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J. Biol. Chem., Vol. 280, Issue 35, 30653-30659, September 2, 2005

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Positive Regulation of Sugar Catabolic Pathways in the Cyanobacterium Synechocystis sp. PCC 6803 by the Group 2 Factor SigE^*

Takashi Osanai, Yu Kanesaki¶, Takayuki Nakano, Hiroyuki Takahashi, Munehiko Asayama**, Makoto Shirai**, Minoru Kanehisa, Iwane Suzuki¶, Norio Murata¶, and Kan Tanaka||

From the Institute of Molecular and Cellular Biosciences, the University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, ^**College of Agriculture, Ibaraki University, Ami, Inashiki, Ibaraki 300-0393, Institute for Chemical Research, Kyoto University, Uji 611-0011, and the ^¶Department of Regulation Biology, National Institute for Basic Biology, Myodaiji, Okazaki 444-8585, Japan

The sigE gene of Synechocystis sp. PCC 6803 encodes a group 2 factor for RNA polymerase and has been proposed to function in transcriptional regulation of nitrogen metabolism. By using microarray and Northern analyses, we demonstrated that the abundance of transcripts derived from genes important for glycolysis, the oxidative pentose phosphate pathway, and glycogen catabolism is reduced in a sigE mutant of Synechocystis maintained under the normal growth condition. Furthermore, the activities of the two key enzymes of the oxidative pentose phosphate pathway, glucose-6-phosphate dehydrogenase and 6-phophogluconate dehydrogenase, encoded by the zwf and gnd genes were also reduced in the sigE mutant. The dark enhancements in both enzyme activity and transcript abundance apparent in the wild type were eliminated by the mutation. In addition, the sigE mutant showed a reduced rate of glucose uptake and an increased intracellular level of glycogen. Moreover, it was unable to proliferate under the light-activated heterotrophic growth conditions. These results indicate that SigE functions in the transcriptional activation of sugar catabolic pathways in Synechocystis sp. PCC 6803.

Received for publication, May 9, 2005 , and in revised form, June 1, 2005.

^* This work was supported in part by Grants-in-aid for Scientific Research on Priority Areas "Genome Biology" 13206011 and for Creative Scientific Research 16GS0304 from the Ministry of Education, Culture, Sports, Science, and Technology of 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.

The on-line version of this article (available at http://www.jbc.org) contains Tables SI and SII.

^|| To whom correspondence should be addressed: Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan. Tel.: 81-3-5841-7825; Fax: 81-3-5841-8476; E-mail: kntanaka{at}iam.u-tokyo.ac.jp.

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