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

Authors

  • F.H. Brembeck
  • T. Schwarz-Romond
  • J. Bakkers
  • S. Wilhelm
  • M. Hammerschmidt
  • W. Birchmeier

Journal

  • Genes & Development

Citation

  • Genes Dev 18 (18): 2225-2230

Abstract

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


DOI

doi:10.1101/gad.317604