Figure 7.
The diagram is divided into three panels representing different contractility states: Endogenous, Low contractility, and High contractility. Each panel shows the state at 0 hours (top) and after 48 hours (bottom) of CHIR treatment. At 0 hours, beta-catenin is degraded and localized at adherens junctions (AJs). The amount of junctional beta-catenin correlates with the level of contractility experienced by human induced pluripotent stem cells (hiPSCs). During differentiation, beta-catenin accumulates in the nucleus and activates a mesoderm program through its binding with TCF4. The diagram includes labels for F-actin, E-cadherin, beta-catenin (intact slash degraded), alpha-catenin, TCF4 slash TCF7L2, and mesoderm program (TBXT, EOMES, etc.). Arrows indicate the direction of beta-catenin movement and interaction with TCF4. The mesoderm conversion efficiency is also depicted.
Working model. Effect of actomyosin contractility on mesoderm lineage commitment. Each panel represents a specific contractile status at the basal state (0 h—top) and after 48 h (bottom) of CHIR treatment. At the basal state, β-catenin is degraded and localized at AJs. The amount of junctional β-catenin correlates with the level of contractility experienced by hiPSCs. During differentiation, β-catenin accumulates in the nucleus and activates a mesoderm program through its binding with TCF4.