Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis
| Autor: | Barry M. Gumbiner, Michael D. Yoder |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
animal structures
Embryo Nonmammalian Xenopus Green Fluorescent Proteins Molecular Sequence Data Notochord Cell Communication Biology Xenopus Proteins Notochord formation FGF and mesoderm formation Article Animals Genetically Modified Paraxial mesoderm Aorta-gonad-mesonephros medicine Cell Adhesion Morphogenesis Animals Protein Precursors Glycoproteins Base Sequence Notochord morphogenesis Gastrulation Gene Expression Regulation Developmental Cell Differentiation Anatomy Cadherins Cell biology medicine.anatomical_structure Gene Knockdown Techniques embryonic structures Intercellular Signaling Peptides and Proteins NODAL Intermediate mesoderm Developmental Biology |
| Zdroj: | Developmental dynamics : an official publication of the American Association of Anatomists. 240(11) |
| ISSN: | 1097-0177 |
| Popis: | The separation and specification of mesoderm into the notochord and somites involves members of the non-clustered δ-protocadherins. Axial (AXPC) and paraxial (PAPC) protocadherins are expressed in the early dorsal mesoderm and later become refined to the developing notochordal and somitic mesoderm, respectively. The role of PAPC in this process has been studied extensively, but the role of AXPC is poorly understood. Partial knockdown of AXPC causes a specific bent-axis phenotype, while more severe knockdown results in the loss of notochord formation. The inability of these embryos to develop a notochord is not due to a cell-sorting event via changes in cell adhesion during gastrulation, but rather this defect is manifested through the loss of axial mesoderm specification, but not general mesoderm induction. The results presented here show that AXPC functions in notochord morphogenesis by directing cell-fate decisions rather than cell-cell adhesion. |
| Databáze: | OpenAIRE |
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