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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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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 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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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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Decoding the function of bivalent chromatin in development and cancer.

Dhirendra Kumar1, Senthilkumar Cinghu1, Andrew J Oldfield1

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Bivalent chromatin, marked by H3K4me3 and H3K27me3, protects genes from DNA methylation, not primes them for rapid activation. Loss of this epigenetic state in cancer increases susceptibility to gene silencing.

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Area of Science:

  • Epigenetics
  • Developmental Biology
  • Cancer Biology

Background:

  • Bivalent chromatin, co-marked by H3K4me3 and H3K27me3, is abundant in embryonic stem cells (ESCs).
  • It is hypothesized to prime developmental genes for rapid activation while maintaining repression.
  • Bivalent promoters are often hypermethylated in human cancers, suggesting a link to aberrant gene silencing.

Purpose of the Study:

  • To investigate the functional role of bivalent chromatin in gene activation and DNA methylation.
  • To test the hypothesis that bivalency poises genes for rapid transcription.
  • To determine if bivalency predisposes genes to aberrant methylation in cancer.

Main Methods:

  • Genome-wide studies in differentiating ESCs.
  • Analysis of histone modifications (H3K4me3, H3K27me3) and DNA methylation.
  • Comparison of gene activation rates between bivalent and other silent genes.
  • Examination of bivalent gene regulation in cancer cell types.

Main Results:

  • Bivalent genes are not activated more rapidly than other silent genes, challenging the role of H3K4me3 in rapid transcription.
  • H3K4me3 at bivalent promoters is stable across cell types and protects against de novo DNA methylation.
  • Loss of H3K4me3/bivalency in cancer correlates with aberrant hypermethylation of previously bivalent genes.
  • Bivalency protects genes from irreversible silencing.

Conclusions:

  • Bivalent chromatin serves to protect genes from aberrant DNA methylation, maintaining epigenetic plasticity.
  • Loss of H3K4me3/bivalency in disease, like cancer, may lead to irreversible gene silencing.
  • The presence of H3K4me3 is not instructive for rapid transcription but rather protective against methylation.