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Planta. 1990 Feb;180(3):445-55. doi: 10.1007/BF00198799.

Potassium channel currents in intact stomatal guard cells: rapid enhancement by abscisic acid.

Author information

1
Botany School, University of Cambridge, Downing Street, CB2 3EA, Cambridge, UK.

Abstract

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.

PMID:
24202027
DOI:
10.1007/BF00198799

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