Research
H2A.Z landscapes and dual modifications in pluripotent and multipotent stem cells underlie complex genome regulatory functions
1 Department of Pathology, Center for Systems Biology and Center for Cancer Research, Massachusetts General Hospital, Simches Research Building, CPZN 8234, Boston, MA 02114, USA
2 Howard Hughes Medical Institute, 4000 Jones Bridge Road, Chevy Chase, MD 20815-6789, USA
3 Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, MA 02142, USA
4 Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
5 Division of Health Sciences and Technology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, E25-519, Cambridge, MA 02139, USA
6 Bioinformatics Program and Department of Biomedical Engineering, Boston University, 24 Cummington Street, Boston, MA 02215, USA
7 RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
Genome Biology 2012, 13:R85 doi:10.1186/gb-2012-13-10-r85
Published: 3 October 2012Additional files
Additional file 1:
Composite plots show H3.3 ChIP-Seq signal enriches at K4me3-only and bivalent promoters (PRC1-positive (+) and PRC1-negative (-)), but is depleted in no-mark promoters in mES cells.
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Additional file 2:
Composite plots show H3 distribution across K4me3-only, bivalent (PRC1-positive and PRC1-negative) or no-mark TSSs (±2.5 kb). Nucleosome-deficient regions are observed at K4me3-only and bivalent promoters, but not at no-mark promoters.
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Additional file 3:
Summary of ChIP-Seq data sets.
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Additional file 4:
Summary of antibody information.
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