Requirement for β-Catenin in Anterior-Posterior Axis Formation in Mice
By J. Huelsken, Regina Vogel, V. Brinkmann, B. Erdmann, C. Birchmeier, W. Birchmeier. Journal of Cell Biology, 2000
706 citations recorded by the source corpus.
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.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/25015f5090290cfeb94091d365ead5e636d18dc3
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- Maternal β-catenin and E-cadherin in mouse development (2004, background): “Lack of β-catenin results in early gastrulation lethality, with no mesoderm formation and a block in anterior-posterior axis formation and head development (Haegel et al., 1995; Huelsken et al., 2000).”
- Multiple roles of mesenchymal β-catenin during murine limb patterning (2006, background): “(Huelsken et al., 2000), to females homozygous for a floxed allele (fl) (Huelsken et al.”
- Canonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytes. (2005, background): “…β-catenin loss-of-function mutant mice (b-cat Prx1/−) S Fwere generated by intercrossing males double heterozygous for a LacZ knockin null allele (Huelsken et al., 2000) and the Prx1-Cre d 2transgenic allele (Logan et al., 2002) with homozygous floxed b-cat- nin females [fl; (Huelsken et…”
- Sequential roles of Hedgehog and Wnt signaling in osteoblast development (2004, positive): “Recently, Smo, which encodes an obligatory component of the Hh pathway, was removed with Wnt1-Cre to eliminate Hh response in cranial neural crest cells (CNCC) that normally give rise to many of the craniofacial bones via intramembranous ossification (Jeong et al., 2004).”
- The many faces and functions of β‐catenin (2012, positive): “A/P axis identity and mesoderm formation is controlled by b -catenin-mediated transcription also in mammals, since mouse embryos lacking b -catenin do not develop a proper A/P axis and fail to form mesoderm, resulting in corrupted gastrulation (Haegel et al , 1995; Huelsken et al , 2000).”
- Inactivation of the beta-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development. (2001, neutral): “Subsequently, β-catenin was found to bind directly to the cytoplasmic domain of E-cadherin and to α-catenin, linking this adhesion complex to the actin cytoskeleton (Aberle et al., 1994; Aberle et al., 1996a; Hülsken et al., 1994; Jou et al., 1995; Rimm et al., 1995).”
- Deletion of β-catenin impairs T cell development (2003, background): “To address the function of β-catenin in T lymphocytes, we generated mice with deletion of the gene encoding β-catenin specifically in thymocytes and T cells, because germline deletion of β-catenin leads to embryonic death due to defective anterior-posterior axis formation and the absence of mesoderm”