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CRISPR-Mediated Reorganization of Chromatin Loop Structure
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Chromatin features constrain structural variation across evolutionary timescales.

Geoff Fudenberg1, Katherine S Pollard1,2,3,4,5,6

  • 1Gladstone Institute of Data Science and Biotechnology, San Francisco, CA 94158; geoff.fudenberg@gladstone.ucsf.edu katherine.pollard@gladstone.ucsf.edu.

Proceedings of the National Academy of Sciences of the United States of America
|January 20, 2019
PubMed
Summary
This summary is machine-generated.

Structural variants impacting topological domains (TADs) can cause disease by enhancer hijacking. Our study shows chromatin structure constrains these variants in healthy individuals, but not in those with developmental delay.

Keywords:
CTCFHi-Cchromatincomparative genomicsevolution

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Area of Science:

  • Genomics
  • Developmental Biology
  • Cancer Research

Background:

  • Structural variants (SVs) can alter gene function through coding sequence changes or by affecting noncoding regulatory elements and chromatin structure.
  • Topological domains (TADs) are crucial for genome organization, and their boundaries can insulate regulatory elements.
  • Disruption of TAD boundaries by SVs has been linked to developmental diseases and cancer, potentially through enhancer hijacking.

Purpose of the Study:

  • To investigate the role of the chromatin landscape in constraining structural variation.
  • To test the hypothesis that TAD boundaries are under negative selection due to their functional importance.
  • To explore the prevalence and distribution of SVs in patients with developmental delay.

Main Methods:

  • Comparative genomics analysis across human and primate genomes.
  • Analysis of structural variant distribution in relation to chromatin features.
  • Examination of SV patterns in a cohort of patients with developmental delay.

Main Results:

  • The chromatin landscape significantly constrains the occurrence of structural variants in healthy humans and across primate evolution.
  • Evidence suggests negative selection acts on structural variants, particularly near TAD boundaries.
  • In contrast, patients with developmental delay exhibit a uniform distribution of variants across genomic features, irrespective of chromatin structure.

Conclusions:

  • Chromatin architecture plays a critical role in maintaining genome stability by limiting structural variation.
  • The disruption of TAD boundaries and subsequent enhancer hijacking may be a significant mechanism in human developmental diseases.
  • The uniform distribution of variants in developmental delay patients suggests a broader impact of enhancer hijacking in disease pathogenesis.