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. 2023 Feb 27;25(3):493–507. doi: 10.1038/s41556-023-01093-0

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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. 6 — a, Pearson correlation analysis of ATACseq replicates of MED8A cells with SMARCD3 KO vs WT. b, Mean accessibility and enrichment of ATACseq data with different insert lengths around transcription start site (TSS). c, Hi-C chromatin interaction map on a region centered in the Dab1 gene of mouse cerebellum (P22). The dashed lines outline TAD borders. d, Pearson correlation analysis of histone marker binding signals from CUT&RUN replicates of MED8A cells with SMARCD3 KO vs WT. e, Histogram of SMARCD3 mRNA expression (FPKM) in 5 G3 patient samples. Each tumor (T) is marked with higher (H), or lower (L), levels of SMARCD3 expression. f, Histone modification signals at CRE1, CRE3, and CRE4 at the locus of the Dab1 gene based on analyzing ChIPseq data of mouse hindbrain or cerebellum samples. These CREs in the mouse are homologous to the human CREs of the DAB1 gene. g, Histogram of Dab1 mRNA expression (TPM) during mouse cerebellar development at indicated time points.