POTASSIUM CHANNEL CURRENTS IN INTACT STOMATAL GUARD-CELLS - RAPID ENHANCEMENT BY ABSCISIC-ACID
POTASSIUM CHANNEL CURRENTS IN INTACT STOMATAL GUARD-CELLS - RAPID ENHANCEMENT BY ABSCISIC-ACID
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DOI：
10.1007/bf00198799
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发表时间：
1990-02-01
期刊：
影响因子：
4.3
通讯作者：
BLATT, MR
中科院分区：
文献类型：
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作者：
BLATT, MR
脱落酸（阿坝）在水分胁迫和促进气孔关闭的信号条件下的作用的证据是令人信服的，但过去的研究留下了一些线索，其分子机制的行动;参数集中在H+泵活性和膜电位的变化，特别是，仍然模棱两可没有一个严格的电生理分析的基本支持。本文研究了蚕豆保卫细胞膜上K+通道对阿坝的反应。膜电位记录之前和暴露于阿坝期间，和全细胞电流进行了测量，在整个时间间隔定量的稳态和时间依赖性的K+通道的特性。在0.1、3或10 mM细胞外K+存在下加入10 μ M阿坝时，自由运行膜电位（Vm）在暴露的前5分钟内负移（-）4-7 mV，此后没有一致的效果。然而，电压钳测量显示，K+通道电流在稳态下上升到对照的1.84- 3.41倍，平均半衰期为1.1 ± 1。0.1通过泄漏的电流返回的可比较变化也是明显的，并解释了Vm的最小响应。计算在Vm，K+电流翻译为平均2.65倍的增加，K+流出阿坝。脱落酸没有观察到改变K+电流激活或失活。这些结果与ABA诱发的K+通道或通道电导的动员一致，而不是植物激素对K+通道门控的直接影响。数据折扣的概念，膜电压的大幅度波动是一个先决条件，以控制保卫细胞K+通量。相反，他们强调了K+通量的膜容量的增加，依赖于K+通道和漏电流的协调调节，并足够快，一般占从保卫细胞和气孔关闭阿坝的K+损失的发病。
Evidence of a role for abscisic acid (ABA) in signalling conditions of water stress and promoting stomatal closure is convincing, but past studies have left few clues as to its molecular mechanism(s) of action; arguments centred on changes in H+-pump activity and membrane potential, especially, remain ambiguous without the fundamental support of a rigorous electrophysiological analysis. The present study explores the response to ABA of K+ channels at the membrane of intact guard cells of Vicia faba L. Membrane potentials were recorded before and during exposures to ABA, and whole-cell currents were measured at intervals throughout to quantitate the steady-state and time-dependent characteristics of the K+ channels. On adding 10 .mu.M ABA in the presence of 0.1, 3 or 10 mM extracellular K+, the free-running membrane potential (Vm) shifted negative-going (-)4-7 mV in the first 5 min of exposure, with no consistent effect thereafter. Voltage-clamp measurements, however, revealed that the K+-channel current rose to between 1.84- and 3.41-fold of the controls in the steady-state with a mean halftime of 1.1 .+-. 0.1 min. Comparable changes in current return via the leak were also evident and accounted for the minimal response in Vm. Calculated at Vm, the K+ currents translated to an average 2.65-fold rise in K+ efflux with ABA. Abscisic acid was not observed to alter either K+-current activation or deactivation. These results are consistent with an ABA-evoked mobilization of K+ channels or channel conductance, rather than a direct effect of the phytohormone on K+-channel gating. The data discount notions that large swings in membrane voltage are a prerequisite to controlling guard-cell K+ flux. Instead, they highlight a rise in membrane capacity for K+ flux, dependent on concerted modulations of K+-channel and leak currents, and sufficiently rapid to account generally for the onset of K+ loss from guard cells and stomatal closure in ABA.