Published 9 December 2002. doi:10.1083/jcb.200207076
© The Rockefeller University Press,
0021-9525/2002/12/731 $5.00
The Journal of Cell Biology, Volume 159, Number 5, 731-737
Microtubule release from the centrosome in migrating cells
Miguel Abal1,
Matthieu Piel1,
Veronique Bouckson-Castaing1,
Mette Mogensen2,
Jean-Baptiste Sibarita1 and
Michel Bornens1
1 Institut Curie/UMR 144 du Centre National de la Recherche Scientifique, 75248 Paris, France
2 School of Biological Sciences, University of East Anglia, Norwich, NR4 7TJ, UK
Address correspondence to Dr. Michel Bornens, Institut Curie/UMR 144 CNRS, 26 rue d'Ulm, 75248 Paris Cedex 05, France. Tel.: 33-1-42-34-64-20. Fax: 33-1-42-34-64 21. E-mail: michel.bornens{at}curie.fr
In migrating cells, force production relies essentially on a polarized actomyosin system, whereas the spatial regulation of actomyosin contraction and substrate contact turnover involves a complex cooperation between the microtubule (MT) and the actin filament networks (Goode, B.L., D.G. Drubin, and G. Barnes. 2000. Curr. Opin. Cell Biol., 12:6371). Targeting and capture of MT plus ends at the cell periphery has been described, but whether or not the minus ends of these MTs are anchored at the centrosome is not known. Here, we show that release of short MTs from the centrosome is frequent in migrating cells and that their transport toward the cell periphery is blocked when dynein activity is impaired. We further show that MT release, but not MT nucleation or polymerization dynamics, is abolished by overexpression of the centrosomal MT-anchoring protein ninein. In addition, a dramatic inhibition of cell migration was observed; but, contrary to cells treated by drugs inhibiting MT dynamics, polarized membrane ruffling activity was not affected in ninein overexpressing cells. We thus propose that the balance between MT minus-end capture and release from the centrosome is critical for efficient cell migration.
Key Words: microtubule anchoring; microtubule dynamics; ninein; EB1-GFP; cell migration

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