Abstract
In the developing central nervous system, transcription factors play a crucial role in the regulation of cell fate. Previously we demonstrated that LHX2 is a critical regulator of the neuron-glia cell fate switch in the developing mouse hippocampus. Here, we test LHX2 target gene Pax6 for a role in this process. We report that Pax6 overexpression is able to suppress the enhanced astrogliogenesis arising due to loss of functional LHX2. Furthermore, we show that like Lhx2, Pax6 is also able to suppress induced astrogliogenesis caused by overexpression of progliogenic factor Nfia. This demonstrates that overexpression of Pax6 can substitute for Lhx2 in the regulation of the neuronal versus glial cell fate in the developing hippocampus, and therefore, supports a role for PAX6 as a mediator of LHX2 function in this process.
MeSH terms
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Animals
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Astrocytes / cytology
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Astrocytes / metabolism*
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Cell Differentiation
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Electroporation
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Embryo, Mammalian
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Female
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Gene Expression Regulation, Developmental*
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Hippocampus / cytology
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Hippocampus / metabolism*
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LIM-Homeodomain Proteins / genetics*
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LIM-Homeodomain Proteins / metabolism
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Male
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Mice
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Mice, Transgenic
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NFI Transcription Factors / genetics*
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NFI Transcription Factors / metabolism
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Neural Stem Cells / cytology
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Neural Stem Cells / metabolism
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Neurogenesis / genetics
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Neurons / cytology
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Neurons / metabolism*
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PAX6 Transcription Factor / genetics*
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PAX6 Transcription Factor / metabolism
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Plasmids / chemistry
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Plasmids / metabolism
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Signal Transduction
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Transcription Factors / genetics*
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Transcription Factors / metabolism
Substances
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LIM-Homeodomain Proteins
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Lhx2 protein, mouse
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NFI Transcription Factors
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Nfia protein, mouse
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PAX6 Transcription Factor
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Pax6 protein, mouse
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Transcription Factors