Nitric Oxide Regulates K+and Cl-Channels in Guard Cells through a Subset of Abscisic Acid-Evoked Signaling Pathways

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 prerequisi...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2003-09, Vol.100 (19), p.11116-11121
Main Authors: Garcia-Mata, Carlos, Gay, Robert, Sokolovski, Sergei, Hills, Adrian, Lamattina, Lorenzo, Blatt, Michael R.
Format: Article
Language:English
Subjects:
Abscisic Acid - metabolism
Biological Sciences
Botany
Calcium
Calcium - metabolism
Cell membranes
Chloride Channels - physiology
Cyclic ADP-Ribose - antagonists & inhibitors
Electric potential
Fluorescence
Guanylate Cyclase - antagonists & inhibitors
Guard cells
Ion channels
Nitric oxide
Nitric Oxide - physiology
Oxides
Physiological regulation
Pipettes
Plant cells
Plasma
Potassium
Potassium Channels - physiology
Signal Transduction
Solutes
Vicia faba - cytology
Vicia faba - metabolism
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Summary: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$Ca^{2+}\!-\!insensitive\>K^+$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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1434381100