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J. Biol. Chem., Vol. 279, Issue 51, 53078-53086, December 17, 2004
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From the aDivision of Cellular Regulation, National Institute for Basic Biology, Okazaki 444-8585, Japan, the bNational Center for Genetic Engineering and Biotechnology, Bangkok 12120, Thailand, the cInstitute of Plant Physiology, Russian Academy of Sciences, Moscow 127276, Russia, the dSatellite Venture Business Laboratory, Ehime University, Matsuyama 790-8577, Japan, the eDepartment of Plant Gene Research, Kazusa DNA Research Institute, Kisarazu, Chiba 292-0818, Japan, the fDepartment of Genetics, Moscow State University, Moscow 119899, Russia, and the gDepartment of Molecular Biomechanics, The Graduate University for Advanced Studies, Okazaki 444-8585, Japan
Microorganisms respond to hyperosmotic stress via changes in the levels of expression of large numbers of genes. Such responses are essential for acclimation to a new osmotic environment. To identify factors involved in the perception and transduction of signals caused by hyperosmotic stress, we examined the response of Synechocystis sp. PCC 6803, which has proven to be a particularly useful microorganism in similar analyses. We screened knockout libraries of histidine kinases (Hiks) and response regulators (Rres) in Synechocystis by DNA microarray and slot-blot hybridization analyses, and we identified several two-component systems, which we designated Hik-Rre systems, namely, Hik33-Rre31, Hik34-Rre1, and Hik10-Rre3, as well as Hik16-Hik41-Rre17, as the transducers of hyperosmotic stress. We also identified Hik2-Rre1 as a putative additional two-component system. Each individual two-component system regulated the transcription of a specific group of genes that were responsive to hyperosmotic stress.
Received for publication, September 3, 2004 , and in revised form, October 7, 2004.
* This work was supported, in part by Grants-in-aid for Scientific Research no. 14086207 (to N. M.) and no. 16013249 (to I. S.) from the Ministry of Education, Science, Sports, and Culture of Japan; and no. 13854002 (to N. M. and I. S.) from the Japan Society for Promotion of Science) and by Grants no. 04-04-48200 (to V. V. Z.) and no. 03-04-48581 (to D. A. L.) from the Russian Foundation for Basic Research. This work was also supported by the Program for Cooperative Research on Stress Tolerance of Plants of the National Institute for Basic Biology, Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
h To whom correspondence should be addressed. Tel.: 81-564-55-7600; Fax: 81-564-54-4866; E-mail: murata{at}nibb.ac.jp.
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