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J Biol Chem, Vol. 273, Issue 9, 5349-5357, February 27, 1998
From the Department of Molecular Biology and Pharmacology,
Washington University Medical School, St. Louis, Missouri 63110
Fibroblast growth factor receptor 3 (FGFR3) has a
complex spatial and temporal pattern of expression and is essential for the normal development of a diverse set of tissues. Recently, mutations
have been identified in FGFR3 that result in constitutive tyrosine
kinase activity and cause a number of different human skeletal
disorders. To examine the regulatory mechanisms governing FGFR3
expression, the promoter for the FGFR3 gene was identified and
characterized. It resides in a CpG island, which encompasses the 5' end
of the FGFR3 gene and lacks classical cis-regulatory motifs. As little as 100 base pairs of sequence 5' to the initiation site can confer a 20-40-fold increase in transcriptional activity upon
a promoter-less vector. The transcriptional activity of these cis-regulatory sequences is further stimulated by elements
found within the first intron. Mapping of the enhancer activity found within intron I identified two purine-rich sequence motifs between +340
and +395. Electrophoretic mobility shift assays demonstrated that
sequences within this region bind members of the Sp1 family of
transcription factors. In a background lacking Sp1-like activity, we
demonstrate that Sp1 can enhance transcription of the minimal promoter
(which contains five classical Sp1 sites), whereas both Sp1 and Sp3 can
enhance transcription through the elements found in intron I. Although
these transcription factors are ubiquitously expressed, we demonstrate
that the sequences between
Regulation of the Fibroblast Growth Factor Receptor 3 Promoter
and Intron I Enhancer by Sp1 Family Transcription Factors
220 and +609 of the FGFR3 gene are
sufficient to promote the tissue-specific expression of a reporter gene
in transgenic mice.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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