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Abstract
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.