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Essential role of BCL9-2 in the switch between β-catenin's adhesive and transcriptional functions

  1. Felix H. Brembeck1,
  2. Thomas Schwarz-Romond1,3,
  3. Jeroen Bakkers2,4,
  4. Sabine Wilhelm1,
  5. Matthias Hammerschmidt2, and
  6. Walter Birchmeier1,5
  1. 1Max Delbrueck Center for Molecular Medicine, 13092 Berlin, Germany; 2Max Planck Institute for Immunobiology, 79108 Freiburg, Germany

Abstract

β-Catenin controls both cadherin-mediated cell adhesion and activation of Wnt _target genes. We demonstrate here that the β-catenin-binding protein BCL9-2, a homolog of the human proto-oncogene product BCL9, induces epithelial-mesenchymal transitions of nontransformed cells and increases β-catenin-dependent transcription. RNA interference of BCL9-2 in carcinoma cells induces an epithelial phenotype and translocates β-catenin from the nucleus to the cell membrane. The switch between β-catenin's adhesive and transcriptional functions is modulated by phosphorylation of Tyr 142 of β-catenin, which favors BCL9-2 binding and precludes interaction with α-catenin. During zebrafish embryogenesis, BCL9-2 acts in the Wnt8-signaling pathway and regulates mesoderm patterning.

Keywords

Footnotes

  • Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.317604.

  • ↵3 Present address: Medical Research Council Laboratory of Molecular Biology, Hills Road, CB2 2QH, Cambridge, UK

  • ↵4 Present address: Hubrecht Laboratorium, Uppsalalaan 8, 3584CT Utrecht, Netherland.

  • ↵5 Corresponding author. E-MAIL wbirch@mdc-berlin.de; FAX 49-30-94062656.

    • Accepted July 20, 2004.
    • Received May 27, 2004.
  1. Published in Advance September 1, 2004, doi: 10.1101/gad.317604 Genes & Dev. 18: 2225-2230 Cold Spring Harbor Laboratory Press

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