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Published January 1, 2000 | Published
Journal Article Open

A role for neural determination genes in specifying the dorsoventral identity of telencephalic neurons


Neurogenin1 (Ngn1), Neurogenin2 (Ngn2), and Mash1 encode bHLH transcription factors with neuronal determination functions. In the telencephalon, the Ngns and Mash1 are expressed at high levels in complementary dorsal and ventral domains, respectively. We found that Ngn function is required to maintain these two separate expression domains, as Mash1 expression is up-regulated in the dorsal telencephalon of Ngn mutant embryos. We have taken advantage of the replacement of the Ngns by Mash1 in dorsal progenitors to address the role of the neural determination genes in neuronal-type specification in the telencephalon. In Ngn2 single and Ngn1; Ngn2 double mutants, a population of early born cortical neurons lose expression of dorsal-specific markers and ectopically express a subset of ventral telencephalic-specific markers. Analysis of Mash1; Ngn2 double mutant embryos and of embryos carrying a Ngn2 to Mash1 replacement mutation demonstrated that ectopic expression of Mash1 is required and sufficient to confer these ventral characteristics to cortical neurons. Our results indicate that in addition to acting as neuronal determinants, Mash1 and Ngns play a role in the specification of dorsal-ventral neuronal identity, directly linking pathways of neurogenesis and regional patterning in the forebrain.

Additional Information

© 2000 Cold Spring Harbor Laboratory Press. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/. Received August 9, 1999; Revised version accepted November 19, 1999. We thank Jean-François Brunet, Christo Goridis, Magdalena Götz, Marion Wassef, and Masato Nakafuku for their critical comments on the manuscript. We also thank Magdalena Götz for helpful discussions, Aitana Perea and Muriel Rhinn for help with the generation of chimeras, and Domingos Henrique for advice on the double RNA in situ hybridization procedure. We also acknowledge the following people for their gifts of probes: Denis Duboule, Gérard Gradwohl, Peter Gruss, Marc Hallonet, Ryoichiro Kageyama, Dan Kaufman, and John Rubenstein. C.F. was supported by fellowships from the Human Frontiers Science Program and Medical Research Council of Canada and S.C. was supported by fellowships from the Association pour la Recherché sur le Cancer and Human Frontiers Science Program. This work was supported by grants from the European Commission Biotech Programme, Association pour la Recherche sur le Cancer, Association Franc¸aise contre les Myopathies and Ministère de l'Enseignement et de la Recherche to F.G., and by institutional funds from INSERM, CNRS, and Hôpital Universitaire de Strasbourg. The publication costs of this article were defrayed in part by payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

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