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. 2018 Nov 19;9:4877. doi: 10.1038/s41467-018-07307-6

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© The Author(s) 2018

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. 9 — Chromatin accessibility in CPCs is shaped by Isl1. a Number of differential chromatin accessibility peaks (log2(FC) > 2, false discovery rate [FDR] < 0.05). b Genome-wide distribution of differential open chromatin peaks grouped by K-means (left), and by distance to promoter and K-means (right). Each row represents one differential peak, normalized to sequencing depth, in sequential comparisons (log2[FC] > 2, FDR < 0.05). c Number of differential peaks and their distance to the nearest promoters. d Boxplots of mRNA expression levels in E8.5 and 9.5 Isl1⁺ CPCs, and of genes that are more accessible (left) or more closed (right) in Isl1 KO cells. Box lines show the median, 25th and 75th percentiles; whiskers represent 5th and 95th percentiles; dots represent outlier data points. p-values were calculated using Student’s t-test. n indicates the genes numbers. e Bubble chart showing the enrichment of transcription factor motifs in differential peaks (p-values were calculated from the hypergeometric distribution)