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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Positive and negative regulation of the transforming growth factor beta/ activin target gene goosecoid by the TFII-I family of transcription factors.

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 beta (TGFbeta)/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 TGFbeta- 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 TGFbeta/ activin signaling and is replaced by the TFII-I/Smad2 complex upon TGFbeta/ activin stimulation. Overexpression of BEN in P19 cells represses the TGFbeta- 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 TGFbeta/ activin signal.[1]


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