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. 2023 Dec 8;24:284. doi: 10.1186/s13059-023-03122-5

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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 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. 3 — PML and H3.3 profiles in H3.3 K27M mutant patient-derived glioma cells. Immunofluorescence of A PML (red) and DAXX (green) and B PML (red) and ATRX (green), in H3.3 K27M in the DIPG XIII patient-derived glioma cell line compared to an H3.3 WT (K27M KO) isogenic control. Scale bar 2 µM. C PML-NBs per cell in H3.3 K27M and H3.3 WT (K27M KO) DIPG XIII cells (n = 103). P-values were calculated using two-tailed Student’s t test (*P < 0.0001). 25th, median, and 75th percentiles are shown. D ChIP-seq read count density heatmaps (normalized for total read counts) of H3.3 ChIP-seq at TSS ± 3 kb in H3.3 WT (K27M KO) and H3.3 K27M DIPG XIII cells. E ChIP-seq read counts at H3K27ac enriched promoters (TSS ± 1 kb) in H3.3 WT (K27M KO) and H3.3 K27M DIPG XIII cells (n = 5108). P-values were calculated using two-tailed Student’s t test (*P < 0.0001). 25th, median, and 75th percentiles are shown. F Composite profile of H3.3 at H3K27ac enriched promoters, centered on transcriptional start sites in H3.3 K27M DIPG XIII glioma cells compared to H3.3 WT (K27M KO) isogenic control. G Representative UCSC genome browser profile of H3.3 ChIP-seq in H3.3 K27M DIPG XIII and H3.3 WT (K27M KO) isogenic control (Ak3; hg38; chr9:4,635,308 – 4,827,283). H–N Experiments repeated across an independent (BT245) H3.3 K27M patient-derived glioma cell line. H Immunofluorescence of PML (red) and DAXX (green) and I PML (red) and ATRX (green), in H3.3 K27M BT245 cells compared to an H3.3 WT (K27M KO) isogenic control. Scale bar 2 µM. J PML-NBs per cell in H3.3 K27M BT245 and H3.3 WT (K27M KO) cells (n = 53). P-values were calculated using two-tailed Student’s t test (*P < 0.0001). K ChIP-seq read count density heatmaps of H3.3 ChIP-seq at TSS ± 3 kb in H3.3 WT (K27M KO) and H3.3 K27M BT245 cells. L ChIP-seq read counts at H3K27ac enriched promoters (TSS ± 1 kb) in H3.3 WT (K27M KO) and H3.3 K27M BT245 cells. P-values were calculated using two-tailed Student’s t test (*P < 0.0001). 25th, median, and 75th percentiles are shown. M Composite profile of H3.3 at promoters, centered on transcriptional start sites in H3.3 K27M BT245 ells compared to H3.3 WT (K27M KO) isogenic control. N Representative UCSC genome browser profile of H3.3 ChIP-seq in H3.3 K27M BT245 and H3.3 WT (K27M KO) isogenic control. Rims2; hg38; chr8:103,455,749 – 103,545,748