Abstract
By using gain-of-function mutations it has been proposed that vertebrate Notch promotes the glial fate. We show in vivo that glial cells are produced at the expense of neurons in the peripheral nervous system of flies lacking Notch and that constitutively activated Notch produces the opposite phenotype. Notch acts as a genetic switch between neuronal and glial fates by negatively regulating glial cell deficient/glial cells missing, the gene required in the glial precursor to induce gliogenesis. Moreover, Notch represses neurogenesis or gliogenesis, depending on the sensory organ type. Numb, which is asymmetrically localized in the multipotent cell that produces the glial precursor, induces glial cells at the expense of neurons. Thus, a cell-autonomous mechanism inhibits Notch signaling.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Differentiation
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Cell Lineage
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DNA-Binding Proteins
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Drosophila Proteins*
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Drosophila melanogaster / embryology
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Gene Expression
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Homeodomain Proteins / genetics
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Juvenile Hormones / genetics
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Membrane Proteins / physiology*
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Mutagenesis
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Neuroglia / cytology*
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Neurons / cytology
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Neurons, Afferent / cytology
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Neuropeptides / genetics
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Peripheral Nervous System / cytology*
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Receptors, Notch
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Signal Transduction / physiology*
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Trans-Activators / genetics
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Transcription Factors
Substances
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DNA-Binding Proteins
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Drosophila Proteins
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GCM protein, Drosophila
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Homeodomain Proteins
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Juvenile Hormones
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Membrane Proteins
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N protein, Drosophila
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Neuropeptides
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Receptors, Notch
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Trans-Activators
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Transcription Factors
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numb protein, Drosophila
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repo protein, Drosophila