的级联反应介导的。NO不能抑制ABA对质膜Ca~(2+)通道和Ca~(2+)不敏感K~+通道的控制作用，也没有清除剂能阻断ABA对这些K~+通道的激活作用。这些结果在ABA参与的钙信号通路的一个分支中没有任何作用，并定义了控制保卫细胞运动的平行信号事件的边界。
Abscisic acid (ABA) triggers a complex sequence of signaling events that lead to concerted modulation of ion channels at the plasma membrane of guard cells and solute efflux to drive stomatal closure in plant leaves. Recent work has indicated that nitric oxide (NO) and its synthesis are a prerequisite for ABA signal transduction in Arabidopsis and Vicia guard cells. Its mechanism(s) of action is not well defined in guard cells and, generally, in higher plants. Here we show directly that NO selectively regulates Ca2+-sensitive ion channels of Vicia guard cells by promoting Ca2+ release from intracellular stores to raise cytosolic-free [Ca2+]. NO-sensitive Ca2+ release was blocked by antagonists of guanylate cyclase and cyclic ADP ribose-dependent endomembrane Ca2+ channels, implying an action mediated via a cGMP-dependent cascade. NO did not recapitulate ABA-evoked control of plasma membrane Ca2+ channels and Ca2+-insensitive K+ channels, and NO scavengers failed to block the activation of these K+ channels evoked by ABA. These results place NO action firmly within one branch of the Ca2+- signaling pathways engaged by ABA and define the boundaries of parallel signaling events in the control of guard cell movements.