Abstract
A major unsolved question in cortical development is how proliferation, neurogenesis, regional growth, regional identity, and laminar fate specification are coordinated. Here we provide evidence, using loss-of-function and gain-of-function manipulations, that the COUP-TFI orphan nuclear receptor promotes ventral cortical fate, promotes cell cycle exit and neural differentiation, regulates the balance of early- and late-born neurons, and regulates the balanced production of different types of layer V cortical projection neurons. We suggest that COUP-TFI controls these processes by repressing Mapk/Erk, Akt, and beta-catenin signaling.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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COUP Transcription Factor I / genetics*
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COUP Transcription Factor I / metabolism*
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Cell Division / physiology
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Female
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MAP Kinase Signaling System / physiology*
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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, Transgenic
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Mitogen-Activated Protein Kinases / metabolism
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Neocortex / cytology
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Neocortex / embryology*
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Neocortex / physiology*
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Neurons / cytology
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Neurons / physiology
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Phosphatidylinositol 3-Kinases / metabolism
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Proto-Oncogene Proteins c-akt / metabolism
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Stem Cells / cytology
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Stem Cells / physiology
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beta Catenin / metabolism*
Substances
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COUP Transcription Factor I
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CTNNB1 protein, mouse
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beta Catenin
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Phosphatidylinositol 3-Kinases
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Proto-Oncogene Proteins c-akt
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Extracellular Signal-Regulated MAP Kinases
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Mitogen-Activated Protein Kinases