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First published online May 11, 2006
doi: 10.1242/10.1242/dev.02345

Development 133, 2105-2113 (2006)
Published by The Company of Biologists 2006
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dILA neurons in the dorsal spinal cord are the product of terminal and non-terminal asymmetric progenitor cell divisions, and require Mash1 for their development

Hendrik Wildner1, Thomas Müller1, Seo-Hee Cho2, Dominique Bröhl1, Constance L. Cepko2, Francois Guillemot3 and Carmen Birchmeier1,*

1 Max-Delbrück-Centrum for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin-Buch, Germany.
2 Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
3 National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.

* Author for correspondence (e-mail: cbirch{at}mdc-berlin.de)

Accepted 3 March 2006

dILA and dILB neurons comprise the major neuronal subtypes generated in the dorsal spinal cord, and arise in a salt-and-pepper pattern from a broad progenitor domain that expresses the bHLH factor Mash1. In this domain, Mash1-positive and Mash1-negative cells intermingle. Using a Mash1GFP allele in mice, we show here that Mash1+ progenitors give rise to dILA and dILB neurons. Using retroviral tracing in the chick, we demonstrate that a single progenitor can give rise to a dILA and a dILB neuron, and that dILA neurons are the product of asymmetric progenitor cell divisions. In Mash1-null mutant mice, the development of dILA, but not of dILB neurons is impaired. We provide evidence that a dual function of Mash1 in neuronal differentiation and specification accounts for the observed changes in the mutant mice. Our data allow us to assign to Mash1 a function in asymmetric cell divisions, and indicate that the factor coordinates cell cycle exit and specification in the one daughter that gives rise to a dILA neuron.

Key words: Asymmetric cell division, Neuronal specification, Spinal cord, Mash1 (Ascl1), Mouse, Chick




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