Cdc42 and noncanonical Wnt signal transduction pathways cooperate to promote cell polarity

被引:154
作者
Schlessinger, Karni
McManus, Edward J.
Hall, Alan
机构
[1] UCL, Canc Res UK Oncogene & Signal Transduct Grp, Med Res Council Lab Mol Cell Biol, London WC1E 6BT, England
[2] UCL, Dept Biochem & Mol Biol, London WC1E 6BT, England
[3] Univ Dundee, Med Res Council Prot Phosphorylat Unit, Dundee DD2 5DQ, Scotland
关键词
D O I
10.1083/jcb.200701083
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Scratch-induced disruption of cultured monolayers induces polarity in front row cells that can be visualized by spatially localized polymerization of actin at the front of the cell and reorientation of the centrosome/Golgi to face the leading edge. We previously reported that centrosomal reorientation and microtubule polarization depend on a Cdc,42-regulated signal transduction pathway involving activation of the Par6/aPKC complex followed by inhibition of GSK-3 beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus ends of leading-edge microtubules. Using monolayers of primary rodent embryo fibroblasts, we show here that dishevelled (Dv vertical bar) and axin, two major components of the Writ signaling pathway are required for centrosome reorientation and that Wnt5a is required for activation of this pathway. We conclude that disruption of cell-cell contacts leads to the activation of a noncanonical Wnt/dishevelled signal transduction pathway that cooperates with Cdc42/Par6/aPKC to promote polarized reorganization of the microtubule cytoskeleton.
引用
收藏
页码:355 / 361
页数:7
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