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J Biol Chem, Vol. 275, Issue 9, 6608-6619, March 3, 2000
From The Hubert H. Humphrey Center for Experimental Medicine and
Cancer Research, The Hebrew University, Hadassah Medical School,
Jerusalem 91120, Israel
The Oct-3/4 transcription factor is expressed in
the earliest stages of embryogenesis, and is thus likely to play an
important role in regulation of initial decisions in development. For
the first time, we have shown that SF1 and Oct-3/4 are co-expressed in
embryonal carcinoma (EC) P19 cells, and their expression is down-regulated with very similar kinetics following retinoic acid (RA)
induced differentiation of these cells, suggesting a functional relationship between the two. Previously, we have shown that the Oct-3/4 promoter harbors an RA-responsive element, RAREoct,
which functions in EC cells as a binding site for positive regulators of transcription, such as RAR and RXR. In this study we have identified in the Oct-3/4 promoter two novel SF1-binding sites: SF1(a)
and SF1(b). The proximal site, SF1(a), is located within the RAREoct, and the distal site, SF1(b), is located between nucleotide
Synergy of SF1 and RAR in Activation of Oct-3/4
Promoter*
193 and
209 of the Oct-3/4 promoter. Both sites contribute to
activation of Oct-3/4 promoter in EC cells, with SF1(a)
playing a more crucial role. SF1, and its isoforms ELP2 and ELP3 bind
to both SF1 sites and activate the Oct-3/4 promoter. This
activation depends on the presence of SF1 DNA-binding domain. Thus,
Oct-3/4 is the first EC-specific gene reported that is
regulated by SF1. Interestingly, SF1 and RAR form a novel complex on
the RAREoct sequence that synergistically activate the
Oct-3/4 promoter. Both RARE and SF1 cis
regulatory elements, as well as the SF1 DNA-binding domain, are needed
for this synergism. SF1 and Oct-3/4 transcription factors play a role
in the same developmental regulatory cascade.
*
This work was supported by a grant from the Israel Cancer
Association (to Y. B.).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.
To whom correspondence should be addressed: P. O. Box 12272, The
Hebrew University-Hadassah Medical School, 91120, Israel. Tel.:
972-2-6758362; Fax: 972-2-6414583; E-mail: yberg@md2.huji.ac.il.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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