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J. Biol. Chem., Vol. 276, Issue 1, 28-34, January 5, 2001
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From the Department of Biochemistry and Molecular Biology
and the University of Southern California/Norris Comprehensive Cancer
Center, Keck School of Medicine of the University of Southern
California, Los Angeles, California 90089-9176
In analyzing cis-regulatory elements important
for cell cycle control of the replication-dependent hamster
histone H3.2 gene, we discovered a binding site for the transcription
factor YY1 embedded within GC-rich sequences between the two tandem
CCAAT repeats proximal to the TATA element. Base mutations that
specifically eliminated YY1 binding resulted in suppression of the S
phase induction of the H3.2 promoter. In addition, we discovered that YY1 is an interactive partner of AP-2, which also binds the H3.2 promoter and regulates its cell cycle-dependent expression.
The critical domains for YY1 and AP-2A interaction are mapped,
revealing that the N-terminal portion of YY1 (amino acids 1-300) and
the DNA-binding/dimerization region of AP-2A are required. Our results suggest that YY1, acting as a transcription factor binding to its site
on the promoter, or through protein-protein interaction with AP-2, may
be part of a regulatory network including key cell cycle regulators
such as c-Myc and Rb in controlling growth- and differentiation-regulated gene expression.
YY1 as a Regulator of Replication-dependent Hamster
Histone H3.2 Promoter and an Interactive Partner of AP-2*
and
*
This work was supported in part by United States Public
Health Service Grant GM31138 (to A. S. L.).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 the USC/Norris Cancer Center predoctoral fellowship.
§
To whom correspondence should be addressed. Tel.: 323-865-0507;
Fax: 323-865-0094; E-mail: amylee@hsc.usc.edu.
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