Delays in neuronal differentiation in Mash1/Ascl1 mutants

Dev Biol. 2006 Jul 1;295(1):67-75. doi: 10.1016/j.ydbio.2006.03.008. Epub 2006 May 4.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / genetics*
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Cell Differentiation / genetics*
  • Ganglia, Autonomic / cytology
  • Ganglia, Autonomic / embryology
  • Ganglia, Sympathetic / cytology
  • Ganglia, Sympathetic / embryology
  • Gene Expression Regulation, Developmental
  • Mice
  • Mice, Mutant Strains
  • Mutation*
  • Neurons / pathology*
  • Neurons / physiology
  • Solitary Nucleus / cytology
  • Solitary Nucleus / embryology*

Substances

  • Ascl1 protein, mouse
  • Basic Helix-Loop-Helix Transcription Factors