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. 2021 May 28;12:3221. doi: 10.1038/s41467-021-23477-2

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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. 5 — a Representation of the chromatin status of H3K18 at the M2M13 locus. Chromatin immunoprecipitation ChIP-Seq analysis of the M2M13 gene in schizont conditions (37 °C) showing H3K18Ac enrichment (blue) on the M2M13 promoter region and H3K18me enrichment (red) on the gene body. b Treatment with the KDMi or KDACi inhibitors impacted the presence of H3K18me1 histone marks on the M2M13 gene. Quantification of the H3K18me1 mark by ChIP-PCR on the M2M13 promoter or gene-body, after treatment with epigenetic inhibitors. c Quantification of H3K18ac mark on the M2M13 gene and promoter following inhibitor treatment. For all experiments n = 3 biologically independent experiments of ChIP qPCR. Error bars represent mean values ± SD. Statistical test Dunnett’s multiple comparison test: ns = not statistically significant p = 0.2979; **p = 0.047; *p = 0.0737.