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Intermediate DNA methylation is a conserved signature of genome regulation

Author

Listed:
  • GiNell Elliott

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Chibo Hong

    (Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)

  • Xiaoyun Xing

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Xin Zhou

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Daofeng Li

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Cristian Coarfa

    (Baylor College of Medicine)

  • Robert J.A. Bell

    (Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco
    Institute for Human Genetics, University of California San Francisco,)

  • Cecile L. Maire

    (Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute)

  • Keith L. Ligon

    (Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute)

  • Mahvash Sigaroudinia

    (Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)

  • Philippe Gascard

    (Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)

  • Thea D. Tlsty

    (Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)

  • R. Alan Harris

    (Baylor College of Medicine)

  • Leonard C. Schalkwyk

    (School of Biological Sciences, University of Essex)

  • Misha Bilenky

    (Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency)

  • Jonathan Mill

    (Social Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, King’s College London
    University of Exeter Medical School, Exeter University, St Luke's Campus)

  • Peggy J. Farnham

    (University of California-Davis)

  • Manolis Kellis

    (The Broad Institute of MIT and Harvard)

  • Marco A. Marra

    (Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency)

  • Aleksandar Milosavljevic

    (Baylor College of Medicine)

  • Martin Hirst

    (Canada's Michael Smith Genome Sciences Centre, BC Cancer Agency
    University of British Columbia)

  • Gary D. Stormo

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Ting Wang

    (Center for Genome Sciences and Systems Biology, Washington University School of Medicine)

  • Joseph F. Costello

    (Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco)

Abstract

The role of intermediate methylation states in DNA is unclear. Here, to comprehensively identify regions of intermediate methylation and their quantitative relationship with gene activity, we apply integrative and comparative epigenomics to 25 human primary cell and tissue samples. We report 18,452 intermediate methylation regions located near 36% of genes and enriched at enhancers, exons and DNase I hypersensitivity sites. Intermediate methylation regions average 57% methylation, are predominantly allele-independent and are conserved across individuals and between mouse and human, suggesting a conserved function. These regions have an intermediate level of active chromatin marks and their associated genes have intermediate transcriptional activity. Exonic intermediate methylation correlates with exon inclusion at a level between that of fully methylated and unmethylated exons, highlighting gene context-dependent functions. We conclude that intermediate DNA methylation is a conserved signature of gene regulation and exon usage.

Suggested Citation

  • GiNell Elliott & Chibo Hong & Xiaoyun Xing & Xin Zhou & Daofeng Li & Cristian Coarfa & Robert J.A. Bell & Cecile L. Maire & Keith L. Ligon & Mahvash Sigaroudinia & Philippe Gascard & Thea D. Tlsty & R, 2015. "Intermediate DNA methylation is a conserved signature of genome regulation," Nature Communications, Nature, vol. 6(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7363
    DOI: 10.1038/ncomms7363
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