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. 2021 Jan 12;12:315. doi: 10.1038/s41467-020-20614-1

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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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Fig. 1 — a PCA analysis of WT, bmi1abc, clf28swn7, emf1-2, lhp1, and ring1ab ATAC-seq replicates at 10 DAG. b Average signal levels at the center of consensus THSs in WT, bmi1abc, clf28swn7, emf1-2, lhp1, and ring1ab mutants. c Distribution of consensus THSs relative to TSS. The percentage of THSs found in different intervals is indicated in different colors. d Average accessibility profile of coding genes at the region surrounding the TSS in WT and mutants. e Average signal levels at the center of WT THSs in WT, bmi1abc, clf28swn7, emf1-2, lhp1, and ring1ab mutants. f Screenshot showing distribution of genotype-specific THSs, consensus THSs, and TFs binding sites (see also Supplementary Data 2). Each genotype is indicated in different color (WT in blue, bmi1abc in red, clf28swn7 in green, emf1-2 in black, ring1ab in pink, and lhp1 in orange). Consensus THSs are indicated in magenta. Gene regions are indicated in dark blue and the binding sites of TFs in greenish blue.