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Published April 1, 2002 | Published
Journal Article Open

Comparison of the generic neuronal differentiation and neuron subtype specification functions of mammalian achaete-scute and atonal homologs in cultured neural progenitor cells


In the vertebrate peripheral nervous system, the proneural genes neurogenin 1 and neurogenin 2 (Ngn1 and Ngn2), and Mash1 are required for sensory and autonomic neurogenesis, respectively. In cultures of neural tube-derived, primitive PNS progenitors NGNs promote expression of sensory markers and MASH1 that of autonomic markers. These effects do not simply reflect enhanced neuronal differentiation, suggesting that both bHLH factors also specify neuronal identity like their Drosophila counterparts. At high concentrations of BMP2 or in neural crest stem cells (NCSCs), however, NGNs like MASH1 promote only autonomic marker expression. These data suggest that that the identity specification function of NGNs is more sensitive to context than is that of MASH1. In NCSCs, MASH1 is more sensitive to Notch-mediated inhibition of neurogenesis and cell cycle arrest, than are the NGNs. Thus, the two proneural genes differ in other functional properties besides the neuron subtype identities they can promote. These properties may explain cellular differences between MASH1- and NGN-dependent lineages in the timing of neuronal differentiation and cell cycle exit.

Additional Information

© 2002 The Company of Biologists Limited. Accepted 7 January 2002. We thank Eric Turner for anti-BRN3A antibody, Christo Goridis and Jean-François Brunet for anti-PHOX2B antibody, Rusty Lansford for introducing us to the pLZRS vectors, Susan Ou for assistance with monoclonal antibody production, Barbara Wold and Jeong Kyo Yoon for super-GFP, Peter Snow for assistance with GST-fusion proteins, Jaesang Kim for pLZRS-SOX10 retrovirus, François Guillemot for communicating unpublished data and for helpful comments on the manuscript, and Gaby Mosconi for laboratory management. This work was supported in part by a grant from the March of Dimes Foundation. E.D. was supported by a fellowship from the Wellcome Trust. D.J.A. is an Investigator of the Howard Hughes Medical Institute.

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