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Published 12 September 2005. doi:10.1083/jcb.200412172
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 170, Number 6, 895-901
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Cdc42 and Par6–PKC{zeta} regulate the spatially localized association of Dlg1 and APC to control cell polarization



Sandrine Etienne-Manneville1,5, Jean-Baptiste Manneville3,5, Sarah Nicholls1, Michael A. Ferenczi3,4, and Alan Hall1,2

1 Medical Research Council Laboratory for Molecular Cell Biology and Cell Biology Unit, Cancer Research UK Oncogene and Signal Transduction Group
2 Department of Biochemistry and Molecular Biology, University College London, London WC1E 6BT, England, UK
3 National Institute for Medical Research, London NW7 1AA, England, UK
4 Department of Biomedical Sciences, Imperial College, London SW7 2AZ, England, UK
5 Institut Curie, Centre National de la Recherche Scientifique, UMR144, Paris 75248, cedex 05, France

Correspondence to Alan Hall: alan.hall{at}ucl.ac.uk


Abstract

Cell polarization is essential in a wide range of biological processes such as morphogenesis, asymmetric division, and directed migration. In this study, we show that two tumor suppressor proteins, adenomatous polyposis coli (APC) and Dlg1-SAP97, are required for the polarization of migrating astrocytes. Activation of the Par6–PKC{zeta} complex by Cdc42 at the leading edge of migrating cells promotes both the localized association of APC with microtubule plus ends and the assembly of Dlg-containing puncta in the plasma membrane. Biochemical analysis and total internal reflection fluorescence microscopy reveal that the subsequent physical interaction between APC and Dlg1 is required for polarization of the microtubule cytoskeleton.

Abbreviations used in this paper: APC, adenomatous polyposis coli; TIRF, total internal reflection fluorescence.


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