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Published June 11, 2002 | Published
Journal Article Open

Transient expression of the bHLH factor neurogenin-2 marks a subpopulation of neural crest cells biased for a sensory but not a neuronal fate

Abstract

Lineage-tracing experiments have indicated that some premigratory neural crest cells (NCCs) are pleuripotent, generating sensory and sympathetic neurons and their associated glia. Using an inducible Cre recombinase-based fate mapping system, we have permanently marked a subpopulation of NCCs that expresses Ngn2, a bHLH transcription factor required for sensory neurogenesis, and compared its fate to the bulk NCC population marked by expression of Wnt1. Ngn2+ progenitors were four times more likely than Wnt1+ NCCs to contribute to sensory rather than sympathetic ganglia. Within dorsal root ganglia, however, both Ngn2- and Wnt1-expressing cells were equally likely to generate neurons or glia. These data suggest that Ngn2 marks an NCC subpopulation with a predictable fate bias, early in migration. Taken together with previous work, these data suggest that NCCs become restricted to sensory or autonomic sublineages before becoming committed to neuronal or glial fates.

Additional Information

© 2002 by the National Academy of Sciences. Communicated by Douglas A. Melton, Harvard University, Cambridge, MA, April 16, 2002 (received for review February 6, 2002) We thank C. Schuurmans and F. Guillemot (Université Louis Pasteur, Strasbourg, France) for providing the Ngn2 genomic construct and Ngn2-lacZ mice; P. Soriano (Fred Hutchinson Cancer Research Center, Seattle) for Rosa26-loxp reporter mice; B. Kennedy, S. Pease, and the staff of Transgenic Animal Facility, California Institute of Technology, for expert help in the generation and maintenance of genetically modified mice; L. Reichardt and F. Rice for anti-Trk antibodies; and C. Birchmeier for the anti-BFABP antibody. We thank G. Kreiman for help with mathematical simulations; J. Yamada for genotyping; and S. Pintchovski and G. Mosconi for help with experiments. Work in A.P.M.'s laboratory was supported by Grant HD 30249 from the National Institutes of Health. D.J.A. is an Investigator of the Howard Hughes Medical Institute.

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