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. 2021 Jul 16;12:4359. doi: 10.1038/s41467-021-24532-8

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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. 4 — a MA plots depicting changes in gene expression in compound H3K9 KMT mutants relative to WT, as determined by RNA sequencing (RNA-seq). From left to right: E1 S1S2, E1E2 G9Gl, and 6KO1. Black dots represent genes whose changes in expression are not statistically significant. Yellow dots represent upregulated genes, and blue dots downregulated genes. b Ingenuity pathway analysis (IPA) of genes differentially expressed in compound H3K9 KMT mutants relative to WT. From left to right: E1 S1S2, E1E2 G9Gl, and 6KO1. The x axis indicates fold change, and the color code indicate the z score for each category (legend on the right). Orange indicates upregulation, and purple downregulation of the pathway. Pathways related to pattern-recognition receptors, interferon signaling, MAP kinase signaling, or cell cycle regulation are highlighted by symbols as indicated below the table. c Genome browser tracks showing RNA expression levels (top) or ATAC accessibility (bottom) of example genes in compound H3K9 KMT mutants. From left to right, Toll-like receptor 3 (Tlr3), interferon regulatory factor 7 (Irf7), cyclin-dependent kinase inhibitor 1 A (Cdkn1a), and cyclin-dependent kinase 1 (Cdk1). For both RNA-seq and ATAC-seq tracks, the top profile corresponds to WT, followed from top to bottom by E1 S1S2, E1E2 G9Gl, and 6KO1 mutants.