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First published online November 20, 2002; 10.1105/tpc.007906

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The Plant Cell, Vol. 14, 3089-3099, December 2002, Copyright © 2002,
American Society of Plant Biologists

Arabidopsis OST1 Protein Kinase Mediates the Regulation of Stomatal Aperture by Abscisic Acid and Acts Upstream of Reactive Oxygen Species Production

Anna-Chiara Mustilli1,a, Sylvain Merlot2,a, Alain Vavasseurb, Francesca Fenzia and Jérôme Giraudata

a Institut des Sciences du Végétal, Centre National de la Recherche Scientifique, Unité Propre de Recherche 2355, 91190 Gif-sur-Yvette, France
b Commissariat à l'Energie Atomique, Direction des Sciences du Vivant, Laboratoire des Echanges Membranaires et Signalisation, F-13108 St. Paul lez Durance Cedex, France

1 To whom correspondence should be addressed. E-mail achmustilli{at}libero.it; fax 33-1-69823695

During drought, the plant hormone abscisic acid (ABA) triggers stomatal closure, thus reducing water loss. Using infrared thermography, we isolated two allelic Arabidopsis mutants (ost1-1 and ost1-2) impaired in the ability to limit their transpiration upon drought. These recessive ost1 mutations disrupted ABA induction of stomatal closure as well as ABA inhibition of light-induced stomatal opening. By contrast, the ost1 mutations did not affect stomatal regulation by light or CO2, suggesting that OST1 is involved specifically in ABA signaling. The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue. In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK). Reactive oxygen species (ROS) were shown recently to be an essential intermediate in guard cell ABA signaling. ABA-induced ROS production was disrupted in ost1 guard cells, whereas applied H2O2 or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production. The relative positions of ost1 and the other ABA-insensitive mutations in the ABA signaling network (abi1-1, abi2-1, and gca2) are discussed.




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