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Published 19 August 2002. doi:10.1083/jcb.200202002
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© The Rockefeller University Press, 0021-9525/2002/8/709 $5.00
The Journal of Cell Biology, Volume 158, Number 4, August 19, 2002 709-718

Article

 Notch1 control of oligodendrocyte differentiation in the spinal cord

Stéphane Genoud1, Corinna Lappe-Siefke2, Sandra Goebbels2, Freddy Radtke3,4, Michel Aguet3, Steven S. Scherer5, Ueli Suter1, Klaus-Armin Nave2 and Ned Mantei1

1 Department of Biology, Institute of Cell Biology, Swiss Federal Institute of Technology, ETH-Hönggerberg, CH-8093 Zürich, Switzerland
2 Department of Neurogenetics, Max-Planck-Institute of Experimental Medicine, D-37075 Göttingen, Germany
3 Swiss Institute of Experimental Cancer Research, CH-1066 Epalinges, Switzerland
4 Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, CH-1066 Epalinges, Switzerland
5 Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, PA 19104

Address correspondence to Ned Mantei, Institute of Cell Biology, Dept. of Biology, Swiss Federal Institute of Technology, ETH-Hönggerberg, CH-8093 Zürich, Switzerland. Tel.: 41-1-633-3685. Fax: 41-1-633-1190. E-mail: mantei{at}cell.biol.ethz.ch

We have selectively inhibited Notch1 signaling in oligodendrocyte precursors (OPCs) using the Cre/loxP system in transgenic mice to investigate the role of Notch1 in oligodendrocyte (OL) development and differentiation. Early development of OPCs appeared normal in the spinal cord. However, at embryonic day 17.5, premature OL differentiation was observed and ectopic immature OLs were present in the gray matter. At birth, OL apoptosis was strongly increased in Notch1 mutant animals. Premature OL differentiation was also observed in the cerebrum, indicating that Notch1 is required for the correct spatial and temporal regulation of OL differentiation in various regions of the central nervous system. These findings establish a widespread function of Notch1 in the late steps of mammalian OPC development in vivo.

Key Words: ectopic expression; brain; Cre-lox P; newborn; apoptosis


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