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Related Concept Videos

Nucleosome Remodeling02:54

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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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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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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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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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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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Chromatin in nervous system development and disease.

Shigeki Iwase1, Donna M Martin2

  • 1Department of Human Genetics, The University of Michigan Medical School, Ann Arbor, MI 48109, United States.

Molecular and Cellular Neurosciences
|December 18, 2017
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Epigenetic factors regulate gene expression in the central nervous system, impacting development and causing disorders like autism and epilepsy. Dysregulation is also linked to brain cancers, highlighting chromatin

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Genetics

Background:

  • Epigenetic regulation is crucial for central nervous system (CNS) development.
  • Pathogenic variants in epigenetic factors are linked to neurodevelopmental disorders (e.g., autism spectrum disorder, intellectual disability, epilepsy).
  • Somatic mutations in epigenetic regulators are observed in brain cancers, suggesting a role in cellular proliferation and differentiation.

Discussion:

  • This special issue reviews recent discoveries on epigenetic modifiers in nervous system development and disease.
  • It explores the mechanisms by which these modifiers function in both normal and pathological states.
  • The articles highlight the connection between chromatin regulation and both development and cancer in the brain.

Key Insights:

  • Epigenetic modifiers play a significant role in the intricate processes of nervous system development.
  • Aberrant epigenetic regulation is a common feature in various neurological disorders and brain cancers.
  • Chromatin regulators are implicated in controlling cellular proliferation and differentiation within the nervous system.

Outlook:

  • Ongoing research continues to uncover the complex roles of epigenetic factors in neurological health and disease.
  • Further investigation into the mechanisms of epigenetic modifiers may reveal novel therapeutic targets for CNS disorders and cancers.
  • This field is rapidly expanding, promising deeper insights into brain function and disease pathogenesis.