Canonical Wnt signalling and E-cadherin-mediated cell adhesion are both involved in mouse embryonic stem (mES) cell maintenance. β-catenin (Ctnnb1) is central to both these processes - it mediates the transactivation of Wnt target genes and also connects E-cadherin to the actin cytoskeleton via α-catenin. But which β-catenin function is absolutely required for mES cell self-renewal and pluripotency? On , Ignacio del Valle and colleagues investigate this controversial question. The researchers use Ctnnb1-/-Eα mES cells in which the constitutive expression of an E-cadherin-α-catenin fusion protein maintains cell adhesion. Preservation of cell adhesion, the researchers report, is sufficient to promote the leukaemia inhibitory factor (Lif) signalling pathway, which is required for mES cell maintenance, and the transcriptional factor network that controls the mES cell state. They also implicate E-cadherin in the activation of Lif signalling by showing that it stabilises the Lifr-Gp130 co-receptor complex. Together, these findings suggest that only the adhesive function of β-catenin is absolutely required for the propagation of mES cells in culture.
