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Mammalian achaete-scute homolog 1 is required for the early development of olfactory and autonomic neurons.

The mouse Mash-1 gene, like its Drosophila homologs of the achaete-scute complex (AS-C), encodes a transcription factor expressed in neural precursors. We created a null allele of this gene by homologous recombination in embryonic stem cells. Mice homozygous for the mutation die at birth with apparent breathing and feeding defects. The brain and spinal cord of the mutants appear normal, but their olfactory epithelium and sympathetic, parasympathetic, and enteric ganglia are severely affected. In the olfactory epithelium, neuronal progenitors die at an early stage, whereas the nonneuronal supporting cells are present. In sympathetic ganglia, the mutation arrests the development of neuronal precursors, preventing the generation of sympathetic neurons, but does not affect glial precursor cells. These observations suggest that Mash-1, like its Drosophila homologs of the AS-C, controls a basic operation in development of neuronal progenitors in distinct neural lineages.

Pubmed ID: 8221886

Authors

  • Guillemot F
  • Lo LC
  • Johnson JE
  • Auerbach A
  • Anderson DJ
  • Joyner AL

Journal

Cell

Publication Data

November 5, 1993

Associated Grants

None

Mesh Terms

  • Adrenal Medulla
  • Animals
  • Animals, Newborn
  • Autonomic Nervous System
  • Base Sequence
  • Basic Helix-Loop-Helix Transcription Factors
  • Chromaffin System
  • DNA-Binding Proteins
  • Epithelium
  • Ganglia
  • Genes, Lethal
  • Mice
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • Mutagenesis
  • Neural Crest
  • Neuroglia
  • Neurons, Afferent
  • Olfactory Mucosa
  • Phenotype
  • Stem Cells
  • Time Factors
  • Transcription Factors