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. 2020 Oct 14;12:147. doi: 10.1186/s13148-020-00941-2

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Effect of H3S10 phosphorylation on chromatin activity in normal and cancer cells. During interphase, enhancers-associated H3S10ph is involved in transcription activation and histone acetylation. By a ‘phospho-methyl switch’ it modulates epigenetic information coming from methylation of neighboring K9—by affecting H3K9me deposition it shields gene regions from heterochromatin. It also dictates spatiotemporal hierarchy of histone modifications. Deregulation of H3S10ph deposition can lead to cellular transformation via activation of protooncogenes, inhibition of developmental genes by heterochromatin spreading, genome instability caused by abnormal R-loops, and H3S10ph-mediated deregulation of inflammatory cytokines, potentially facilitating immune escape. During cell division H3S10ph is needed for proper chromosome condensation, kinetochore function and chromosome segregation. Deregulation of the deposition of this mark causes genome instability and aneuploidy caused by chromosome lagging or abnormal cytokinesis