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. 2019 Nov 11;10:5116. doi: 10.1038/s41467-019-13060-1

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© This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 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. 9 — Identification of potential direct target genes for RUNX1 and/or FOXL2. a Pie-chart identifying the genes significantly changed in XX Runx1/Foxl2 DKO gonads that are nearest to peaks for FOXL2 and/or RUNX1. Genome browser view of two key genes significantly changed in XX Runx1/Foxl2 DKO gonads and bound by RUNX1 and FOXL2 in E14.5 ovaries. Blue arrows: gene orientation; orange highlighted area: significant binding peaks identified by HOMER. b–d Examples of genes affected in XX Runx1/Foxl2 DKO gonads and bound by FOXL2 or/and RUNX1. For each gene, we show the genome browser view of RUNX1 and/or FOXL2 binding in E14.5 ovaries, the gene expression by quantitative PCR in XX Runx1/Foxl2 single and double knockouts gonads at E15.5 (n = 4/genotype; mean ± SEM; one-way ANOVA, p < 0.05.; bars with different letters (a, b) are significantly different) and the gene expression in fetal Sertoli and granulosa cells from E11.5 to E13.5⁴⁰. Source data are provided as a Source Data file