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. 2019 Jul 5;9:9736. doi: 10.1038/s41598-019-45841-5

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© The Author(s) 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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Induction of Etv2 promotes cellular proliferation in EBs. (a–d) FACS analysis (a,c) and quantification (b,d) of EdU-labelled cells from EBs in the absence (−Dox) and presence (+Dox) of Dox between D2-D3 and D2-D4. Dox induction of Etv2 resulted in significantly increased EdU labelling at both time points. Blue boxes indicate the timing of Dox treatment. (e) qPCR analysis of cell cycle gene expression in iHA-Etv2 ES/EBs differentiated in the absence (−Dox) and presence (+Dox) of Dox. Pro-proliferative cell cycle genes Ccnd2,Ccna2 and Ccne1 show increased expression with induction of Etv2. Expression of Cdkn1b, a cell cycle repressor, was not affected by Etv2 induction. Data are presented as mean ± SEM (n = 3 replicates; *p < 0.05).