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The CRISPR-Cas system serves as a bacterial defense mechanism against invading genetic elements such as viruses and plasmids, forming the foundation for its adaptation as a powerful genome-editing tool. Originally discovered in prokaryotes, this system has been repurposed to revolutionize genetic engineering across a wide range of organisms, including plants, animals, and humans. The core component, Cas9, is an endonuclease derived from Streptococcus pyogenes, capable of introducing...
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Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced...
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CRISPR-Mediated Reorganization of Chromatin Loop Structure
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Cas9 Functionally Opens Chromatin.

Amira A Barkal1,2, Sharanya Srinivasan1,2, Tatsunori Hashimoto2

  • 1Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.

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|April 1, 2016
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Summary
This summary is machine-generated.

The Cas9 gene editing tool can be repurposed to increase accessibility in the genome, enabling transcription factor binding and gene activation at previously inaccessible sites.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Epigenetics

Background:

  • The Cas9 system is primarily known for its gene editing capabilities.
  • Understanding how to control chromatin accessibility is crucial for regulating gene expression.

Purpose of the Study:

  • To investigate the potential of a nuclease-dead Cas9 mutant to alter chromatin accessibility.
  • To determine if Cas9-induced chromatin opening can facilitate transcription factor binding and gene activation.

Main Methods:

  • Utilized a nuclease-dead Cas9 mutant.
  • Assessed chromatin accessibility at genomic loci.
  • Examined transcription factor binding and activation using retinoic acid receptor.

Main Results:

  • Cas9 reproducibly induced chromatin accessibility at previously inaccessible genomic loci.
  • Cas9-mediated chromatin opening was sufficient to allow binding of the retinoic acid receptor to previously unbound motifs.
  • This led to transcriptional activation adjacent to the Cas9 binding site.

Conclusions:

  • A nuclease-dead Cas9 mutant can be used to enhance local chromatin accessibility.
  • This method provides a novel way to control transcription factor binding and alter gene transcription.