Nature Neuroscience 8, 451 - 457 (2005)
Published online: 20 March 2005; Corrected online: 14 December 2005 | doi:10.1038/nn1428
There is a Corrigendum (January 2006) associated with this Article.
Protocadherin Celsr3 is crucial in axonal tract developmentFadel Tissir1, 3, Isabelle Bar2, 3, Yves Jossin1, Olivier De Backer2
& Andre M Goffinet11
Developmental Neurobiology Unit, University of Louvain Medical School, 73, avenue Mounier, Box DENE7382, B-1200 Brussels, Belgium. 2
Molecular Physiology Research Unit, University of Namur Medical School, 61, rue de Bruxelles, B5000 Namur, Belgium. 3
These authors contributed equally to this work.
Correspondence should be addressed to andre.goffinet@dene.ucl.ac.be In the embryonic CNS, the development of axonal tracts is required for the formation of connections and is regulated by multiple genetic and microenvironmental factors. Here we show that mice with inactivation of Celsr3, an ortholog of Drosophila melanogaster flamingo (fmi; also known as starry night, stan) that encodes a seven-pass protocadherin, have marked, selective anomalies of several major axonal fascicles, implicating protocadherins in axonal development in the mammalian CNS for the first time. In flies, fmi controls planar cell polarity (PCP) in a frizzled-dependent but wingless-independent manner. The neural phenotype in Celsr3 mutant mice is similar to that caused by inactivation of Fzd3, a member of the frizzled family. Celsr3 and Fzd3 are expressed together during brain development and may act in synergy. Thus, a genetic pathway analogous to the one that controls PCP is key in the development of the axonal blueprint.
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