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. 2019 Nov 27;10:5412. doi: 10.1038/s41467-019-13404-x

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© The Author(s) 2019

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 — Characterization of a CTCF boundary deletion upstream of the α-globin locus. Gene annotation is shown at the top, with the α-globin genes in bold and genes upregulated by the CTCF boundary deletion highlighted in green. Open chromatin (ATAC in WT erythroid cells) is shown below, with the α-globin enhancers highlighted. CTCF occupancy in WT (blue) and D3839 (red) erythroid cells is shown underneath, with the orientation of the CTCF-binding motifs indicated by arrowheads (forward orientation in red; reverse orientation in blue). CTCF-binding sites of interest are highlighted and the deleted CTCF-binding sites are indicated with a black cross. The profiles below show Capture-C interactions from the viewpoint of the R2 enhancer (indicated with a black arrow) in WT (blue) and D3839 (red) erythroid cells, with a differential profile at the bottom. Profiles represent the mean number of normalized unique interaction counts per restriction fragment in n = 3 biological replicates. Coordinates (mm9): chr11:32,070,000–32,250,000.