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Related Concept Videos

Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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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.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
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Chromatin Structure Regulates pre-mRNA Processing02:41

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In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
The chromatin structure, especially...
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Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
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Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
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Histone Modification02:32

Histone Modification

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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.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
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Nucleosome Remodeling02:54

Nucleosome Remodeling

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Related Experiment Video

Updated: Jun 5, 2025

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark

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Dynamic Regulation OF The Chromatin Environment By Ash1L Modulates Human Neuronal Structure And Function.

Megha Jhanji, Joseph A Ward, Calvin S Leung

    Biorxiv : the Preprint Server for Biology
    |December 16, 2024
    PubMed
    Summary

    The histone methyltransferase ASH1L is crucial for brain development. Its dysfunction causes reduced neurite outgrowth and gene dysregulation, offering insights into neuropsychiatric disorders and potential therapies.

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    Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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    Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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    Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

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    Area of Science:

    • Neuroscience
    • Epigenetics
    • Molecular Biology

    Background:

    • Precise chromatin regulation via histone modifications is vital for brain development and function.
    • Mutations in histone-modifying enzymes are linked to complex brain disorders.
    • The histone methyltransferase ASH1L, implicated in neuropsychiatric disorders, has underexplored pathobiology.

    Purpose of the Study:

    • To investigate the role of ASH1L in human neuronal development and its link to neuropsychiatric diseases.
    • To elucidate the molecular mechanisms underlying ASH1L-associated pathobiology.
    • To identify potential therapeutic strategies for ASH1L-related disorders.

    Main Methods:

    • Generation of human isogenic stem cells with a mutation in ASH1L's catalytic domain.
    • Analysis of chromatin profiles, including activating and repressive histone marks.
    • Assessment of gene expression patterns related to neuronal structure and function.
    • Identification of regulatory networks involving transcription factors and ASH1L.
    • Rescue of cellular defects using epigenetic mechanisms promoting transcriptional activation.

    Main Results:

    • ASH1L dysfunction leads to reduced neurite outgrowth in human stem cells.
    • Altered chromatin marks and dysregulated gene programs associated with neuronal function were observed.
    • A novel regulatory axis involving SP and Krüppel-like transcription factors and ASH1L was identified.
    • Cellular defects were rescued by promoting transcriptional activation through epigenetic mechanisms.

    Conclusions:

    • ASH1L plays an essential role in human brain development through an epigenetic and transcriptional axis.
    • ASH1L dysfunction contributes to the pathobiology of complex brain disorders.
    • The findings provide insights into potential therapeutic strategies for ASH1L-related neuropsychiatric disorders.