Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis

Michael D. Yoder, Barry M. Gumbiner

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2495-2504
Number of pages10
JournalDevelopmental Dynamics
Volume240
Issue number11
DOIs
StatePublished - Nov 1 2011

All Science Journal Classification (ASJC) codes

  • Developmental Biology

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