Abstract
Juxtanodin (JN) is a cytoskeleton-related oligodendrocyte-specific gene, and its underlying mechanism still needs detailed exploration. In this study, we tested whether a 1.9 kb fragment from the 5'-flanking region of JN is sufficient to specifically deliver the gene expression in oligodendrocytes. By reporter assay, we found that the 1.9 kb fragment specifically activated in C6 cells, which is further upregulated by ATRA-induced oligodendrocyte lineage differentiation. Bioinformatics study revealed that Nkx2.2 might be a transcription factor involved in the process. qPCR results showed that ATRA upregulated endogenous expression of Nkx2.2 in C6 cells. Further study revealed that Nkx2.2 could bind JN promoter and its overexpression increase the promoter activity of JN. In summary, our study here suggests that Nkx2.2 is one of the essential transcription factors delivering the specificity of JN promoter in oligodendrocytes.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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COS Cells
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Cell Differentiation / drug effects*
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Cell Differentiation / genetics
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Cell Line
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Chlorocebus aethiops
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Cloning, Molecular
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Gene Expression Regulation / drug effects
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HeLa Cells
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Homeobox Protein Nkx-2.2
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Homeodomain Proteins / metabolism
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Homeodomain Proteins / physiology
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Humans
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Microfilament Proteins / genetics*
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Microfilament Proteins / metabolism
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Molecular Sequence Data
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Nuclear Proteins
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Oligodendroglia / drug effects*
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Oligodendroglia / metabolism*
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Oligodendroglia / physiology
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Promoter Regions, Genetic*
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Rats
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Sequence Analysis
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Transcription Factors / metabolism
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Transcription Factors / physiology
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Transcription, Genetic / genetics*
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Tretinoin / pharmacology*
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Zebrafish Proteins
Substances
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Ermn protein, rat
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Homeobox Protein Nkx-2.2
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Homeodomain Proteins
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Microfilament Proteins
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NKX2-2 protein, human
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Nkx2-2 protein, rat
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Nuclear Proteins
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Transcription Factors
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Zebrafish Proteins
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nkx2.2b protein, zebrafish
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Tretinoin