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. 2020 Mar;43:101688. doi: 10.1016/j.scr.2019.101688

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© 2020 The Author(s)

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Fig 1 — (A) Phase contrast images showing colonies of both DMD iPSC lines. Scale bar 100 μm. (B) Immunofluorescence staining showing pluripotency-associated markers (NANOG, SOX2 and OCT3/4) in UCLi011-A and UCLi012-A iPSCs. Hoechst: nuclei. Scale bar: 75 μm. (C) Quantitative real-time PCR analysis showing expression of mRNAs of pluripotency-associated factors (NANOG, SOX2 and OCT3/4) in UCLi011-A and UCLi012-A iPSCs and their absence in parental fibroblasts. (D) Upper images: normal karyotype of UCLi011-A and UCLi012-A iPSCs (46,XY). Lower images: electropherograms confirming presence of pathogenic mutations in exon 68 (c.9851G>A (p.Trp3284X) and 70 c.10141C>T (p.Arg3381X) of the dystrophin gene. (E) Embryoid body formation assay. Upper phase contract images show morphology of UCLi011-A and UCLi012-A embryoid bodies. Lower panels show immunofluorescence staining of the same embryoid bodies with lineage-specific markers: α-smooth muscle actin (mesoderm), βIII-tubulin (ectoderm) and SOX17 (endoderm). Hoechst: nuclei. Scale bar: 75 μm. Bottom images: merged pictures showing magnified areas of each lineage-specific staining.