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. 2021 Jan 15;25(3):1661–1676. doi: 10.1111/jcmm.16268

FIGURE 1.

FIGURE 1

MYOM1−/− hESCs have normal pluripotency and ability to differentiate into MYOM1−/− hESC‐CMs. (A) Schematic illustration of human myomesin‐1’s total exons and the guide RNA designed for CRISPR/Cas9 mutagenesis. (B) Excision of 7 nucleotides resulting in frameshift mutation of whole protein from exon‐4. (C,D) Immunostaining and mRNA level of MYOM1−/− hESCs for the pluripotency markers (Scalebar, 50 μm). (E) Schematic representation of small molecule‐based cardiac differentiation. (F) Western blot of MYOM1 protein and GAPDH from WT and KO CMs at day 20. (G,H) Flow cytometry of day 20 cardiomyocytes from two groups stained with troponin T (TNNT2/cTNT) without purification. (I,J) Immunostaining of day 20 CMs with MLC2v(MYL2) and MLC2a (MYL7) (Scalebar, 50 μm). Data are analysed with two‐sample t test and shown as means ± SD. ns, not significant