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First published online October 2, 2003; 10.1104/pp.103.025916 Plant Physiology 133:1148-1157 (2003) © 2003 American Society of Plant Biologists Seed 1-Cysteine Peroxiredoxin Antioxidants Are Not Involved in Dormancy, But Contribute to Inhibition of Germination during Stress1Division of Cell and Molecular Biology, Department of Biology, University of Oslo, P.O. Box 1031 Blindern, N–0315 Oslo, Norway
Peroxiredoxins (Prx) are thiol-dependent antioxidants containing one (1-cysteine [-Cys]) or two (2-Cys) conserved Cys residues that protect lipids, enzymes, and DNA against reactive oxygen species. In plants, the 1-Cys Prxs are highly expressed during late seed development, and the expression pattern is dormancy related in mature seeds. We have expressed the Arabidopsis 1-Cys Prx AtPER1 in Escherichia coli and show that this protein has antioxidant activity in vitro and protects E. coli in vivo against the toxic oxidant cumene hydroperoxide. Although some 1-Cys Prxs are targeted to the nucleus, a green fluorescent protein-AtPER1 fusion protein was also localized to the cytoplasm in an onion epidermis subcellular localization assay. It has been proposed that seed Prxs are involved in maintenance of dormancy and/or protect the embryo and aleurone layer surviving desiccation against damage caused by reactive oxygen species. These hypotheses were tested using transgenic Arabidopsis lines overexpressing the barley (Hordeum vulgare) 1-Cys PER1 protein and lines with reduced levels of AtPER1 due to antisensing or RNA interference. We found no correlation between Prx levels and the duration of the after-ripening period required before germination. Thus, Prxs are unlikely to contribute to maintenance of dormancy. RNA interference lines almost devoid of AtPER1 protein developed and germinated normally under standard growth room conditions. However, seeds from lines overexpressing PER1 were less inclined to germinate than wild-type seeds in the presence of NaCl, mannitol, and methyl viologen, suggesting that Prx can sense harsh environmental surroundings and play a part in the inhibition of germination under unfavorable conditions.
Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.103.025916. 1 This work was supported by the University of Oslo (grant to C.H.) and by the Research Council of Norway (project no. 140429/130). 2 Present address: Department of Tumor Biology, Institute for Cancer Research, The Norwegian Radiumhospital, Montebello, N–0310 Oslo, Norway. 3 Present address: Department of Genetics, The Norwegian Radiumhospital, Montebello, N–0310 Oslo, Norway. 4 Present address: Department of Molecular Biology, Institute of Medical Microbiology, University of Oslo, National Hospital, N–0027 Oslo, Norway. * Corresponding author; e-mail reidunn.aalen{at}bio.uio.no; fax 47–22854605. Received April 23, 2003; returned for revision June 2, 2003; accepted July 29, 2003. This article has been cited by other articles:
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