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Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions that take up more dye are called heterochromatin. Heterochromatin is further classified into two forms – constitutive heterochromatin and facultative heterochromatin.
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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 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.
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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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  11. The Chromatin Remodeler Dek Promotes Proliferation Of Mammary Epithelium And Is Associated With H3k27me3 Epigenetic Modifications

The chromatin remodeler DEK promotes proliferation of mammary epithelium and is associated with H3K27me3 epigenetic modifications

Megan Johnstone, Ashley Leck, Taylor Lange

    Biorxiv : the Preprint Server for Biology
    |September 24, 2024

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    View abstract on PubMed

    Summary
    This summary is machine-generated.

    The DEK protein promotes mammary epithelial cell proliferation by regulating the cell cycle. It also plays a novel role in mammary gland development and histone methylation.

    Area of Science:

    • * Molecular Biology
    • * Developmental Biology
    • * Epigenetics

    Background:

    • * The DEK chromatin remodeling protein is known to drive oncogenic phenotypes in mammary epithelial cells.
    • * Its specific function in normal mammary gland development was previously uncharacterized.
    • * Understanding DEK's role in normal tissue is crucial for its broader biological implications.

    Purpose of the Study:

    • * To investigate the function of the DEK protein in normal mammary gland biology *in vivo*.
    • * To elucidate the molecular mechanisms underlying DEK's effects on mammary epithelial cells.
    • * To explore DEK's role in mammary gland development, stem cell function, and epigenetic regulation.

    Main Methods:

    • * Development of novel mouse models for mammary gland-specific DEK overexpression and knockout.

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  • * Analysis of mammary gland phenotypes, including cell proliferation and alveolar development.
  • * Transcriptional profiling and single-cell RNA-sequencing analysis.
  • * Investigation of DEK's interaction with Ezh2 and its impact on histone H3 trimethylation (H3K27me3).

    • Main Results:

    • * DEK overexpression led to mammary epithelial cell hyperproliferation and altered gene expression related to cell cycle and stem/progenitor functions.
    • * DEK knockout mice displayed significant defects in alveologenesis and lactation, impacting pup survival.
    • * *Dek* expression is highest in mammary stem and alveolar progenitor cells.
    • * DEK was identified as a modifier of Ezh2 activity, influencing H3K27me3 levels and gene transcription.

    Conclusions:

    • * DEK promotes mammary epithelial cell proliferation through cell cycle deregulation.
    • * DEK plays a critical role in normal mammary gland alveologenesis and lactation.
    • * DEK functions in epigenetic regulation by modulating histone H3 K27 trimethylation.