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. 2023 Sep 4;55(9):1567–1578. doi: 10.1038/s41588-023-01476-x

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© The Author(s) 2023

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 — H3–H4 asymmetry in MCM2-2A cells creates a lagging strand largely devoid of parental histone PTMs, which affects the accuracy of chromatin restoration and creates a permissive environment for unscheduled expression in every cell cycle. This broadly alters the histone PTM epigenome with both local and global changes in repressive modifications. MCM2-2A cells show loss of H3K9me3-based repeat repression, misregulation of H3K27me3 and bivalent genes, and reduced ESC plasticity and embryonic differentiation. Naïve, naïve pluripotency; primed, lineage-primed states; new histones, green; parental histones, purple.