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First published online December 18, 2003; 10.1104/pp.103.031674

Plant Physiology 134:81-91 (2004)
© 2004 American Society of Plant Biologists

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CELL BIOLOGY AND SIGNAL TRANSDUCTION

Characterization of Mutants in Arabidopsis Showing Increased Sugar-Specific Gene Expression, Growth, and Developmental Responses1

Margarete Baier2,3, Georg Hemmann3, Rachel Holman, Fiona Corke, Rod Card, Caroline Smith, Fred Rook and Michael W. Bevan*

Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, United Kingdom

Sugars such as sucrose serve dual functions as transported carbohydrates in vascular plants and as signal molecules that regulate gene expression and plant development. Sugar-mediated signals indicate carbohydrate availability and regulate metabolism by co-coordinating sugar production and mobilization with sugar usage and storage. Analysis of mutants with altered responses to sucrose and glucose has shown that signaling pathways mediated by sugars and abscisic acid interact to regulate seedling development and gene expression. Using a novel screen for sugar-response mutants based on the activity of a luciferase reporter gene under the control of the sugar-inducible promoter of the ApL3 gene, we have isolated high sugar-response (hsr) mutants that exhibit elevated luciferase activity and ApL3 expression in response to low sugar concentrations. Our characterization of these hsr mutants suggests that they affect the regulation of sugar-induced and sugar-repressed processes controlling gene expression, growth, and development in Arabidopsis. In contrast to some other sugar-response mutants, they do not exhibit altered responses to ethylene or abscisic acid, suggesting that the hsr mutants may have a specifically increased sensitivity to sugars. Further characterization of the hsr mutants will lead to greater understanding of regulatory pathways involved in metabolite signaling.


Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.103.031674.

1 This work was supported by Syngenta (grant no. PMC19), by the Deutsche Forschungsgemeinschaft (grant no. Ba2011/1–1), and by the Biotechnology and Biological Sciences Research Council (core strategic grant to the John Innes Centre).

2 Present address: Biochemistry and Physiology of Plants, University of Bielefeld, Universitätsstrasse 25, 33615 Bielefeld, Germany.

3 These authors contributed equally to this work.

* Corresponding author; e-mail michael.bevan{at}bbsrc.ac.uk; fax 01603–450025.

Received August 11, 2003; returned for revision September 16, 2003; accepted October 17, 2003.




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