DNA Research Advance Access originally published online on October 17, 2006
DNA Research 2006 13(5):185-195; doi:10.1093/dnares/dsl010
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Nitrogen Induction of Sugar Catabolic Gene Expression in Synechocystis sp. PCC 6803
1 Institute of Molecular and Cellular Biosciences, The University of Tokyo 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan
2 Laboratory of Molecular Genetics, College of Agriculture, Ibaraki University, Ami Inashiki, Ibaraki 300-0393, Japan
3 Department for Regulation Biology, National Institute for Basic Biology Myodaiji, Okazaki 444-8585, Japan
Nitrogen starvation requires cells to change their transcriptome in order to cope with this essential nutrient limitation. Here, using microarray analysis, we investigated changes in transcript profiles following nitrogen depletion in the unicellular cyanobacterium Synechocystis sp. PCC 6803. Results revealed that genes for sugar catabolic pathways including glycolysis, oxidative pentose phosphate (OPP) pathway, and glycogen catabolism were induced by nitrogen depletion, and activities of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD), two key enzymes of the OPP pathway, were demonstrated to increase under this condition. We recently showed that a group 2 sigma factor SigE, which is under the control of the global nitrogen regulator NtcA, positively regulated these sugar catabolic pathways. However, increases of transcript levels of these sugar catabolic genes under nitrogen starvation were still observed even in a sigE-deficient mutant, indicating the involvement of other regulatory element(s) in addition to SigE. Since these nitrogen activations were abolished in an ntcA mutant, and since these genes were not directly included in the NtcA regulon, we suggested that sugar catabolic genes were induced by nitrogen depletion under complex and redundant regulations including SigE and other unknown factor(s) under the control of NtcA.
Key words: cyanobacteria; sugar catabolism; NtcA; SigE; nitrogen starvation
*To whom correspondence should be addressed. Tel. +81-3-5841-7825, Fax. +81-3-5841-8476, E-mail: kntanaka{at}iam.u-tokyo.ac.jp
Communicated by Satoshi Tabata
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