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. 2020 Apr 11;10:8. doi: 10.1186/s13395-020-00227-4

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 10 — Skeletal muscles from FSHD-like mouse models develop centralized nuclei. Soleus and TA muscle histological sections from control ACTA1-MCM (blue) and mild (green), moderate (yellow), and severe (red) FSHD-like model mice that had undergone treadmill exhaustion analysis 2× per week (see Figs. 7 and 8), were stained with H&E and counted for myofibers with centralized nuclear. Muscles were assayed at the indicated time points for each model. The ACTA1-MCM +TMX controls were assayed at MD28 and SD9, as appropriate. Data is plotted as percent of myofibers with centralized nuclei. Data are mean ± S.D. with significance calculated by one-way ANOVA using Prism 7. *p < .05, **p < .01, ***p < .001, ^#p < .001 for ACTA1-MCM compared with all other samples in the group.