Nitrogen Induction of Sugar Catabolic Gene Expression in Synechocystis sp. PCC 6803
Author(s) -
Takashi Osanai,
S. Imamura,
Munehiko Asayama,
Makoto Shirai,
Iwane Suzuki,
Norio Murata,
Kan Tanaka
Publication year - 2006
Publication title -
dna research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 98
eISSN - 1756-1663
pISSN - 1340-2838
DOI - 10.1093/dnares/dsl010
Subject(s) - pentose phosphate pathway , catabolism , regulon , biology , dehydrogenase , biochemistry , transcriptome , sugar , synechocystis , mutant , sigma factor , gene , glycolysis , metabolic pathway , microbiology and biotechnology , enzyme , gene expression , promoter
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.
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