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. 2016 Jan 13;44(8):3659–3674. doi: 10.1093/nar/gkv1516

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© The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — UTX resolves the bivalency of many RA-inducible bivalent genes during RA-driven differentiation of mouse ESCs. (A and C) Comparison of average ChIP-Seq reads densities for H3K4me3 and H3K27me3 between RA-treated and untreated WT cells (A) and between RA-treated and untreated Utx-null cells (C). The average values of three biological replicates of the 637 RA-inducible bivalent genes (top), the rest of bivalent genes (middle) and non-bivalent genes (bottom) were plotted from -5K to 5K around the transcription start site (TSS). (B and D) ChIP-Seq enrichment profiles for H3K4me3 (first column) and H3K27me3 (second column) levels and for RA-induced changes in H3K4me3 (third column) and H3K27me3 (fourth column) levels in WT (B) and Utx-null (D) mouse ESCs. (E) Comparison of ChIP-Seq reads densities for H3K4me3 and H3K27me3 between RA-treated and untreated WT cells and between RA-treated and untreated Utx-null cells. The 316 RA-inducible bivalent genes downregulated by UTX loss were used.