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J. Biol. Chem., Vol. 282, Issue 3, 1916-1924, January 19, 2007

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The ATP Binding Cassette Transporter AtMRP5 Modulates Anion and Calcium Channel Activities in Arabidopsis Guard Cells^*

Su Jeoung Suh¹², Yong-Fei Wang¹, Annie Frelet¹, Nathalie Leonhardt¹³, Markus Klein, Cyrille Forestier^¶, Bernd Mueller-Roeber^||, Myeon H. Cho^**, Enrico Martinoia⁴, and Julian I. Schroeder⁵

From the Institut für Pflanzenbiologie, University Zurich, Zollikerstrasse 107, 8008 Zurich, Switzerland, the Divison of Biological Sciences, Cell & Developmental Biology Section, University of California San Diego, La Jolla, California 92093-0116, the ^¶CEA Cadarache, UMR 163 CEA-CNRS, Départment d'Ecophysiologie Végétale et de Microbiologie (DEVM)-Laboratoire des Echanges Membrangire et Signalisation (LEMS), BP 1, F-13108 St. Paul Lez Durance, France, the ^||University of Potsdam, Karl-Liebknecht-Strasse 24-25, 14476 Potsdam-Golm, Germany, and the ^**Department of Biology, Yonsei University, Seoul, 120749 South Korea

Stomatal guard cells control CO₂ uptake and water loss between plants and the atmosphere. Stomatal closure in response to the drought stress hormone, abscisic acid (ABA), results from anion and K⁺ release from guard cells. Previous studies have shown that cytosolic Ca²⁺ elevation and ABA activate S-type anion channels in the plasma membrane of guard cells, leading to stomatal closure. However, membrane-bound regulators of abscisic acid signaling and guard cell anion channels remain unknown. Here we show that the ATP binding cassette (ABC) protein AtMRP5 is localized to the plasma membrane. Mutation in the AtMRP5 ABC protein impairs abscisic acid and cytosolic Ca²⁺ activation of slow (S-type) anion channels in the plasma membrane of guard cells. Interestingly, atmrp5 insertion mutant guard cells also show impairment in abscisic acid activation of Ca²⁺-permeable channel currents in the plasma membrane of guard cells. These data provide evidence that the AtMRP5 ABC transporter is a central regulator of guard cell ion channel during abscisic acid and Ca²⁺ signal transduction in guard cells.

Received for publication, August 18, 2006 , and in revised form, November 1, 2006.

^* This work was supported by National Institutes of Health Grant R01GM060396 and National Science Foundation Grant MCB0417118 (to J. I. S.), by the Swiss National Foundation (Grant 3100A0-103911 to E. M.), and partly by Grant R01-2006-000-11026-0 from KOSEF (to M. H. C.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2.

¹ These authors contributed equally to this work.

² Present address: Dept. of Biological Sciences, Seoul National University, Seoul 151-747, Korea.

³ Present address: CEA Cadarache, UMR 163 CEA-CNRS, DEVM-LEMS, BP 1, F-13108 St. Paul Lez Durance, France.

⁴ To whom correspondence may be addressed. Tel.: 41-1-634-8222; Fax: 41-44-634-8204; E-mail: enrico.martinoia{at}botinst.unizh.ch. ⁵ To whom correspondence may be addressed. Tel.: 858-534-7759; Fax: 858-534-7108; E-mail: julian{at}biomail.ucsd.edu.

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