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Related Concept Videos

Nucleosome Remodeling02:54

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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 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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Related Experiment Video

Updated: Aug 9, 2025

CD Spectroscopy to Study DNA-Protein Interactions
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Till SMARCA5 loss do nucleosomes part.

Jane Jialu Xu1, Aaron D Viny1

  • 1Columbia Stem Cell Initiative, Columbia University Irving Medical Center, New York, NY, USA; Department of Medicine, Division of Hematology & Oncology, Columbia University Irving Medical Center, New York, NY, USA.

Molecular Cell
|February 22, 2023
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Summary
This summary is machine-generated.

Loss of SMARCA5 in human cells causes CTCF protein to be removed and increases nucleosome repeat length. This occurs without directly affecting gene activity.

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Area of Science:

  • Molecular biology
  • Cell biology
  • Genomics

Background:

  • SMARCA5 is a key component of the SWI/SNF family of chromatin remodelers.
  • Chromatin structure plays a crucial role in regulating gene expression.
  • CTCF is a transcription factor involved in genome organization.

Purpose of the Study:

  • To investigate the functional consequences of acute SMARCA5 loss in human cells.
  • To determine the impact of SMARCA5 depletion on CTCF binding and chromatin structure.
  • To assess the effect of SMARCA5 loss on transcriptional activity.

Main Methods:

  • CRISPR-Cas9 mediated gene editing to deplete SMARCA5.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to analyze CTCF occupancy.
  • Nucleosome spacing assays to measure nucleosome repeat length.
  • RNA sequencing to evaluate transcriptional changes.

Main Results:

  • Acute SMARCA5 loss resulted in the eviction of CTCF binding sites genome-wide.
  • A significant increase in nucleosome repeat length was observed upon SMARCA5 depletion.
  • Despite changes in chromatin structure and CTCF binding, global transcriptional activity remained largely unaffected.

Conclusions:

  • SMARCA5 is essential for maintaining CTCF localization and proper nucleosome organization.
  • The data suggest a regulatory role for SMARCA5 in chromatin architecture independent of direct transcriptional control.
  • These findings provide new insights into the function of chromatin remodelers in genome regulation.