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Drosophila CBP represses the transcription factor TCF to antagonize Wingless signalling

Author

Listed:
  • Lucas Waltzer

    (MRC Laboratory of Molecular Biology)

  • Mariann Bienz

    (MRC Laboratory of Molecular Biology)

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.

Suggested Citation

  • Lucas Waltzer & Mariann Bienz, 1998. "Drosophila CBP represses the transcription factor TCF to antagonize Wingless signalling," Nature, Nature, vol. 395(6701), pages 521-525, October.
    • Handle: RePEc:nat:nature:v:395:y:1998:i:6701:d:10.1038_26785
    DOI: 10.1038/26785
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