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Letters to Nature

Nature 406, 731-734 (17 August 2000) | doi:10.1038/35021067; Received 14 February 2000; Accepted 18 May 2000

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

Zhen-Ming Pei1,4, Yoshiyuki Murata1,4, Gregor Benning3, Sébastien Thomine1, Birgit Klüsener1, Gethyn J. Allen1, Erwin Grill3 & Julian I. Schroeder1

  1. Division of Biology, Cell and Developmental Biology, and Center for Molecular Genetics, University of California at San Diego, La Jolla, California 92093-0116, USA
  2. Technische Universität München, Lehrstuhl für Botanik, D-85350 Freising–Weihenstephan , Germany
  3. These authors contributed equally to this work

Correspondence to: Julian I. Schroeder1 Correspondence and requests for materials should be addressed to J.I.S. (e-mail: Email: julian@biomail.ucsd.edu).

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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 Ca 2+ 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 [Ca 2+]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 H2O 2-activated Ca2+ channels are important mechanisms for ABA-induced stomatal closing.