Requirement for β-Catenin in Anterior-Posterior Axis Formation in Mice

Abstract

The anterior-posterior axis of the mouse embryo is defined before formation of the primitive streak, and axis specification and subsequent anterior development involves signaling from both embryonic ectoderm and visceral endoderm. Τhe Wnt signaling pathway is essential for various developmental processes, but a role in anterior-posterior axis formation in the mouse has not been previously established. β-Catenin is a central player in the Wnt pathway and in cadherin-mediated cell adhesion. We generated β-catenin–deficient mouse embryos and observed a defect in anterior-posterior axis formation at embryonic day 5.5, as visualized by the absence of Hex and Hesx1 and the mislocation of cerberus-like and Lim1 expression. Subsequently, no mesoderm and head structures are generated. Intercellular adhesion is maintained since plakoglobin substitutes for β-catenin. Our data demonstrate that β-catenin function is essential in anterior-posterior axis formation in the mouse, and experiments with chimeric embryos show that this function is required in the embryonic ectoderm.

β-Catenin up-regulates Nanog expression through interaction with Oct-3/4 in embryonic stem cells

“…Furthermore, several studies, including ours, suggest that β-catenin plays an important role in the self-renewal of ES cells [12,13]. Establishment of β-catenin-null ES cells, however, has also been reported [23]. Since we observed that γ-catenin, a protein highly homologous to β-catenin, can partially maintain the undifferentiated state of ES cells ( Figure S2), it is possible that γ-catenin compensates for the loss of β-catenin.…”

Expression of all Wnt genes and their secreted antagonists during mouse blastocyst and postimplantation development

“…Moreover, a mutation in the beta-Catenin gene (Catnb), a cellular effector of the Wnt pathway, leads to a lack of mesoderm, confirming the role of Wnt in axis formation. However, in these mutant embryos, the visceral endodermal cells do not migrate from the distal tip of the pregastrula embryo to the presumptive anterior side to form the aVE signaling center (Huelsken et al, 2000). This phenotype is not identical to the Wnt3 phenotype and suggests that an unidentified Wnt factor is involved in breaking the radial symmetry.…”

“…Wnt2b and Wnt3 may also be partially redundant because their expression domains are largely overlapping. Indeed, Wnt2b has been shown to trigger the canonical Wnt pathway and could eventually be responsible for part of the phenotype of the beta-Catenin mutant embryo (lack of anterior migration of the distal visceral endoderm at 5.5 dpc) that is not mimicked in the Wnt3 mutant (Liu et al, 1999;Huelsken et al, 2000;Kubo et al, 2003).…”

The Recruitment of Phosphatidylinositol 3-Kinase to the E-cadherin-Catenin Complex at the Plasma Membrane Is Required for Calcium-induced Phospholipase C-γ1 Activation and Human Keratinocyte Differentiation

“…5B). In contrast, ␥-catenin, which can replace ␤-catenin in adherens junctions (53,54), was not increased by ␤-catenin knockdown (Fig. 5C).…”