This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 135/3/1685    most recent pp.104.041921v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Web of Science (17) Citing Articles via Google Scholar Google Scholar Articles by Avsian-Kretchmer, O. Articles by Ben-Hayyim, G. Search for Related Content PubMed PubMed Citation Articles by Avsian-Kretchmer, O. Articles by Ben-Hayyim, G. Agricola Articles by Avsian-Kretchmer, O. Articles by Ben-Hayyim, G. Related Collections Reactive Oxygen Species

ENVIRONMENTAL STRESS AND ADAPTATION

The Salt-Stress Signal Transduction Pathway That Activates the gpx1 Promoter Is Mediated by Intracellular H₂O₂, Different from the Pathway Induced by Extracellular H₂O₂^[w]

Department of Fruit-Tree Breeding and Molecular Genetics, ARO, The Volcani Center, Bet Dagan 50250, Israel (O.A.-K., Y.G.-D., R.G., G.B.-H.); and Department of Biology, Faculty of Science and Science Education, University of Haifa-Oranim, Tivon 36006, Israel (S.L.-Y.)

Several genes encoding putative glutathione peroxidase have been isolated from a variety of plants, all of which show the highest homology to the phospholipid hydroperoxide isoform. Several observations suggest that the proteins are involved in biotic and abiotic stress responses. Previous studies on the regulation of gpx1, the Citrus sinensis gene encoding phospholipid hydroperoxide isoform, led to the conclusion that salt-induced expression of gpx1 transcript and its encoded protein is mediated by oxidative stress. In this paper, we describe the induction of gpx1 promoter:uidA fusions in stable transformants of tobacco (Nicotiana tabacum) cultured cells and plants. We show that the induction of gpx1 by salt and oxidative stress occurs at the transcriptional level. gpx1 promoter analysis confirmed our previous assumption that the salt signal is transduced via oxidative stress. We used induction of the fusion construct to achieve better insight into, and to monitor salt-induced oxidative stress. The gpx1 promoter responded preferentially to oxidative stress in the form of hydrogen peroxide, rather than to superoxide-generating agents. Antioxidants abolished the salt-induced expression of gpx1 promoter, but were unable to eliminate the induction by H₂O₂. The commonly employed NADPH-oxidase inhibitor diphenyleneiodonium chloride and catalase inhibited the H₂O₂-induced expression of gpx1 promoter, but did not affect its induction by salt. Our results led us to conclude that salt induces oxidative stress in the form of H₂O₂, its production occurs in the intracellular space, and its signal transduction pathway activating the gpx1 promoter is different from the pathway induced by extracellular H₂O₂.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.041921.

^* Corresponding author; e-mail vhgozal{at}agri.gov.il; fax 972–3–9669583.

Received March 2, 2004; returned for revision April 20, 2004; accepted May 2, 2004.

This article has been cited by other articles:

				T. Xue, X. Li, W. Zhu, C. Wu, G. Yang, and C. Zheng Cotton metallothionein GhMT3a, a reactive oxygen species scavenger, increased tolerance against abiotic stress in transgenic tobacco and yeast J. Exp. Bot., January 1, 2009; 60(1): 339 - 349. [Abstract] [Full Text] [PDF]

				X. Hu, A. Zhang, J. Zhang, and M. Jiang Abscisic Acid is a Key Inducer of Hydrogen Peroxide Production in Leaves of Maize Plants Exposed to Water Stress Plant Cell Physiol., November 1, 2006; 47(11): 1484 - 1495. [Abstract] [Full Text] [PDF]

				M. Baier and K.-J. Dietz Chloroplasts as source and target of cellular redox regulation: a discussion on chloroplast redox signals in the context of plant physiology J. Exp. Bot., June 1, 2005; 56(416): 1449 - 1462. [Abstract] [Full Text] [PDF]