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. 2022 Jan 14;7:5. doi: 10.1038/s41536-021-00201-8

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© The Author(s) 2022

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. 7 — a–d Co-cultures of all combinations of mutant and control FAPs and MuSCs were examined. Control MuSCs cultured with Acvr1^R206H/+ FAPs show reduced efficiency of myofiber formation (c), while control FAPs cultured with Acvr1^R206H/+ MuSCs form mature myofibers that fuse in vitro (d) rescuing the myogenic failure of Acvr1^R206H/+ MuSCs cultured with Acvr1^R206H/+ FAPs (b). e Quantification of the fusion index percentage in all co-culture conditions. f–i All combinations of mutant and control MuSCs with conditioned media (CM) from mutant and control FAPs were examined. MuSC cultures were stained with the mature muscle marker myosin heavy chain (α-MyHC). Acvr1^R206H/+ MuSCs cultured with control FAP-conditioned media for 7 days partially rescued the poor differentiation in Acvr1^R206H/+ MuSCs (i). j Quantification of the fusion index percentage in all CM conditions, n = 3–4 for each genotype (mean ± SEM). Scale bars for all images = 100 µm. Statistical significance determined by one-way ANOVA, ***p < 0.0002, ^#p < 0.0001.