Abstract
The ability of the mature mammalian nervous system to continually produce neuronal precursors is of considerable importance, as manipulation of this process might one day permit the replacement of cells lost as a result of injury or disease. In mammals, the anterior subventricular zone (SVZa) region is one of the primary sites of adult neurogenesis. Here we show that doublecortin (DCX), a widely used marker for newly generated neurons, when deleted in mice results in a severe morphological defect in the rostral migratory stream and delayed neuronal migration that is independent of direction or responsiveness to Slit chemorepulsion. DCX is required for nuclear translocation and maintenance of bipolar morphology during migration of these cells. Our data identifies a critical function for DCX in the movement of newly generated neurons in the adult brain.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Active Transport, Cell Nucleus / genetics
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Animals
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Cell Differentiation / genetics
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Cell Movement / physiology*
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Cell Proliferation*
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Cell Shape / genetics
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Chemotaxis / genetics
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Doublecortin Domain Proteins
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Doublecortin Protein
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Female
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Gene Expression Regulation, Developmental / genetics
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Male
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Mice, Transgenic
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Microtubule-Associated Proteins / genetics
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Microtubule-Associated Proteins / physiology*
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Nerve Tissue Proteins / genetics
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Neurites / metabolism
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Neurites / ultrastructure
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Neurons / cytology
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Neurons / metabolism*
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Neuropeptides / genetics
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Neuropeptides / physiology*
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Phenotype
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Prosencephalon / cytology
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Prosencephalon / metabolism*
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Protein Transport / genetics
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Stem Cells / cytology
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Stem Cells / metabolism*
Substances
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Dcx protein, mouse
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Doublecortin Domain Proteins
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Doublecortin Protein
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Microtubule-Associated Proteins
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Nerve Tissue Proteins
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Neuropeptides
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Slit1 protein, mouse