Different levels of repressor activity assign redundant and specific roles to Nkx6 genes in motor neuron and interneuron specification

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Item Type:	Article
Title:	Different levels of repressor activity assign redundant and specific roles to Nkx6 genes in motor neuron and interneuron specification
Creators Name:	Vallstedt, A., Muhr, J., Pattyn, A., Pierani, A., Mendelsohn, M., Sander, M., Jessell, T.M. and Ericson, J.
Abstract:	Specification of neuronal fate in the vertebrate central nervous system depends on the profile of transcription factor expression by neural progenitor cells, but the precise roles of such factors in neurogenesis remain poorly characterized. Two closely related transcriptional repressors, Nkx6.2 and Nkx6.1, are expressed by progenitors in overlapping domains of the ventral spinal cord. We provide genetic evidence that differences in the level of repressor activity of these homeodomain proteins underlies the diversification of interneuron subtypes, and provides a fail-safe mechanism during motor neuron generation. A reduction in Nkx6 activity further permits V0 neurons to be generated from progenitors that lack homeodomain proteins normally required for their generation, providing direct evidence for a model in which progenitor homeodomain proteins direct specific cell fates by actively suppressing the expression of transcription factors that direct alternative fates.
Keywords:	Cell Differentiation, Cell Lineage, Central Nervous System, Chick Embryo, Eye Proteins, Fetus, Developmental Gene Expression Regulation, Homeobox Protein Nkx-2.2, Homeodomain Proteins, Immunohistochemistry, In Situ Hybridization, Interneurons, Motor Neurons, PAX6 Transcription Factor, Paired Box Transcription Factors, Repressor Proteins, Spinal Cord, Stem Cells, Transcription Factors, Genetic Transcription, Zebrafish Proteins, Animals, Mice, Knockout Mice
Source:	Neuron
ISSN:	0896-6273
Publisher:	Cell Press
Volume:	31
Number:	5
Page Range:	743-55
Date:	13 September 2001
Official Publication:	https://doi.org/10.1016/s0896-6273(01)00412-3
PubMed:	View item in PubMed

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