Figure 5

Schematic summarizing the role of N-cadherin in the maintenance of AHF-CPCs. In wild-type mice, N-cadherin expression by CPCs allows the cells to be properly adhered in the microenvironment of the pharyngeal mesoderm, thereby allowing the cells to be sufficiently exposed to paracrine factors that promote multipotency and proliferation. In addition, N-cadherin serves to maintain β-catenin levels by sequestering the molecules at the cell membrane. These allow the AHF-CPCs from wild-type mice to achieve higher Wnt signaling activity as compared to single mutant (AHF-Cre;Cdh2^fl/fl), where an overall downregulation of Wnt signaling activity was observed, which consequently resulted in premature differentiation of CPCs to cardiomyocytes in the AHF. Expectedly, activating Wnt signaling by overexpression of β-catenin in the double mutant (AHF-Cre; Cdh2^fl/fl ; bCat(e3)^fl/+) was able to partially rescue the premature differentiation phenotype of the CPCs observed in Cdh2 single mutant.