Neuronal position in the developing brain is regulated by mouse disabled-1

Brian W. Howell (), Richard Hawkes, Philippe Soriano and Jonathan A. Cooper
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Brian W. Howell: Fred Hutchinson Cancer Research Center
Richard Hawkes: University of Calgary
Philippe Soriano: Fred Hutchinson Cancer Research Center
Jonathan A. Cooper: Fred Hutchinson Cancer Research Center

Nature, 1997, vol. 389, issue 6652, 733-737

Abstract: Abstract During mammalian brain development, immature neurons migrate radially from the neuroectoderm to defined locations, giving rise to characteristic cell layers1,2. Here we show that targeted disruption of the mouse disabled1 ( mdab1 ) gene3 disturbs neuronal layering in the cerebral cortex, hippocampus and cerebellum. The gene encodes a cytoplasmic protein, mDab1 p80, which is expressed and tyrosine-phosphorylated in the developing nervous system3. It is likely to be an adaptor protein, docking to others through its phosphotyrosine residues and protein-interacting domain4. The mdab1 mutant phenotype is very similar to that of the reeler mouse5,6,7. The product of the reeler gene, Reelin, is a secreted protein that has been proposed to act as an extracellular signpost for migrating neurons8,9,10. Because mDab1 is expressed in wild-type cortical neurons, and Reelin expression is normal in mdab1 mutants, mDab1 may be part of a Reelin-regulated or parallel pathway that controls the final positioning of neurons.

Date: 1997
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DOI: 10.1038/39607

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