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Fibroblast Growth Factor Receptor 3 Gene: Regulation by Serum Response Factor

Department of Pathology (M.I.R., M.C.N.), University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229; and Lineberger Comprehensive Cancer Center (D.G.M.), University of North Carolina, Chapel Hill, North Carolina 27599

Address all correspondence and requests for reprints to: Michael C. Naski, M.D., Ph.D., Department of Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900. E-mail: naski{at}pathology.uthscsa.edu.

We have previously identified a cis-acting sequence in the proximal promoter of the fibroblast growth factor receptor 3 (FGFR3) gene that strongly activates transcription in chondrocytic cells. Here we report that the transcriptional activity of this sequence (FRE3) requires serum response factor and its cognate recognition motif, serum response element. Although the FRE3 contains consensus sequence motifs for several transcription factors, the serum response element is paramount for the transcriptional activity of the FRE3. Additionally, the transcriptional activity of the proximal promoter of the FGFR3 gene is suppressed by mutation of the serum response element. Serum response factor binds to the FRE3 as evidenced by gel shift experiments and antibody supershift experiments and expression of a dominant negative form of serum response factor suppresses the activity of FRE3. Additionally, serum response factor binds to the FGFR3 gene in vivo, as demonstrated by chromatin immunoprecipitation. Serum response factor is an important regulator of cardiac, skeletal, and smooth muscle gene expression; these data suggest that serum response factor is also an important determinant of chondrocyte gene expression.

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