Abstract
The transcription factor Sox2 is expressed at high levels in neural stem and progenitor cells. Here, we inactivated Sox2 specifically in the developing brain by using Cre-loxP system. Although mutant animals did not survive after birth, analysis of late gestation embryos revealed that loss of Sox2 causes enlargement of the lateral ventricles and a decrease in the number of neurosphere-forming cells. However, although their neurogenic potential is attenuated, Sox2-deficient neural stem cells retain their multipotency and self-renewal capacity. We found that expression level of Sox3 is elevated in Sox2 null developing brain, probably mitigating the effects of loss of Sox2.
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* / genetics
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DNA-Binding Proteins / biosynthesis
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology*
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Embryonic Stem Cells / cytology*
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Embryonic Stem Cells / metabolism
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Gene Silencing
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HMGB Proteins / genetics
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HMGB Proteins / physiology*
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High Mobility Group Proteins / biosynthesis
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Lateral Ventricles / cytology
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Lateral Ventricles / embryology*
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Lateral Ventricles / metabolism
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Mice
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Neurons / cytology*
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Neurons / metabolism
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Receptors, Notch / metabolism
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SOXB1 Transcription Factors
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Signal Transduction / genetics
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Transcription Factors / biosynthesis
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Transcription Factors / genetics
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Transcription Factors / physiology*
Substances
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DNA-Binding Proteins
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HMGB Proteins
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High Mobility Group Proteins
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Receptors, Notch
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SOXB1 Transcription Factors
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Sox2 protein, mouse
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Sox3 protein, mouse
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Transcription Factors