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First published online 15 December 2008
doi: 10.1242/dev.027193

Development 136, 295-305 (2009)
Published by The Company of Biologists 2009
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The bHLH transcription factor Olig3 marks the dorsal neuroepithelium of the hindbrain and is essential for the development of brainstem nuclei

Robert Storm1,*, Justyna Cholewa-Waclaw1,*, Katja Reuter1,*, Dominique Bröhl1, Martin Sieber1,{dagger}, Mathias Treier2, Thomas Müller1 and Carmen Birchmeier1,{ddagger}

1 Max-Delbrück-Centrum for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
2 EMBL, Meyerhofstrasse 1, 69117 Heidelberg, Germany.

{ddagger} Author for correspondence (cbirch{at}mdc-berlin.de)

Accepted 6 November 2008

The Olig3 gene encodes a bHLH factor that is expressed in the ventricular zone of the dorsal alar plate of the hindbrain. We found that the Olig3+ progenitor domain encompassed subdomains that co-expressed Math1, Ngn1, Mash1 and Ptf1a. Olig3+ cells give rise to neuronal types in the dorsal alar plate that we denote as class A neurons. We used genetic lineage tracing to demonstrate that class A neurons contribute to the nucleus of the solitary tract and to precerebellar nuclei. The fate of class A neurons was not correctly determined in Olig3 mutant mice. As a consequence, the nucleus of the solitary tract did not form, and precerebellar nuclei, such as the inferior olivary nucleus, were absent or small. At the expense of class A neurons, ectopic Lbx1+ neurons appeared in the alar plate in Olig3 mutant mice. By contrast, electroporation of an Olig3 expression vector in the chick hindbrain suppressed the emergence of Lbx1+ neurons. Climbing fiber neurons of the inferior olivary nucleus express Foxd3 and require Olig3 as well as Ptf1a for the determination of their fate. We observed that electroporation of Olig3 and Ptf1a expression vectors, but not either alone, induced Foxd3. We therefore propose that Olig3 can cooperate with Ptf1a to determine the fate of climbing fiber neurons of the inferior olivary nucleus.

Key words: Fate mapping, Neuronal fate, Transcription factor, Mouse


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