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

被引：266
|
作者：
Brembeck, FH
Schwarz-Romond, T
Bakkers, J
Wilhelm, S
Hammerschmidt, M
Birchmeier, W [1 ]
机构：
[1] Max Delbruck Ctr Mol Med, D-13092 Berlin, Germany
[2] Max Planck Inst Immunbiol, D-79108 Freiburg, Germany
来源：
GENES & DEVELOPMENT | 2004年 / 18卷 / 18期
关键词：
BCL9/legless; alpha-catenin; Wnt8; tyrosine phosphorylation; epithelial-mesenchymal transition; mesoderm patterning;
D O I：
10.1101/gad.317604
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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.
引用
收藏
页码：2225 / 2230
页数：6
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