341 Modeling and Rescue of PLN-R14del Cardiomyopathy Phenotype in Human iPSC-Derived Cardiac Spheroids 12 Supplementary Figure 5 Supplementary Figure 5. SPLiT Sequencing mapping, sources of biological variability in hiPSC donors and cell type-specific gene patterns. (A). UMAP plot of single-cell profile with each cell color-coded for D12, D24, and D90 cardiomyocytes (Grancharova et al.,). Different cell clusters are colored and labeled as indicated. (B) clustered mapping of all labels based on mapping in A (Grancharova et al.,) (C) UMAP of the individual cells derived from cardiac spheroid per iPSC donor. (D) Fraction of cells for the three cell types; CMs group 1 (CM1), CMs group 2 (CM2), and fibroblasts (fibro) in healthy controls and PLN-R14del spheroid groups. (E) Top 10 genes of each cell cluster. Wilcoxon rank-sum test identifies differentially expressed genes in each cluster and the top 10 genes are displayed in a heatmap. (F) Expression levels of cardiac genes TNNT2 and MYH7 per individual cells derived from cardiac spheroid per iPSC donor. (G) UMAP from Fig. 3 colored by transcript abundance of DCC and FAM155A, highlighting cardiomyocyte cluster 1, TNNT2, and RYR2, highlighting cardiomyocyte cluster 2 and FN1 and COL1A1, highlighting the fibroblast cluster. (H) Transcript abundance distributions are shown for CM1, CM2, and fibroblast clusters. Max value = maximum value of log1p normalized counts; dot = median.
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