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. 2021 Jan 29;12:694. doi: 10.1038/s41467-020-20716-w

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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 Schematic of experimental approach. 5-aza-dC is used to hypomethylate cells and the kinetics of methylation recovery are compared for different CGIs. b H3K36me3 marked CGIs preferentially recover methylation following 5-aza-dC treatment. Boxplots of relative methylation at H3K36me3 marked CGIs (n = 369) and all other CGIs methylated (n = 8285) in HCT116 cells. P-values are from two-sided Wilcoxon rank sum tests. Lines = median; box = 25th–75th percentile; whiskers = 1.5 × interquartile range from box. c The rate of methylation gain is higher at H3K36me3 CGIs in HCT116 cells. Barplot of the median normalised rate of methylation gain for H3K36me3 marked CGIs and other CGIs methylated in HCT116 cells and DNMT KO cells (n = 369, 371 and 284 for K36me3 CGIs and 8285, 8284 and 6519 for other CGIs in HCT116, DNM3B KO and DNMT1 KO, respectively). The rate of methylation recovery was estimated by fitting linear models to the RRBS data for each CGI. P-values are from two-sided Wilcoxon rank sum tests. Source data are provided as a Source Data file.