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Developmental Biology
Article
License: Elsevier Non-Commercial
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Developmental Biology
Article . 2006
License: Elsevier Non-Commercial
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Developmental Biology
Article . 2006 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
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Delays in neuronal differentiation in Mash1/Ascl1 mutants

Authors: Pattyn, Alexandre; Guillemot, François; Brunet, Jean-François;

Delays in neuronal differentiation in Mash1/Ascl1 mutants

Abstract

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.

Keywords

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

  • BIP!
    Impact byBIP!
    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    82
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
82
Top 10%
Top 10%
Top 10%
hybrid