Abstract
The molecular mechanisms that activate morphogenesis of cerebral cortex are currently the subject of intensive experimental analysis. Transcription factor genes of the homeobox, basic helix-loop-helix (bHLH) and zinc-finger families have recently been shown to have essential roles in this process. However, the actual selector genes activating corticogenesis have not yet been identified. Here we show that high-level expression of at least one functional allele of either of the homeobox genes Emx2 or Pax6 in the dorsal telencephalon is necessary and sufficient to stably activate morphogenesis of cerebral cortex and to repress that of adjacent structures, such as striatum.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alleles
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Animals
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Antigens, Differentiation / biosynthesis
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Antigens, Differentiation / genetics
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Basal Ganglia / abnormalities*
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Basal Ganglia / metabolism
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Basal Ganglia / pathology
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Cell Differentiation
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Cerebral Cortex / abnormalities*
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Cerebral Cortex / metabolism
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Cerebral Cortex / pathology
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Down-Regulation
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Eye Proteins
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Gene Expression Regulation, Developmental
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Homeodomain Proteins / genetics
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Homeodomain Proteins / metabolism*
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Immunohistochemistry
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In Situ Hybridization
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Mice
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Mice, Knockout
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Mice, Mutant Strains
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Morphogenesis
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Nervous System Malformations / embryology*
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Nervous System Malformations / metabolism
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Nervous System Malformations / pathology
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PAX6 Transcription Factor
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Paired Box Transcription Factors
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RNA, Messenger / analysis
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RNA, Messenger / biosynthesis
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Repressor Proteins
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Stem Cells / cytology
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Transcription Factors
Substances
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Antigens, Differentiation
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Eye Proteins
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Homeodomain Proteins
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PAX6 Transcription Factor
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Paired Box Transcription Factors
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Pax6 protein, mouse
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RNA, Messenger
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Repressor Proteins
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Transcription Factors
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empty spiracles homeobox proteins