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J. Biol. Chem., Vol. 276, Issue 16, 13136-13144, April 20, 2001
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From Le Centre de Recherche en Cancérologie de
l'Université Laval, L'Hôtel-Dieu de Québec,
Département de Biologie Médicale, Faculté de
Médecine, Québec G1R 2J6, Canada
Fetoprotein transcription factor
(FTF) is an orphan nuclear receptor that activates the
The Mouse Fetoprotein Transcription Factor (FTF) Gene Promoter Is
Regulated by Three GATA Elements with Tandem E Box and Nkx Motifs, and
FTF in Turn Activates the Hnf3
,
Hnf4
, and Hnf1 Gene Promoters*
,
1-fetoprotein gene during early liver developmental growth. Here we sought to define better the position of
FTF in transcriptional cascades leading to hepatic differentiation. The
mouse FTF gene was isolated and assigned to chromosome 1 band E4 (one
mFTF pseudogene was also found). Exon/intron mapping shows an mFTF gene
structure similar to that of its close homologue SF1, with two more
N-terminal exons in the mFTF gene; exon mapping also delimits several
FTF mRNA 5'- and 3'-splice variants. The mFTF transcription
initiation site was located in adult liver at 238 nucleotides from the
first translation initiator codon, with six canonical GATA, E box, and
Nkx motifs clustered between 
50/140 base pairs (bp) from the cap
site; DNA/protein binding assays also pinpointed an HNF4-binding
element at +36 bp and an FTF-binding element at 257 bp. Transfection
assays and point mutations showed that the mFTF promoter is activated
by GATA, HNF4, FTF, Nkx, and basic helix-loop-helix factors, with
marked cooperativity between GATA and HNF4. A tandem GATA/E box
activatory motif in the proximal mFTF promoter is strikingly similar to
a composite motif coactivated by differentiation inducers in the hematopoietic lineage; a tandem GATA-Nkx motif in the distal mFTF promoter is also similar to a composite motif transducing
differentiation signals from transforming growth factor-
-like
receptors in the cardiogenic lineage. Three genes encoding
transcription factors critical to early hepatic differentiation,
Hnf3, Hnf4, and
Hnf1, each contain dual FTF-binding elements
in their proximal promoters, and all three promoters are activated by
FTF in transfection assays. Direct DNA binding action and cooperativity
was demonstrated between FTF and HNF3 on the Hnf3
promoter and between FTF and HNF4 on the Hnf1
promoter. These combined results suggest that FTF is an early
intermediary between endodermal specification signals and downstream
genes that establish and amplify the hepatic phenotype.
*
This work was supported in part by Grant MT-6478 from the
Canadian Institutes for Health Research.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 doctoral studentship from Fonds de la Recherche en
Santé du Québec and Fonds pour la Formation de Chercheurs et l'Aide à la Recherche.
§
To whom correspondence should be addressed:
Cancer Research Centre, L'Hôtel-Dieu de Québec,
Québec G1R 2J6, Canada. Tel.: 418-691-5543; Fax: 418-691-5489;
E-mail: luc.belanger@crhdq.ulaval.ca.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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