1. Evolutionary Biology
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Silencing of transposable elements may not be a major driver of regulatory evolution in primate iPSCs

  1. Michelle C Ward  Is a corresponding author
  2. Siming Zhao
  3. Kaixuan Luo
  4. Bryan J Pavlovic
  5. Mohammad M Karimi
  6. Matthew Stephens
  7. Yoav Gilad  Is a corresponding author
  1. University of Chicago, United States
  2. Imperial College London, United Kingdom
Research Article
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Cite this article as: eLife 2018;7:e33084 doi: 10.7554/eLife.33084

Abstract

Transposable elements (TEs) comprise almost half of primate genomes and their aberrant regulation can result in deleterious effects. In pluripotent stem cells, rapidly-evolving KRAB-ZNF genes target TEs for silencing by H3K9me3. To investigate the evolution of TE silencing, we performed H3K9me3 ChIP-seq experiments in induced pluripotent stem cells from ten human and seven chimpanzee individuals. We identified four million orthologous TEs and found the SVA and ERV families to be marked most frequently by H3K9me3. We found little evidence of inter-species differences in TE silencing, with as many as 82% of putatively silenced TEs marked at similar levels in humans and chimpanzees. TEs that are preferentially silenced in one species are a similar age to those silenced in both species, and are not more likely to be associated with expression divergence of nearby orthologous genes. Our data suggest limited species-specificity of TE silencing across six million years of primate evolution.

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Author details

  1. Michelle C Ward

    Department of Human Genetics, University of Chicago, Chicago, United States
    For correspondence
    mcward@uchicago.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-1485-320X
  2. Siming Zhao

    Department of Human Genetics, University of Chicago, Chicago, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Kaixuan Luo

    Department of Human Genetics, University of Chicago, Chicago, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Bryan J Pavlovic

    Department of Human Genetics, University of Chicago, Chicago, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-7751-5315
  5. Mohammad M Karimi

    MRC London Institute of Medical Sciences, Imperial College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  6. Matthew Stephens

    Department of Human Genetics, University of Chicago, Chicago, United States
    Competing interests
    The authors declare that no competing interests exist.
  7. Yoav Gilad

    Department of Human Genetics, University of Chicago, Chicago, United States
    For correspondence
    gilad@uchicago.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8284-8926

Funding

National Institute of General Medical Sciences (GM077959)

  • Yoav Gilad

EMBO Long-Term Fellowship/European Commission Marie Curie Actions (ALTF 751-2014)

  • Michelle C Ward

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Patricia J Wittkopp, University of Michigan, United States

Publication history

  1. Received: October 28, 2017
  2. Accepted: April 11, 2018
  3. Accepted Manuscript published: April 12, 2018 (version 1)
  4. Version of Record published: May 9, 2018 (version 2)

Copyright

© 2018, Ward et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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