Botany School, University of Cambridge, Downing Street, CB2 3EA, Cambridge, UK.
Planta. 1990 Feb;180(3):445-55. doi: 10.1007/BF00198799.
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 μM ABA in the presence of 0.1, 3 or 10 mM extracellular K(+), the free-running membrane potential (V m) 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 V m. Calculated at V m, 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, thev 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.
脱落酸（ABA）在信号传递水分胁迫条件和促进气孔关闭方面的作用的证据令人信服，但过去的研究几乎没有提供其作用机制的线索；围绕 H（+）-泵活性和膜电位变化的争论，在没有严格的电生理分析的基本支持下，仍然模棱两可。本研究探讨了 ABA 对 intact guard cells 膜上 K(+)通道的反应。在暴露于 ABA 之前和期间记录膜电位，并且在整个过程中每隔一段时间测量全细胞电流，以量化 K(+)通道的稳态和时变特性。在 0.1、3 或 10 mM 细胞外 K(+)存在下添加 10 μM ABA 时，暴露的前 5 分钟内自由运行的膜电位（V m）负向移动-4-7 mV，此后没有一致的影响。然而，电压钳测量显示，在稳态下，K(+)通道电流增加到对照的 1.84-3.41 倍，平均半衰期为 1.1 ± 0.1 min。通过泄漏返回的电流也发生了类似的变化，并且解释了 V m 的最小响应。以 V m 计算，K(+)电流的翻译为 ABA 时 K(+)流出的平均 2.65 倍增加。未观察到 ABA 改变 K(+)电流的激活或失活。这些结果与 ABA 诱导的 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。这些数据否定了膜电压大幅波动是控制 guard-cell K(+)通量的前提的观点。相反，突出了膜对 K(+)通量的容量增加，这依赖于 K(+)通道和泄漏电流的协同调制，并且足够快，可以普遍解释 ABA 中 guard-cell K(+)流失和气孔关闭的开始。
