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A map of direct TF-DNA interactions in the human genome

View ORCID ProfileMarius Gheorghe, View ORCID ProfileGeir Kjetil Sandve, View ORCID ProfileAziz Khan, Jeanne Chèneby, View ORCID ProfileBenoit Ballester, View ORCID ProfileAnthony Mathelier
doi: https://doi.org/10.1101/394205
Marius Gheorghe
1Centre for Molecular Medicine Norway (NCMM), University of Oslo, Oslo, Norway
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Geir Kjetil Sandve
2Department of Informatics, University of Oslo, Oslo, Norway
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Aziz Khan
1Centre for Molecular Medicine Norway (NCMM), University of Oslo, Oslo, Norway
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Jeanne Chèneby
3Aix-Marseille Université, INSERM, TAGC, UMR_S1090, Marseille, France
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Benoit Ballester
3Aix-Marseille Université, INSERM, TAGC, UMR_S1090, Marseille, France
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Anthony Mathelier
1Centre for Molecular Medicine Norway (NCMM), University of Oslo, Oslo, Norway
4Department of Cancer Genetics, Institute for Cancer Research, Radiumhospitalet, Oslo, Norway
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  • For correspondence: anthony.mathelier@ncmm.uio.no
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ABSTRACT

Chromatin immunoprecipitation followed by sequencing (ChIP-seq) is the most popular assay to identify genomic regions, called ChIP-seq peaks, that are bound in vivo by transcription factors (TFs). These regions are derived from direct TF-DNA interactions, indirect binding of the TF to the DNA (through a co-binding partner), nonspecific binding to the DNA, and noise/bias/artifacts. Delineating the bona fide direct TF-DNA interactions within the ChIP-seq peaks remains challenging. We developed a dedicated software, ChIP-eat, that combines computational TF binding models and ChIP-seq peaks to automatically predict direct TF-DNA interactions. Our work culminated with predicted interactions covering >4% of the human genome, obtained by uniformly processing 1,983 ChIP-seq peak data sets from the ReMap database for 232 unique TFs. The predictions were a posteriori assessed using protein binding microarray and ChIP-exo data, and were predominantly found in high quality ChIP-seq peaks. The set of predicted direct TF-DNA interactions suggested that high-occupancy target regions are likely not derived from direct binding of the TFs to the DNA. Our predictions derived co-binding TFs supported by protein-protein interaction data and defined cis-regulatory modules enriched for disease- and trait-associated SNPs. Finally, we provide this collection of direct TF-DNA interactions and cis-regulatory modules in the human genome through the UniBind web-interface (http://unibind.uio.no).

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license.
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Posted August 17, 2018.
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A map of direct TF-DNA interactions in the human genome
Marius Gheorghe, Geir Kjetil Sandve, Aziz Khan, Jeanne Chèneby, Benoit Ballester, Anthony Mathelier
bioRxiv 394205; doi: https://doi.org/10.1101/394205
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A map of direct TF-DNA interactions in the human genome
Marius Gheorghe, Geir Kjetil Sandve, Aziz Khan, Jeanne Chèneby, Benoit Ballester, Anthony Mathelier
bioRxiv 394205; doi: https://doi.org/10.1101/394205

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