Assmann S M, Wu W H
Department of Biology, Pennsylvania State University, University Park 16802, USA.
Symp Soc Exp Biol. 1994;48:193-202.
Abscisic acid (ABA) affects a number of ion transport mechanisms in guard cells. One effect of ABA is to inhibit inward K+ channels, an effect that can contribute to the inhibition of stomatal opening. One model of the signal transduction cascade mediating this response involves ABA-activation of a G-protein, which in turn activates phospholipase C, resulting in production of inositol 1,4,5-trisphosphate (IP3), elevation of cytosolic free Ca2+ levels (Cai), and activation of a Ca(2+)-dependent phosphatase (protein phosphatase 2B; PP2B) which mediates channel inhibition. A review of the literature reveals that several of the links in this putative signal transduction chain have been established. The G-protein activator, GTP gamma S, inhibits inward K+ currents. Exogenous IP3 inhibits inward K+ currents. Exogenous IP3 elevates Cai. Elevated Cai inhibits inward K+ currents, and the inhibition by ABA of inward K+ currents does require Ca2+. Exogenous PP2B inhibits inward K+ currents, and an endogenous Ca(2+)-dependent phosphatase activity is present in guard cells. However, significant gaps in the chain remain. There is no direct evidence that ABA activates a G-protein. The presence or absence of a G-protein-activated phospholipase C in guard cells has not been investigated. Elevation of Cai by ABA is variable, and the reasons for this variability remain to be established. It is not known whether or not activation of a guard-cell PP2B homolog is the exclusive mechanism by which Ca2+ inhibits the channels.
脱落酸（ABA）影响保卫细胞中的多种离子转运机制。ABA的一个作用是抑制内向钾离子通道，这种作用有助于抑制气孔开放。介导这种反应的信号转导级联的一种模型涉及ABA激活G蛋白，G蛋白进而激活磷脂酶C，导致肌醇1,4,5-三磷酸（IP3）的产生、胞质游离钙离子水平（Cai）的升高以及一种钙依赖性磷酸酶（蛋白磷酸酶2B；PP2B）的激活，该磷酸酶介导通道抑制。对文献的综述表明，这个假定的信号转导链中的几个环节已经得到证实。G蛋白激活剂GTPγS抑制内向钾离子电流。外源性IP3抑制内向钾离子电流。外源性IP3升高Cai。升高的Cai抑制内向钾离子电流，并且ABA对内向钾离子电流的抑制确实需要钙离子。外源性PP2B抑制内向钾离子电流，并且保卫细胞中存在内源性钙依赖性磷酸酶活性。然而，该链中仍存在显著差距。没有直接证据表明ABA激活G蛋白。尚未研究保卫细胞中是否存在G蛋白激活的磷脂酶C。ABA引起的Cai升高是可变的，这种变异性的原因尚待确定。尚不清楚保卫细胞PP2B同源物的激活是否是钙离子抑制通道的唯一机制。
