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. 2018 Jan 19;8:1189. doi: 10.1038/s41598-017-19114-y

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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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A model of the mechanism for the effective myogenic differentiation of hPSCs with siPOU5F1 and synMYOD1. (a) In hPSCs, POU5F1 directly represses the expression of the genes related to extracellular matrix and early myogenic genes such as PAX3 and PAX7. Additionally, when synMYOD1 alone is introduced in hPSCs, POU5F1 inhibits the access of the translated MYOD1 protein to the target late myogenic genes such as MEF2C and MYOG, which results in the failure of myogenic differentiation. (b) Knockdown of POU5F1 with siPOU5F1 causes the activation of extracellular matrix genes and early myogenic genes. Consequently, when synMYOD1 is introduced, the translated MYOD1 protein can access to the promoters of the late myogenic genes to activate terminal myogenic gene activation. These mechanisms facilitate the rapid and highly efficient myogenic differentiation in hPSCs.