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. 2021 Jun 7;53(7):1075–1087. doi: 10.1038/s41588-021-00878-z

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© The Author(s) 2021

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. 7 — a, RPB1 ChIP-seq signal across genes normalized to spike-in K562. b, RPB1 ChIP-seq signal across human genes in spike-in K562 cells. For a & b, Wild type (wt), morpholino control (ctrl), rpb1 morpholino knock-down (rpb1 kd), rpb1 rescue (rpb1 rsc), all experiments were conducted in two biological replicates. c, Effect of transcription inhibition on embryo development. Transcription inhibition with α-amanitin was repeated for at least two times with similar results. d, Arrowhead corner score distribution. e, TAD size distribution. f, Percentage of genome folds in TADs.