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Papers In Press, published online ahead of print April 13, 2004
Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto 606-8507
Corresponding Author: amurakam{at}virus.kyoto-u.ac.jp
Fgf-3 is expressed in a dynamic and complex spatio-temporal pattern during mouse development. Previous studies identified GATA-4 as a transcription factor that binds the key regulatory element PS4A of the Fgf-3 promoter and stimulates transcription. Here we show that members of the SOX family of transcription factors also bind PS4A and differentially modulate transcription. At least five SOX genes, Sox2, Sox6, Sox7, Sox13 and Sox17 were expressed in F9 cells, and of these, Sox7 and Sox17 were dramatically induced in parallel with Fgf-3 following differentiation into parietal endoderm-like cells with retinoic acid and dibutyryl cAMP. Complexes could be detected on PS4A with SOX2, SOX7 and SOX17 using nuclear extracts from differentiated F9 cells. However, only Sox7 expression markedly activated the Fgf-3 promoter in these cells. By contrast, SOX2 was a poor activator of Fgf-3 transcription, and when Sox2 was co-expressed with Gata4 it negatively modulated the strong activation mediated by GATA-4. More detailed analyses showed that SOX7 competes with GATA-4 for PS4A occupancy, and to activate the Fgf-3 promoter. In situ hybridization analysis showed that Sox7 is co-expressed with Fgf-3 and Gata4 in the parietal endoderm of E7.5 mouse embryos. In culture, GATA-4 deficient ES cells were shown to express Fgf-3 upon differentiation into embryoid bodies, although at lower levels than were found in wild type ES cells. This Fgf-3 expression was virtually abolished when Sox7 expression was suppressed by RNA interference. These results show that SOX7 is a potent activator of Fgf-3 transcription.
J. Biol. Chem, 10.1074/jbc.M313814200
Submitted on December 17, 2003
Revised on April 13, 2004
Accepted on April 13, 2004
SOX7 and GATA-4 are competitive activators of Fgf-3 transcription
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