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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
Selective Regulation of ptsG Expression by Fis
FORMATION OF EITHER ACTIVATING OR REPRESSING NUCLEOPROTEIN
COMPLEX IN RESPONSE TO GLUCOSE*
Dongwoo
Shin §,
Namwook
Cho ¶,
Sunggi
Heu , and
Sangryeol
Ryu **
From the 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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Copyright © 2003 by the American Society for Biochemistry and Molecular Biology.
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