Cdc42 and noncanonical Wnt signal transduction pathways cooperate to promote cell polarity
- Author(s)
- Schlessinger, K; McManus, EJ; Hall, A;
- Details
- Publication Year 2007-07-30,Volume 178,Issue #3,Page 355-361
- Journal Title
- JOURNAL OF CELL BIOLOGY
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- ROCKEFELLER UNIV PRESS
- Keywords
- MICROTUBULE-ORGANIZING CENTER; SUBCELLULAR-LOCALIZATION; PLANAR POLARITY; BETA-CATENIN; POLARIZATION; KINASE; MIGRATION; ACTIVATION; ACTIN; PHOSPHORYLATION
- Publisher's Version
- https://doi.org/10.1083/jcb.200701083
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2007-07-30 12:00:00