Published April 12, 2018
| Version v1
Journal article
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Silencing of transposable elements may not be a major driver of regulatory evolution in primate iPSCs
Creators
- 1. University of Chicago
- 2. Imperial College
Description
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 10 human and 7 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 6 million years of primate evolution.
Data availability
The following data sets were generated:
Ward MC (2017) Epigenomic conservation of transposable element silencing Publicly available at the NCBI Gene Expression Omnibus (accession no: GSE96712). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE96712
The following previously published data sets were used:
Rosenbloom (2013) ENCODE data in the UCSC Genome Browser Publicly available at the UCSC Genome Browser. http://hgdownload.cse.ucsc.edu/goldenPath/hg19/database
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Silencing-of-transposable-elements-may-not-be-a-major-driver-of-regulatory-evolution-in-primate-iPSCs.pdf
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Additional details
Identifiers
- DOI
- 10.7554/eLife.33084
- Other
- oai:uchicago.tind.io:5743
Funding
- National Institute of General Medical Sciences
- GM077959
- EMBO Long-Term Fellowship/European Commission Marie Curie Actions
- ALTF 751-2014