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. 2018 Dec 18;9:5375. doi: 10.1038/s41467-018-07787-6

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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. 8 — Model of SCL’s functions in blood lineage specification. Single mesodermal cells co-express blood (Scl), cardiac (Mesp1) and paraxial (Tbx6)-affiliated transcriptional regulators at low levels, establishing multi-lineage priming and cellular plasticity. As differentiation progresses, Scl levels increase in FLK1⁺PDGFRα^– cells. SCL establishes a global repressive environment by activating potent transcriptional repressors (Rybp/Pcgf5/Eto2) and ensuring genome-wide, high H2AK119Ub levels. This leads to decreased Mesp1 and Tbx6 levels and repression of alternative fates. Activation of blood/endothelial gene expression programmes together with decreased plasticity allows consolidation of the blood fate and specification of the hematopoietic lineage