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Related Concept Videos

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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Chromatin Modification in iPS Cells01:32

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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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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.
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Histone Modification02:32

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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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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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Position-effect Variegation02:32

Position-effect Variegation

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In 1928, a German botanist Emil Heitz observed the moss nuclei with a DNA binding dye. He observed that while some chromatin regions decondense and spread out in the interphase nucleus, others do not. He termed them euchromatin and heterochromatin, respectively. He proposed that the heterochromatin regions reflect a functionally inactive state of the genome. It was later confirmed that heterochromatin is transcriptionally repressed, and euchromatin is transcriptionally active chromatin.
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Updated: Oct 8, 2025

Lentiviral Vector Platform for the Efficient Delivery of Epigenome-editing Tools into Human Induced Pluripotent Stem Cell-derived Disease Models
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Epigenomic Remodeling in Huntington's Disease-Master or Servant?

Geraldine Zimmer-Bensch1

  • 1Division of Functional Epigenetics in the Animal Model, Institute for Biology II, RWTH Aachen University, Worringerweg 3, 52074 Aachen, Germany.

Epigenomes
|December 30, 2021
PubMed
Summary

Huntington's disease (HD) is a fatal neurodegenerative disorder caused by genetic mutations. Epigenetic changes, influenced by environment, are increasingly recognized as key factors in HD pathogenesis, offering potential therapeutic targets.

Keywords:
DNA methylationDNMT1HTTMeCP2PCR2RESThistone modificationshistone variantstranscriptional dysregulation

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Area of Science:

  • Neuroscience
  • Genetics
  • Epigenetics

Background:

  • Neurodegenerative disorders pose a growing challenge due to aging populations.
  • Huntington's disease (HD) is an incurable, hereditary neurodegenerative disorder.
  • HD results from CAG trinucleotide repeat expansion in the huntingtin gene.

Purpose of the Study:

  • To explore the role of epigenetic mechanisms in Huntington's disease pathogenesis.
  • To discuss how environmental factors influence HD through epigenetics.
  • To identify potential therapeutic strategies based on epigenetic modifications in HD.

Main Methods:

  • Review of existing literature on HD genetics and epigenetics.
  • Analysis of epigenomic remodeling in HD patients and animal models.
  • Examination of epigenetic signatures like DNA methylation and histone modifications.

Main Results:

  • Dynamic epigenomic remodeling is evident in HD.
  • Epigenetic signatures influence gene expression and neuronal function in HD.
  • Environmental factors may impact HD risk and progression via epigenetic pathways.

Conclusions:

  • Epigenetic mechanisms are critically involved in Huntington's disease pathogenesis.
  • Understanding these epigenetic alterations may lead to novel therapeutic approaches for HD.
  • Targeting epigenetic modifications presents a promising avenue for future HD treatments.