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Originally published In Press as doi:10.1074/jbc.M010501200 on December 19, 2000
J. Biol. Chem., Vol. 276, Issue 12, 9478-9485, March 23, 2001
A 72-Base Pair AT-rich DNA Sequence Element Functions as a
Bacterial Gene Silencer*
Chien-Chung
Chen,
Ming
Fang,
Arundhati
Majumder, and
Hai-Young
Wu
From the Department of Pharmacology, School of Medicine, Wayne
State University, Detroit, Michigan 48201
We have previously demonstrated that sequential
activation of the bacterial ilvIH-leuO-leuABCD gene
cluster involves a promoter-relay mechanism. In the current study, we
show that the final activation of the leuABCD operon is
through a transcriptional derepression mechanism. The
leuABCD operon is transcriptionally repressed by the
presence of a 318-base pair AT-rich upstream element. LeuO is required
for derepressing the repressed leuABCD operon. Deletion analysis of the repressive effect of the 318-bp element has led to the
identification of a 72-bp AT-rich (78% A+T) DNA sequence element, AT4,
which is capable of silencing a number of unrelated promoters in
addition to the leuABCD promoter. AT4-mediated gene silencing is orientation-independent and occurs within a distance of
300 base pairs. Furthermore, an increased gene-silencing effect was
observed with a tandemly repeated AT4 dimer. The possible mechanism of
AT4-mediated gene silencing in bacteria is discussed.
*
This work was supported by a National Institutes of Health
Grant GM-53617.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.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF106956 and AF106955.
To whom correspondence should be addressed: Dept. of Pharmacology,
Wayne State University, School of Medicine, 540 E. Canfield Ave.,
Detroit, MI 48201. Tel.: 313-577-1584; Fax: 313-577-6739; E-mail:
haiwu@med.wayne.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
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