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Related Concept Videos

Epigenetic Regulation01:46

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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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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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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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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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.
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Related Experiment Video

Updated: May 5, 2026

Detection of Modified Forms of Cytosine Using Sensitive Immunohistochemistry
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DNA demethylation dynamics.

Nidhi Bhutani1, David M Burns, Helen M Blau

  • 1Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5175, USA.

Cell
|September 20, 2011
PubMed
Summary
This summary is machine-generated.

DNA demethylation, initially thought simple, involves complex active and passive mechanisms by TET and AID/APOBEC enzymes. This dynamic DNA methylation process in mammals relies on DNA repair pathways for regulation.

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Related Experiment Videos

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Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Genetics

Background:

  • Cytosine hydroxymethylation (5hmC) was initially proposed as a straightforward DNA demethylation pathway.
  • Early understanding suggested a simple mechanism for gene activation via DNA demethylation.

Purpose of the Study:

  • To elucidate the complex mechanisms of DNA demethylation.
  • To investigate the roles of TET and AID/APOBEC enzymes in DNA methylation dynamics.
  • To understand the regulatory processes governing DNA methylation in mammalian cells.

Main Methods:

  • Investigated passive and active DNA demethylation pathways.
  • Focused on the enzymatic activities of ten-eleven translocation (TET) family enzymes.
  • Examined the functions of AID/APOBEC family enzymes in DNA modification.

Main Results:

  • DNA demethylation involves intricate active and passive mechanisms.
  • TET and AID/APOBEC enzymes play crucial roles in active DNA demethylation.
  • DNA repair pathways are integral to cytosine methylation removal in mammalian cells.

Conclusions:

  • DNA methylation is a dynamic, not a fixed, epigenetic mark.
  • Continuous regulation of DNA methylation is essential in specific cellular contexts.
  • The interplay between DNA methylation, demethylation, and repair highlights epigenetic plasticity.