Delays in neuronal differentiation in Mash1/Ascl1 mutants
pmid: 16677628
Delays in neuronal differentiation in Mash1/Ascl1 mutants
The inactivation of a developmental transcription factor may lead to the complete absence of a specific cell type. More commonly, though, it only partially impairs its generation. The modalities of this partial effect have rarely been documented in any detail. Here, we report a novel function for the bHLH transcription factor Ascl1/Mash1 in the generation of the nucleus of the solitary tract (nTS). In Mash1(-/-) late embryos, the nTS is markedly atrophic. Tracing back the origin of this atrophy, we show that nTS precursors appear in the mutants 1 day later than in the wild type and then accumulate at a slower pace. We also show that the previously reported atrophy of the sympathetic chain in Mash1 mutants is similarly preceded by a delay of 1 to 2 days in the appearance of differentiated ganglionic cells. Finally, we provide evidence that the acceleration imposed by Mash1, regardless of the production of post-mitotic cells, affects differentiation itself, both generic and type-specific.
Neurons, Ganglia, Sympathetic, Mouse, Gene Expression Regulation, Developmental, Cell Differentiation, Cell Biology, Mice, Mutant Strains, Sympathetic ganglia, Mice, Nucleus of the solitary tract, Knock-out, Neuronal differentiation, Proneural gene, Mutation, Basic Helix-Loop-Helix Transcription Factors, Solitary Nucleus, Animals, Transcription factor, Mash1/Ascl1, Molecular Biology, Ganglia, Autonomic, Developmental Biology
Neurons, Ganglia, Sympathetic, Mouse, Gene Expression Regulation, Developmental, Cell Differentiation, Cell Biology, Mice, Mutant Strains, Sympathetic ganglia, Mice, Nucleus of the solitary tract, Knock-out, Neuronal differentiation, Proneural gene, Mutation, Basic Helix-Loop-Helix Transcription Factors, Solitary Nucleus, Animals, Transcription factor, Mash1/Ascl1, Molecular Biology, Ganglia, Autonomic, Developmental Biology
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