This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ku, M. Articles by Hata, A. Search for Related Content PubMed PubMed Citation Articles by Ku, M. Articles by Hata, A.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, August 2005, p. 7144-7157, Vol. 25, No. 16
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.16.7144-7157.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Positive and Negative Regulation of the Transforming Growth Factor ß/Activin Target Gene goosecoid by the TFII-I Family of Transcription Factors

Molecular Cardiology Research Institute, Tufts-New England Medical Center and Department of Biochemistry,¹ Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111,³ Department of Molecular, Cell, and Developmental Biology, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1020, New York, NY 10029²

Received 30 November 2004/ Returned for modification 14 February 2005/ Accepted 23 May 2005

Goosecoid (Gsc) is a homeodomain-containing transcription factor present in a wide variety of vertebrate species and known to regulate formation and patterning of embryos. Here we show that in embryonic carcinoma P19 cells, the transcription factor TFII-I forms a complex with Smad2 upon transforming growth factor ß (TGFß)/activin stimulation, is recruited to the distal element (DE) of the Gsc promoter, and activates Gsc transcription. Downregulation of endogenous TFII-I by small inhibitory RNA in P19 cells abolishes the TGFß-mediated induction of Gsc. Similarly, Xenopus embryos with endogenous TFII-I expression downregulated by injection of TFII-I-specific antisense oligonucleotides exhibit decreased Gsc expression. Unlike TFII-I, the related factor BEN (binding factor for early enhancer) is constitutively recruited to the distal element in the absence of TGFß/activin signaling and is replaced by the TFII-I/Smad2 complex upon TGFß/activin stimulation. Overexpression of BEN in P19 cells represses the TGFß-mediated transcriptional activation of Gsc. These results suggest a model in which TFII-I family proteins have opposing effects in the regulation of the Gsc gene in response to a TGFß/activin signal.

This article has been cited by other articles:

• Chimge, N.-O., Makeyev, A. V., Ruddle, F. H., Bayarsaihan, D. (2008). Identification of the TFII-I family target genes in the vertebrate genome. Proc. Natl. Acad. Sci. USA 105: 9006-9010 [Abstract] [Full Text]  
• Lazebnik, M. B., Tussie-Luna, M. I., Roy, A. L. (2008). Determination and Functional Analysis of the Consensus Binding Site for TFII-I Family Member BEN, Implicated in Williams-Beuren Syndrome. J. Biol. Chem. 283: 11078-11082 [Abstract] [Full Text]  
• Hartwell, K. A., Muir, B., Reinhardt, F., Carpenter, A. E., Sgroi, D. C., Weinberg, R. A. (2006). The Spemann organizer gene, Goosecoid, promotes tumor metastasis. Proc. Natl. Acad. Sci. USA 103: 18969-18974 [Abstract] [Full Text]  
• Lagna, G., Nguyen, P. H., Ni, W., Hata, A. (2006). BMP-dependent activation of caspase-9 and caspase-8 mediates apoptosis in pulmonary artery smooth muscle cells.. Am. J. Physiol. Lung Cell. Mol. Physiol. 291: L1059-L1067 [Abstract] [Full Text]  
• Ogura, Y., Azuma, M., Tsuboi, Y., Kabe, Y., Yamaguchi, Y., Wada, T., Watanabe, H., Handa, H. (2006). TFII-I down-regulates a subset of estrogen-responsive genes through its interaction with an initiator element and estrogen receptor {alpha}. GENES CELLS 11: 373-381 [Abstract] [Full Text]  
• Ku, M., Howard, S., Ni, W., Lagna, G., Hata, A. (2006). OAZ Regulates Bone Morphogenetic Protein Signaling through Smad6 Activation. J. Biol. Chem. 281: 5277-5287 [Abstract] [Full Text]