Nitric oxide regulates K+ and Cl- channels in guard cells through a subset of abscisic acid-evoked signaling pathways

Carlos Garcia-Mata, Robert Gay, Sergei Sokolovski, Adrian Hills, Lorenzo Lamattina, Michael R. Blatt*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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 Ca 2+-signaling pathways engaged by ABA and define the boundaries of parallel signaling events in the control of guard cell movements.

Original languageEnglish
Pages (from-to)11116-11121
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number19
Publication statusPublished - 16 Sept 2003

Bibliographical note

Funding: This work was supported by Biotechnology and Biological Sciences Research Council Grants P09640, C10234, and P09561 to M.R.B., Agencia Nacional de Promoción de Ciencia y Tecnología, and a Foundation Antorchas travel grant to L.L. and C.G.-M.


  • cGMP-mediated signaling
  • Cyclic ADP ribose
  • Cytosolic-free [Ca] elevation
  • Stress physiology
  • Vicia


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