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. 2021 Jun 4;28(11):3161–3175. doi: 10.1038/s41418-021-00808-w

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© The Author(s) 2021

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. 7 — A Principal component analysis demonstrating the separation of IBD patients (n = 30) displaying low (in blue) or high (in red) expression of RNF20/40-regulated genes detected by mRNA-seq in murine IECs. B Heatmap displaying the expression of genes differentially marked with H3K27ac between a subset of IBD patients with markedly low (n = 5) or high (n = 4) expression of RNF20/40-dependent genes. C Venn diagram showing the overlap between genes differentially bound by H3K27ac in IBD patients showing low or high expression of RNF20/40-regulated genes and genes which have lost H3K4me3 occupancy in Rnf20/40^fl/fl IECs. D Example occupancy profiles of H3K27ac on VDR, ABCB1, and TSPAN3 revealed decreased H3K27ac occupancy in enhancer and promoter regions in IBD patients with low (blue) compared to high (red) expression of RNF20/40-dependent genes.