Calcium channels activated by hydrogen peroxide mediate abscisic acid signalling in guard cells

Zhen-Ming Pei, Yoshiyuki Murata, Gregor Benning, Sébastien Thomine, Birgit Klüsener, Gethyn J. Allen, Erwin Grill and Julian I. Schroeder ()
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Zhen-Ming Pei: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego
Yoshiyuki Murata: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego
Gregor Benning: Technische Universität München, Lehrstuhl für Botanik
Sébastien Thomine: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego
Birgit Klüsener: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego
Gethyn J. Allen: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego
Erwin Grill: Technische Universität München, Lehrstuhl für Botanik
Julian I. Schroeder: Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego

Nature, 2000, vol. 406, issue 6797, 731-734

Abstract: Abstract Drought is a major threat to agricultural production. Plants synthesize the hormone abscisic acid (ABA) in response to drought, triggering a signalling cascade in guard cells that results in stomatal closure, thus reducing water loss1. ABA triggers an increase in cytosolic calcium in guard cells ([Ca2+]cyt)2,3,4,5,6 that has been proposed to include Ca2+ influx across the plasma membrane3,5,7,8,9. However, direct recordings of Ca2+ currents have been limited3 and the upstream activation mechanisms of plasma membrane Ca2+ channels remain unknown. Here we report activation of Ca2+-permeable channels in the plasma membrane of Arabidopsis guard cells by hydrogen peroxide. The H2O2-activated Ca2+ channels mediate both influx of Ca2+ in protoplasts and increases in [Ca2+]cyt in intact guard cells. ABA induces the production of H2O2 in guard cells. If H2O2 production is blocked, ABA-induced closure of stomata is inhibited. Moreover, activation of Ca2+ channels by H2O2 and ABA- and H2O2-induced stomatal closing are disrupted in the recessive ABA-insensitive mutant gca2. These data indicate that ABA-induced H2O2 production and the H2O2-activated Ca2+ channels are important mechanisms for ABA-induced stomatal closing.

Date: 2000
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DOI: 10.1038/35021067

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