TY - JOUR
T1 - Mammalian achaete-scute homolog 1 is required for the early development of olfactory and autonomic neurons
AU - Guillemot, François
AU - Lo, Li Ching
AU - Johnson, Jane E.
AU - Auerbach, Anna
AU - Anderson, David J.
AU - Joyner, Alexandra L.
N1 - Funding Information:
We gratefully acknowledge K. Harpal for advice and assistance with histological procedures; Drs. T. Edlund, E. E. Geisert, T. Jessell, A. Klar, R. Klein, F. L. Margolis, 8. Motro, V. Pachnis, and M. Tessier-Lavigne for the gifts of probes and antibodies; and Drs. A. Calof, C. C. Hui, and B. Motro for critical reading of the manuscript. We thank B. N. Yoshida for his contributions to the early stages of this work (Anderson laboratory). This research was funded by grants from the National Cancer Institute of Canada and Bristol-Myers Squibb Limited to A. L. J. F. G. was supported by the Medical Research Council (MRC) of Canada and J. E. J. by a Young Investigator’s Award from the National Neurofibromatosis Foundation. D. J. A. is an Associate Investigator of the Howard Hughes Medical Institute. A. L. J. is an MRC Scientist and a Howard Hughes international Scholar.
PY - 1993/11/5
Y1 - 1993/11/5
N2 - 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.
AB - 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.
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U2 - 10.1016/0092-8674(93)90381-Y
DO - 10.1016/0092-8674(93)90381-Y
M3 - Article
C2 - 8221886
AN - SCOPUS:0027420712
SN - 0092-8674
VL - 75
SP - 463
EP - 476
JO - Cell
JF - Cell
IS - 3
ER -