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CpG island-mediated global gene regulatory modes in mouse embryonic stem cells

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  • Samuel Beck

    (The University of Texas at Austin)

  • Bum-Kyu Lee

    (The University of Texas at Austin)

  • Catherine Rhee

    (The University of Texas at Austin)

  • Jawon Song

    (Texas Advanced Computing Center, The University of Texas at Austin)

  • Andrew J. Woo

    (School of Medicine and Pharmacology, Royal Perth Hospital Unit, The University of Western Australia)

  • Jonghwan Kim

    (The University of Texas at Austin
    Institute for Cellular and Molecular Biology, The University of Texas at Austin
    Center for Systems and Synthetic Biology, The University of Texas at Austin)

Abstract

Both transcriptional and epigenetic regulations are fundamental for the control of eukaryotic gene expression. Here we perform a compendium analysis of >200 large sequencing data sets to elucidate the regulatory logic of global gene expression programs in mouse embryonic stem (ES) cells. We define four major classes of DNA-binding proteins (Core, PRC, MYC and CTCF) based on their target co-occupancy, and discover reciprocal regulation between the MYC and PRC classes for the activity of nearly all genes under the control of the CpG island (CGI)-containing promoters. This CGI-dependent regulatory mode explains the functional segregation between CGI-containing and CGI-less genes during early development. By defining active enhancers based on the co-occupancy of the Core class, we further demonstrate their additive roles in CGI-containing gene expression and cell type-specific roles in CGI-less gene expression. Altogether, our analyses provide novel insights into previously unknown CGI-dependent global gene regulatory modes.

Suggested Citation

  • Samuel Beck & Bum-Kyu Lee & Catherine Rhee & Jawon Song & Andrew J. Woo & Jonghwan Kim, 2014. "CpG island-mediated global gene regulatory modes in mouse embryonic stem cells," Nature Communications, Nature, vol. 5(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6490
    DOI: 10.1038/ncomms6490
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