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. 2018 Mar 13;9:1057. doi: 10.1038/s41467-018-03476-6

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© The Author(s) 2018, corrected publication 2022

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 — Atrx-dependent epigenetic and transcriptional alterations correlate with H3.3 composition. a, b H3.3 ChIP qPCR from Atrx-bound genomic loci approximating Gna13 and Gfap reveals differential enrichment between Atrx+ and Atrx- mNPCs at many points. Positioning of loci subjected to qPCR relative to Atrx binding peaks and open reading frames (Gna13 and Gfap) is also shown (left panels). c sample trace showing relationship of Atrx ChIP-seq peaks (black) to sites of significantly differential H3.3 composition (ΔH3.3) arising with Atrx deficiency (red). d H3.3 ChIP qPCR from Atrx-bound genomic loci approximating GNA13 reveals differential enrichment between ATRX+ (TS 603) and ATRX- (GS 5-22) human GSCs (right panels; *P < 0.05; **P < 0.001; ***P < 0.0001. In all cases, error bars reflect standard deviation and P values determined by unpaired two-tailed t-test