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. 2021 Jun 7;12:3337. doi: 10.1038/s41467-021-23630-x

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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. 8 — SPFs engage their target sequences in closed chromatin and in the presence of DNA methylation. Upon binding, most SPFs drive DNA demethylation through active processes, mainly mediated by the TET enzymes, while SOX2 leads to passive DNA demethylation. Loss of DNA methylation allows the binding of methylation-sensitive PFs. Nucleosome remodelling and deposition of histone modifications associated with open chromatin regions, mediated by both SPFs and PFs, create a favourable environment for the binding of settler TFs.