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Histone Variants at the Centromere02:30

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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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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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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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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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An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
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Alterations in Chromatin Folding Patterns in Cancer Variant-Enriched Loci.

Alan Perez-Rathke1, Samira Mali1, Lin Du1

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|June 4, 2021
PubMed
Summary
This summary is machine-generated.

Genomic regions with cancer mutations show altered chromatin folding patterns. This study used Hi-C data to compare healthy and cancer cells, finding significant differences in chromatin interactions and A/B compartments.

Keywords:
CancerChromatin foldingHi-CNuclear organization

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Area of Science:

  • Genomics
  • Epigenetics
  • Cancer Biology

Background:

  • Cancer development is linked to genomic alterations.
  • Chromatin folding influences gene regulation and cellular function.
  • Understanding cancer-associated changes in 3D genome organization is crucial.

Purpose of the Study:

  • To investigate whether genomic regions with high cancer variant mutation frequencies exhibit distinct chromatin folding patterns compared to regions without such enrichment.
  • To analyze differences in A/B compartmentalization and physical chromatin interactions between healthy and cancer cells.
  • To statistically evaluate the significance of observed chromatin folding alterations in cancer-associated loci.

Main Methods:

  • Utilized publicly available Hi-C data from healthy (GM12878) and cancer (K562) cell lines.
  • Characterized chromatin folding by assessing A/B compartmentalization status.
  • Analyzed random versus non-random chromatin physical interaction patterns.
  • Performed statistical tests to compare chromatin folding in cancer variant-enriched loci versus non-enriched loci.

Main Results:

  • Significant differences in chromatin folding patterns were observed in loci associated with cancer variants.
  • Statistical analysis revealed significantly altered A/B compartmentalization in cancer-enriched regions (FDR < 0.05).
  • Non-random chromatin physical interactions showed significant changes in cancer variant-enriched loci.

Conclusions:

  • Genomic regions frequently mutated in cancer display significantly altered chromatin folding.
  • Chromatin folding alterations, including A/B compartments and physical interactions, are characteristic of cancer variant-enriched loci.
  • These findings highlight the role of 3D genome organization changes in cancer biology.