Drosophila CBP represses the transcription factor TCF to antagonize Wingless signalling

Lucas Waltzer and Mariann Bienz ()
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Lucas Waltzer: MRC Laboratory of Molecular Biology
Mariann Bienz: MRC Laboratory of Molecular Biology

Nature, 1998, vol. 395, issue 6701, 521-525

Abstract: Abstract T-cell factor (TCF), a high-mobility-group domain protein, is the transcription factor activated by Wnt/Wingless signalling1,2,3,4. When signalling occurs, TCF binds to its coactivator, beta-catenin/Armadillo, and stimulates the transcription of the target genes of Wnt/Wingless by binding to TCF-responsive enhancers1,5. Inappropriate activation of TCF in the colon epithelium and other cells leads to cancer6,7,8. It is therefore desirable for unstimulated cells to have a negative control mechanism to keep TCF inactive. Here we report that Drosophila CREB-binding protein (dCBP)9,10 binds to dTCF. dCBP mutants show mild Wingless overactivation phenotypes in various tissues. Consistent with this, dCBP loss-of-function suppresses the effects of armadillo mutation. Moreover, our data show that dCBP acetylates a conserved lysine in the Armadillo-binding domain of dTCF, and that this acetylation lowers the affinity of Armadillo binding to dTCF. Although CBP is a coactivator of other transcription factors11,12, our data show that CBP represses TCF.

Date: 1998
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DOI: 10.1038/26785

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