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. 2019 Jan 21;10:348. doi: 10.1038/s41467-018-08255-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — BAP1.com is dispensable for Polycomb-mediated silencing. a Western blot analysis of EZH2 and RING1B in wild-type (WT), RING1B KO, and EZH2 KO cells. Lamin B1 is used as a loading control. A two-point titration (1:2 ratio) is shown for each condition. b PCA analysis of WT, RING1B, EZH2, ASXL1, ASXL2, and BAP1 KO transcriptome. c Venn diagram showing the overlap between genes upregulated in BAP1, EZH2, or RING1B KO cells. d Heatmaps showing H2AK119ub1, H3K27me3, and H3K4me3 distribution in a −5/ + 5 kb window around the transcription start site (TSS) of genes upregulated in BAP1 KO cells in wild-type and BAP1 KO cells. Corresponding average profiles are plotted on top of each heatmap. e, f Correlation heatmap of H3K27me3 (e) and H2AK119ub1 (f) distribution between wild-type cells and the different KO conditions indicated. g Plots showing average enrichment of H2AK119ub1 and H3K27me3 in wild-type and BAP1 KO cells at regions that gain H2AK119ub1 upon BAP1 loss