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Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis
Author(s) -
Yoder Michael D.,
Gumbiner Barry M.
Publication year - 2011
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22754
Subject(s) - notochord , mesoderm , lateral plate mesoderm , biology , gastrulation , intermediate mesoderm , paraxial mesoderm , microbiology and biotechnology , morphogenesis , nodal , anatomy , embryogenesis , embryo , genetics , embryonic stem cell , gene
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. Developmental Dynamics 240:2495–2504, 2011. © 2011 Wiley Periodicals, Inc.