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JXB Advance Access published online on July 30, 2004

Journal of Experimental Botany, doi:10.1093/jxb/erh202
© 2004 by Oxford University Press
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Received March 4, 2004
Accepted May 17, 2004

Sulphur Metabolism Special Issue Article

Regulation of calcium signalling and gene expression by glutathione

L. D. Gomez 1, G. Noctor 2, M. R. Knight 3, C. H. Foyer 4*

1 Crop Performance and Improvement Division, Rothamsted Research, Harpenden, Herts AL5 2JQ, UK; Present address: Centre for Novel Agricultural Products, Department of Biology, University of York, PO Box 373, York YO10 5 YW, UK
2 Institut de Biotechnologie des Plantes, Bâtiment 630, Université Paris XI, F-91405 Orsay cedex, France
3 Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RB, UK
4 Crop Performance and Improvement Division, Rothamsted Research, Harpenden, Herts AL5 2JQ, UK

* To whom correspondence should be addressed. E-mail: christine.foyer{at}bbsrc.ac.uk.


   Abstract

The glutathione redox couple is an information-rich redox buffer that interacts with numerous cellular components. To explore the role of glutathione in redox signalling, leaf contents were increased either chemically, by feeding reduced glutathione (GSH), or genetically, by over-expressing the first enzyme of the GSH biosynthetic pathway, {gamma}-glutamylcysteine synthetase ({gamma}-ECS). Leaf discs were also fed glutathione disulphide (GSSG), leading to increases in both GSH and GSSG. The effects of increases in GSH were compared with non-specific changes in leaf thiol status induced by feeding dithiothreitol (DTT) or the monothiol {beta}-mercaptoethanol ({beta}-ME). Photosynthesis measurements showed that none of the feeding treatments greatly disrupted leaf physiology. Transgenic plants expressing aequorin were used to analyse calcium signatures during the feeding treatments. Calcium release occurred soon after the onset of GSH or GSSG feeding, but was unaffected by DTT or {beta}-ME. Pathogenesis-related protein 1 (PR-1) was induced both in the {gamma}-ECS overexpressors and by feeding GSH, but not GSSG. Feeding DTT also induced PR-1. Key transcripts encoding antioxidative enzymes were much less affected, although glutathione synthetase was suppressed by feeding thiols or GSSG. It is concluded that modulation of glutathione contents transmits information through diverse signalling mechanisms, including (i) the establishment of an appropriate redox potential for thiol/disulphide exchange and (ii) the release of calcium to the cytosol.

Keywords: Calcium signalling; cytosol; dithiothreitol; gene expression; glutathione; {beta}-mercaptoethanol; regulation.
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