Essential role of BCL9-2 in the switch between β-catenin's adhesive and transcriptional functions
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.
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Footnotes
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Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.317604.
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↵3 Present address: Medical Research Council Laboratory of Molecular Biology, Hills Road, CB2 2QH, Cambridge, UK
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↵4 Present address: Hubrecht Laboratorium, Uppsalalaan 8, 3584CT Utrecht, Netherland.
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↵5 Corresponding author. E-MAIL wbirch{at}mdc-berlin.de; FAX 49-30-94062656.
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- Accepted July 20, 2004.
- Received May 27, 2004.
- Cold Spring Harbor Laboratory Press
