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First published online August 19, 2005; 10.1104/pp.105.065698

Plant Physiology 139:267-274 (2005)
© 2005 American Society of Plant Biologists

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ENVIRONMENTAL STRESS AND ADAPTATION

Enhancing Arabidopsis Salt and Drought Stress Tolerance by Chemical Priming for Its Abscisic Acid Responses1

Gabor Jakab2,*, Jurriaan Ton2,3, Victor Flors, Laurent Zimmerli, Jean-Pierre Métraux and Brigitte Mauch-Mani

Institute of Botany, Biochemistry, University of Neuchâtel, CH–2007 Neuchatel, Switzerland (G.J., J.T., V.F., L.Z., B.M.-M.); Department of Biology, Plant Biology, University of Fribourg, CH–1700 Fribourg, Switzerland (G.J., J.-P.M.); and Departamento de Ciencias Experimentales, Área de Fisiología Vegetal, Universitat Jaume I, 12071 Castellon, Spain (V.F.)

Drought and salt stress tolerance of Arabidopsis (Arabidopsis thaliana) plants increased following treatment with the nonprotein amino acid {beta}-aminobutyric acid (BABA), known as an inducer of resistance against infection of plants by numerous pathogens. BABA-pretreated plants showed earlier and higher expression of the salicylic acid-dependent PR-1 and PR-5 and the abscisic acid (ABA)-dependent RAB-18 and RD-29A genes following salt and drought stress. However, non-expressor of pathogenesis-related genes 1 and constitutive expressor of pathogenesis-related genes 1 mutants as well as transgenic NahG plants, all affected in the salicylic acid signal transduction pathway, still showed increased salt and drought tolerance after BABA treatment. On the contrary, the ABA deficient 1 and ABA insensitive 4 mutants, both impaired in the ABA-signaling pathway, could not be protected by BABA application. Our data demonstrate that BABA-induced water stress tolerance is based on enhanced ABA accumulation resulting in accelerated stress gene expression and stomatal closure. Here, we show a possibility to increase plant tolerance for these abiotic stresses through effective priming of the preexisting defense pathways without resorting to genetic alterations.


1 This work was supported by the National Center of Competence in Research on Plant Survival in Natural and Agricultural Ecosystems (grant to B.M.-M.), the Swiss National Science Foundation (grant nos. 3100–064024 to B.M.-M. and 3100A0–104224/1 to J.-P.M.), and the Agència Valenciana de Ciència i Tecnologia, Generalitat Valenciana, Spain (grant to V.F.).

2 These authors contributed equally to the paper.

3 Present address: Section of Phytopathology, Faculty of Biology, Utrecht University, 3584 CA Utrecht, The Netherlands.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.065698.

* Corresponding author; e-mail gabor.jakab{at}unine.ch; fax 41–32–718–2201.

Received May 17, 2005; returned for revision June 17, 2005; accepted June 17, 2005.




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