Human Molecular Genetics Advance Access published online on March 28, 2006
Human Molecular Genetics, doi:10.1093/hmg/ddl062
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1 Institut Cochin, Département de Génétique et Développement, Paris, F-75014 France. INSERM U567, Paris, France. CNRS UMR 8104, Paris, France. Université Paris Descartes, Paris V, 75014 Paris, France
* To whom correspondence should be addressed.
Received January 4, 2006
Revised March 10, 2006
Accepted March 10, 2006
Article
Branching and nucleokinesis defects in migrating interneurons derived from doublecortin knockout mice
Caroline Kappeler 1,
Yoann Saillour 1,
Jean-Pierre Baudoin 2,
Françoise Phan Dinh Tuy 1,
Chantal Alvarez 2,
Christophe Houbron 3,
Patricia Gaspar 2,
Ghislaine Hamard 3,
Jamel Chelly 1,
Christine Métin 2,
and
Fiona Francis 1 *
2 U616 INSERM, Hôpital Pitié-Salpêtrière, 47, Bld de l'Hôpital, 75651 Paris Cédex 13
3 Homologous recombination laboratory, Institut Cochin, 75014 Paris
Fiona Francis, E-mail: francis{at}cochin.inserm.fr
Type I lissencephaly results from mutations in the doublecortin (DCX) and LIS1 genes. We generated Dcx knockout mice to further understand the pathophysiological mechanisms associated with this cortical malformation. Dcx is expressed in migrating interneurons in developing human and mouse brains. Video microscopy analyses of such tangentially migrating neuron populations derived from the medial ganglionic eminence show defects in migratory dynamics. Specifically, the formation and division of growth cones, leading to the production of new branches, are more frequent in knockout cells, although branches are less stable. Dcx-deficient cells thus migrate in a disorganised manner, extending and retracting short branches and making less long distant movements of the nucleus. Despite these differences, migratory speeds and distances remain similar to wild type cells. These novel data thus highlight a role for Dcx, a microtubule associated protein enriched at the leading edge, in the branching and nucleokinesis of migrating interneurons.
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