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Vol. 15, No. 14, pp. 1808-1816, July 15, 2001

RESEARCH PAPER
Inactivation of AtRac1 by abscisic acid is essential for stomatal closure

Emmanuel Lemichez,1 Yan Wu,1 Juan-Pablo Sanchez,1 Amel Mettouchi,2 Jaideep Mathur,3 and Nam-Hai Chua1,4

1 Laboratory of Plant Molecular Biology, Rockefeller University, New York, New York 10021-6399, USA; 2 Cellular Biochemistry and Biophysics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA; 3 Laboratory of Plant Cell Biology, Institute of Molecular Agrobiology, National University of Singapore, Kent Ridge 117604, Singapore

Plant water homeostasis is maintained by the phytohormone abscisic acid (ABA), which triggers stomatal pore closure in response to drought stress. We identified the Arabidopsis small guanosine triphosphatase (GTPase) protein AtRac1 as a central component in the ABA-mediated stomatal closure process. ABA treatment induced inactivation of AtRac GTPases and disruption of the guard cell actin cytoskeleton. In contrast, in the ABA-insensitive mutant abi1-1, which is impaired in stomatal closure, neither AtRac inactivation nor actin cytoskeleton disruption was observed on ABA treatment. These observations indicate that AtRac1 inactivation is a limiting step in the ABA-signaling cascade leading to stomatal closure. Consistent with these findings, expression of a dominant-positive mutant of AtRac1 blocked the ABA-mediated effects on actin cytoskeleton and stomatal closure in wild-type plants, whereas expression of a dominant-negative AtRac1 mutant recapitulated the ABA effects in the absence of the hormone. Moreover, the dominant-negative form of AtRac1 could also restore stomatal closure in abi1-1. These results define AtRac1 as a central element for plant adaptation to drought.

[Key Words: Abscisic acid; guard cell; actin; Rac; PP2C; turgor pressure]


4 Corresponding author.


GENES & DEVELOPMENT 15:1808-1816 © 2001 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/01 $5.00

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