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Related Concept Videos

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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Related Experiment Video

Updated: Jan 13, 2026

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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Histone Demethylase KDM6B Promotes Postnatal Oligodendrocyte Development and Cortical Myelination.

Ruth Lambries, Zihan Shen, George I Mias

    Biorxiv : the Preprint Server for Biology
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    The histone demethylase KDM6B is crucial for postnatal cortical myelination. It promotes oligodendrocyte development by regulating the SOX10 gene, essential for brain development and function.

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    Area of Science:

    • Neuroscience
    • Epigenetics
    • Developmental Biology

    Background:

    • Postnatal cortical myelination is vital for proper brain function.
    • Epigenetic regulation, specifically histone modifications, plays a key role in activating oligodendrocyte gene networks necessary for myelination.

    Purpose of the Study:

    • To investigate the role of the histone H3K27me3 demethylase KDM6B in postnatal cortical myelination.
    • To elucidate the molecular mechanisms by which KDM6B influences oligodendrocyte development and myelination.

    Main Methods:

    • Conditional KDM6B deletion (Kdm6b-cKO) in Emx1-expressing progenitors in mice.
    • Lineage-specific RNA-sequencing (RNA-seq) to analyze gene expression.
    • Chromatin immunoprecipitation (ChIP) assays to assess H3K27me3 levels.

    Main Results:

    • Kdm6b deletion resulted in delayed cortical myelination and impaired oligodendrocyte maturation.
    • Reduced expression of the oligodendrocyte master regulator SOX10 and myelination effectors was observed.
    • Increased H3K27me3 at the SOX10 promoter indicated KDM6B's role in de-repression.
    • Partial rescue of myelination was achieved by inducing SOX10 expression.

    Conclusions:

    • KDM6B acts through a KDM6B→SOX10 axis to promote oligodendrocyte development and cortical myelination.
    • KDM6B facilitates myelination by removing repressive H3K27me3 marks and maintaining active chromatin.
    • These findings have implications for understanding KDM6B-related neurodevelopmental disorders.