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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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Extended Data Fig. 5 — a, Fraction of reads in peaks (FRiP) as quality control for H3K27me3 ChIP-seq peaks. Fewer reads fall into peaks in MCM2-2A clones compared to WT cells, indicating that peak calling for H3K27me3 is affected in MCM2-2A (n = 2 biological replicates for each clone). b, Density plots (top) showing distribution of H3K27me3 signal in genome-wide 5-kb bins. Two-sided Wilcoxon signed-rank test P values. Bar plots (bottom) showing quantification of bins in the indicated signal categories. Three MCM2-2A clones (left; average of n = 2 biological replicates) and MCM2-R cells (right; average of n = 3 biological replicates) demonstrate similar trends across mutant clones and rescue of signal redistribution upon restoration of symmetric recycling. c, Violin plots showing H3K27me3 signal in bins non-overlapping WT peaks in early, mid-early, mid-late and late replicating regions, related to Fig. 2d. Two-sided Wilcoxon signed-rank test P values. n = 3 biological replicates. d, Violin plot showing H3K27me3 signal in 5 kb bins overlapping WT H3K36me2 peaks. Two-sided Wilcoxon signed-rank test P values. n = 3 biological replicates. e, Violin plot showing H3K27ac signal in 2.5-kb bins overlapping WT H3K36me3 peaks. Two-sided Wilcoxon signed-rank test P values. n = 2 biological replicates. f, Violin plot showing absolute differences in H3K27me3 signal between WT and MCM2-2A in bins of H3K27me3 gains and H3K27me3 losses. Two-sided Wilcoxon signed-rank test P values. n = 3 biological replicates. Related to Fig. 2f. g, Increased SUZ12 binding to chromatin in MCM2-2A cells shown by box plots of mean SUZ12 levels in 1 kb windows of SUZ12 peaks quantified by qChIP-seq. Two-sided Wilcoxon signed-rank test P values. n = 3 biological replicates. c-g, Box plots as in Fig. 2a. h, Venn diagrams illustrating strong overlap of SUZ12 peaks in WT, MCM2-2A#1 and MCM2-2A#2 clones (n = 3 biological replicates). i, Individual SUZ12 SCAR-seq replicates related to Fig. 2j, including two MCM2-2A clones. H3K27me3 SCAR-seq was performed in parallel as control for crosslinked SCAR-seq. SCAR-seq is represented as in Fig. 1.