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