Calcium-dependent ABA induction of stomatal closure


Calcium elevation-dependent and attenuated resting calcium-dependent abscisic acid induction of stomatal closure and abscisic acid-induced enhancement of calcium sensitivities of S-type anion and inward-rectifying K channels in Arabidopsis guard cells.

by Siegel R. S., Xue S., Murata Y., Yang Y., Nishimura N., Wang A., Schroeder J. I. (2009)

Robert S. Siegel,1,* Shaowu Xue,1 Yoshiyuki Murata,1,2 Yingzhen Yang,1 Noriyuki Nishimura,1 Angela Wang,1and Julian I. Schroeder1

1 Division of Biological Sciences, Cell and Developmental Biology Section, and Center for Molecular Genetics, University of California, San Diego, 9500 Gilman Drive 0116 La Jolla, California 92093-0116, USA
2 Department of Agriculture, Okayama University, Tsushima, Okayama 700-8530, JAPAN



in Plant J. 59, 207–220. – doi: 10.1111/j.1365-313X.2009.03872.x –

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text – [PMC free article] [PubMed] –


Stomatal closure in response to abscisic acid depends on mechanisms that are mediated by intracellular [Ca2+] ([Ca2+]i), and also on mechanisms independent of [Ca2+]i in guard cells.

In this study we address three important questions in reference to these two predicted pathways in Arabidopsis thaliana.

1. How large is the relative abscisic acid (ABA)-induced stomatal closing response from a [Ca2+]i-elevation-independent pathway?

2. How do ABA-insensitive mutants affect a [Ca2+]i-elevation-independent pathway?

3. Does ABA enhance (prime) the Ca2+-sensitivity of anion and inward-rectifying K+ channel regulation?

We monitored stomatal responses to ABA while experimentally inhibiting [Ca2+]i elevations and clamping [Ca2+]i to resting levels. The absence of [Ca2+]i-elevations was confirmed in ratiometric [Ca2+]i imaging experiments.

ABA-induced stomatal closing in the absence of [Ca2+]i-elevations above the physiological resting [Ca2+]i showed only ≈30% of the stomatal closure response and was greatly slowed compared to the presence of [Ca2+]i-elevations.

The ABA-insensitive mutants ost1-2, abi2-1, gca2 showed partial stomatal closing responses that correlate with [Ca2+]i-dependent ABA signaling. Interestingly, patch clamp experiments show that exposure of guard cells to ABA greatly enhances the ability of cytosolic Ca2+to both activate S-type anion channels and down-regulate inward K+ channels, providing strong evidence for the Ca2+ sensitivity priming hypothesis.

The present study shows and quantifies an attenuated and slowed ABA response, while directly inhibiting [Ca2+]i-elevations in guard cells. A minimal model is discussed, in which ABA increases (primes) the [Ca2+]i sensitivity of stomatal closing mechanisms.


Published by

Willem Van Cotthem

Honorary Professor of Botany, University of Ghent (Belgium). Scientific Consultant for Desertification and Sustainable Development.

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