Fig. S9.

β-Catenin and YAP1 is synergistically required to induce hPSC-CM proliferation in hCO in support of the data presented in Fig. 7. (A) Heat map with gene names of YAP targets down-regulated hCOs in MM; n = 4 experiments from RNA-seq data. Log₂ expression relative to mean for all conditions. (B) Delivery of constitutively active β-catenin or YAP1 individually does not activate proliferation (Ki-67 intensity) in hCOs cultured in MM; n = 11–13 from three experiments. (C) Delivery of constitutively active β-catenin or YAP1 individually does not activate proliferation (Ki-67) of hPSC-CMs (α-actinin) in hCOs cultured in MM; n = 10 from three experiments. The 17,214 hPSC-CMs were manually counted. (D) Delivery of constitutively active β-catenin or YAP1 individually does not activate mitosis (pH3) of hPSC-CMs (α-actinin) in hCOs cultured in MM; n = 6 from two experiments. The 10,243 hPSC-CMs were manually counted. (E) Delivery of constitutively active β-catenin or YAP1 individually does not activate BIRC5 in hCOs cultured in MM; n = 7–8 from two experiments. (F) Delivery of constitutively active β-catenin and YAP1 cooperates to activate proliferation (Ki-67 intensity) in hCOs cultured in MM; n = 11–14 from three experiments. (G) β-Catenin and YAP1 cooperate in hCOs cultured in MM to induce expression of BIRC5; n = 6–7 from two experiments. (H) Force of contraction is not affected by overexpression of constitutively active β-catenin and YAP1; n = 9–12. (I) Chemical structure of compound 6.28. (J) Dose–response curves for compound 6.28. (K) Volcano plot illustrating the differential analysis of the proteomics data for hCO treated with compound 6.28 for 2 d; n = 2 for DMSO control and n = 4 for compound 6.28. Data are mean ± SEM. **P < 0.01, using t test (F and G). FC, fold change.