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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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Heterochromatin02:38

Heterochromatin

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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.
Constitutive heterochromatin: It is a highly compact region of chromatin that is mostly concentrated in the centromere and telomere. Unlike euchromatin, the amino acid at...
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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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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.
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Co-activators and Co-repressors02:04

Co-activators and Co-repressors

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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Chromatin Position Affects Gene Expression02:35

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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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Related Experiment Video

Updated: Jun 14, 2025

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin.

Elena Grossi1,2,3, Christie B Nguyen1,2,3,4, Saul Carcamo3,5

  • 1Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Biorxiv : the Preprint Server for Biology
|September 4, 2024
PubMed
Summary

The Polybromo-associated BAF (PBAF) chromatin remodeler complex helps silence neuronal genes in melanoma. Loss of ARID2 disrupts PBAF, leading to increased expression of these genes in patients.

Keywords:
ARID2PBAFRESTSWI/SNFmelanoma

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Area of Science:

  • Chromatin biology
  • Cancer epigenetics
  • Molecular mechanisms of gene regulation

Background:

  • SWI/SNF chromatin remodelers exist in distinct complexes with varied functions.
  • Mutations in SWI/SNF subunits, like ARID2 in melanoma, alter chromatin accessibility.
  • The interplay between PBAF, PRC2, and transcription factors in cancer is not fully understood.

Purpose of the Study:

  • To investigate the role of PBAF complexes in melanoma epigenomics.
  • To understand how ARID2 mutations affect chromatin states and gene expression in melanoma.
  • To elucidate the functional relationship between PBAF, PRC2, and the REST transcription factor.

Main Methods:

  • Comprehensive epigenomic profiling of SWI/SNF complexes in melanoma and melanocytes.
  • Time-resolved assays to assess chromatin remodeling sensitivity.
  • Analysis of transcription factor binding (REST) at PBAF-occupied regions.
  • Correlation of gene expression signatures with ARID2 mutation status in patient cohorts.

Main Results:

  • Identified PBAF-exclusive regions co-localized with PRC2 and repressive chromatin.
  • PBAF-bound regions exhibit lower sensitivity to ATPase-mediated remodeling compared to BAF sites.
  • PBAF/PRC2-bound loci are enriched for the repressive transcription factor REST.
  • ARID2 loss disrupts PBAF, impairing REST binding and leading to upregulation of synaptic/neuronal genes.
  • This gene signature is conserved in melanoma patients with ARID2 mutations.

Conclusions:

  • PBAF plays a unique role in facilitating REST accessibility at repressed chromatin.
  • ARID2 mutations in melanoma disrupt PBAF function, leading to aberrant gene expression.
  • These findings highlight a novel epigenetic mechanism in melanoma pathogenesis with potential therapeutic implications.