Abstract
The autosomal recessive mouse mutation reeler leads to impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. Here we use a previously characterized reeler allele (rl(tg)) to close a gene, reelin, deleted in two reeler alleles. Normal but not mutant mice express reelin in embryonic and postnatal neurons during periods of neuronal migration. The encoded protein resembles extracellular matrix proteins involved in cell adhesion. The reeler phenotype thus seems to reflect a failure of early events associated with brain lamination which are normally controlled by reelin.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alleles
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Amino Acid Sequence
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Animals
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Base Sequence
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Brain / cytology
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Brain / embryology
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Brain / growth & development
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Cell Adhesion Molecules, Neuronal / chemistry
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Cell Adhesion Molecules, Neuronal / genetics*
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Cell Movement / genetics
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Cloning, Molecular
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Embryonic and Fetal Development / genetics
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Extracellular Matrix Proteins / chemistry
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Extracellular Matrix Proteins / genetics*
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Gene Deletion
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Mice
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Mice, Neurologic Mutants / embryology
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Mice, Neurologic Mutants / genetics*
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Mice, Neurologic Mutants / growth & development
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Molecular Sequence Data
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Nerve Tissue Proteins
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Neurons / physiology
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Phenotype
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RNA, Messenger / biosynthesis
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Reelin Protein
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Serine Endopeptidases
Substances
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Cell Adhesion Molecules, Neuronal
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Extracellular Matrix Proteins
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Nerve Tissue Proteins
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RNA, Messenger
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Reelin Protein
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Reln protein, mouse
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Serine Endopeptidases