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. 2023 Jun 15;24(7):1188–1199. doi: 10.1038/s41590-023-01528-8

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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. 1 — a. Plot of WT microglia enhancers ranked by normalized H3K27ac tag count. Dotted line represents the cutoff for an enhancer to be considered a super-enhancer. b. Genome browser of the human SALL1 super-enhancer with H3K27ac ChIP, ATAC, and PU.1 ChIP. Regions conserved with the mouse Sall1 super-enhancer Region A and Region C are marked above the H3K27ac. Conserved TF binding sites are annotated in the region homologous to mouse Region C. c. Genome browser of the mouse Sall1 super-enhancer and the overlap of mouse H3K27ac in microglia and embryonic/early postnatal kidney. d. Genome browser showing input DNA from microglia and the Sall1 SE deletion (n = 4–6 mice/geno- type over > 3 experiments). Primers used for genotyping are marked below, and results from geno- typing are shown on the right. Genotyping was performed for all mice utilized in this study (>40 mice over >12 experiments).