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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. 1 — Atrx deficiency alters the morphology and gene expression profiles of mNPCs. a Western blot demonstrating effective cre-recombinase-mediated Atrx inactivation. p53 levels are also shown (Vinculin loading control). b micrographs showing mNPC morphology at 5 passages following Atrx inactivation (representative of three biological replicates; scale bar 100 µm). c heat map showing differentially expressed genes across isogenic mNPCs (Tp53^+/+ Atrx+ : yellow, Tp53^+/+ Atrx−: green, Tp53^−/− Atrx+ : orange, and Tp53^−/− Atrx-: blue). d, e heat map showing ssGSEA correlations between mNPC expression profiles and transcriptional signatures derived from glioma subtypes (d) and mature murine nervous system constituents (e). Glioma subtypes exhibiting high rates of ATRX deficiency shown in red. EPL early progenitor-like, PG pre-glioblastoma, Oligo oligodendrocyte, Astro astrocyte, OPC oligodendroglial precursor cell, Astro (cult) cultured astrocyte