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Originally published In Press as doi:10.1074/jbc.M213248200 on February 14, 2003

J. Biol. Chem., Vol. 278, Issue 17, 14776-14781, April 25, 2003
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Selective Regulation of ptsG Expression by Fis
FORMATION OF EITHER ACTIVATING OR REPRESSING NUCLEOPROTEIN COMPLEX IN RESPONSE TO GLUCOSE*

Dongwoo ShinDagger §, Namwook ChoDagger , Sunggi Heu||, and Sangryeol RyuDagger **

From the Dagger  Department of Food Science and Technology, School of Agricultural Biotechnology and Center for Agricultural Biomaterials, Seoul National University, Suwon 441-744 and || Plant Pathology Division, National Institute of Agricultural Science and Technology, Suwon 441-707, Korea

Transcription of ptsG encoding glucose-specific permease, enzyme IICBGlc, in Escherichia coli is initiated from two promoters, P1 and P2. ptsG transcription is repressed by Mlc, a glucose-inducible regulator of carbohydrate metabolism. The regulation of ptsG P1 transcription is also under positive control by cyclic AMP receptor protein and cyclic AMP complex (CRP·cAMP) as observed in other Mlc regulon. We report here that Fis, one of the nucleoid-associated proteins, plays a key role in glucose induction of Mlc regulon. ptsG transcription was induced when wild-type cells were grown in the presence of glucose. However, in a fis mutant, the basal level of ptsG transcription was higher but decreased when cells were grown in the presence of glucose, which implies the possibility of regulatory interactions among Fis, Mlc, and CRP·cAMP. Footprinting experiments with various probes and transcription assays revealed that Fis assists both Mlc repression and CRP·cAMP activation of ptsG P1 through the formation of Fis·CRP·Mlc or Fis·CRP nucleoprotein complexes at ptsG P1 promoter depending on the availability of glucose in the growth medium. ptsG P2 transcription was inhibited by Fis and Mlc. Tighter Mlc repression and enhanced CRP·cAMP activation of ptsG P1 by Fis enable cells to regulate Mlc regulon efficiently by selectively controlling the concentration of enzyme IICBGlc that modulates Mlc activity.


* This work was supported in part by Korea Research Foundation Grant KRF-2001-015-DP0503.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Recipient of a grant for doctoral candidates provided by Korea Research Foundation (KRF-2001-908-GN0016).

Recipient of the graduate fellowship provided by the Ministry of Education through the Brain Korea 21 Project.

** To whom correspondence should be addressed. Tel.: 82-31-290-2584; Fax: 82-31-293-4789; E-mail: sangryu@snu.ac.kr.


Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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