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First published online December 4, 2003; 10.1104/pp.103.033480 Plant Physiology 134:275-285 (2004) © 2004 American Society of Plant Biologists A Methyl Viologen-Resistant Mutant of Arabidopsis, Which Is Allelic to Ozone-Sensitive rcd1, Is Tolerant to Supplemental Ultraviolet-B Irradiation1Division of Biological Sciences, Graduate School of Environmental Earth Science, Hokkaido University, Sapporo, 060-0810 Japan (T.F., K.T.Y.); Environmental Biology Division, National Institute for Environmental Studies, Tsukuba, 305-0053 Japan (H.S.); Low Temperature Institute, Hokkaido University, Sapporo, 060-0819 Japan (K.A.); Kihara Institute for Biological Research, Graduate School of Integrated Science, Yokohama City University, 641-12 Maioka-cho, Totsuka-ku, Yokohama, 244-0813 Japan (N.Y.); and Department of Bioscience and Technology, School of Engineering, Hokkaido Tokai University, Sapporo, 005-8601 Japan (Y.T.)
To better understand the role of active oxygen species (AOS) in acquired resistance to increased levels of ultraviolet (UV)-B irradiation in plants, we isolated an Arabidopsis mutant that is resistant to methyl viologen, and its sensitivity to UV-B was investigated. A complementation test revealed that the obtained mutant was allelic to the ozone-sensitive radical-induced cell death1-1 (rcd1-1). Therefore, this mutant was named rcd1-2. rcd1-2 was recessive and nearly 4-fold more resistant to methyl viologen than wild type. It exhibited a higher tolerance to short-term UV-B supplementation treatments than the wild type: UV-B-induced formation of cyclobutane pyrimidine dimers was reduced by one-half after 24 h of exposure; the decrease in quantum yield of photosystem II was also diminished by 40% after 12 h of treatment. Furthermore, rcd1-2 was tolerant to freezing. Steady-state mRNA levels of plastidic Cu/Zn superoxide dismutase and stromal ascorbate peroxidase were higher in rcd1-2 than in wild type, and the mRNA level of the latter enzyme was enhanced by UV-B exposure more effectively in rcd1-2. UV-B-absorbing compounds were more accumulated in rcd1-2 than in wild type after UV-B exposure for 24 h. These findings suggest that rcd1-2 methyl viologen resistance is due to the enhanced activities of the AOS-scavenging enzymes in chloroplasts and that the acquired tolerance to the short-term UV-B exposure results from a higher accumulation of sunscreen pigments. rcd1 appears to be a mutant that constitutively shows stress responses, leading to accumulation of more pigments and AOS-scavenging enzymes without any stresses.
1 This work was supported in part by Grants-in-Aid and the Special Coordination Fund from the Ministry of Education, Culture, Sports, Science and Technology (to K.T.Y. and H.S., respectively) and by the Research for the Future Program of the Japan Society for the Promotion of Science (to K.A., Y.T., and K.T.Y.). 2 Present address: Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, 060-0810 Japan. 3 Present address: Laboratory of Plant Science, Department of Biological Sciences, Graduate School of Science, University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113-0033 Japan. Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.103.033480. * Corresponding author; e-mail kty{at}sci.hokudai.ac.jp; fax 81-11-706-2739. Received September 16, 2003; returned for revision October 10, 2003; accepted October 20, 2003. This article has been cited by other articles:
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