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Open Access Highly Accessed Research article

PAPC and the Wnt5a/Ror2 pathway control the invagination of the otic placode in Xenopus

Barbara Jung12, Almut Köhler1, Alexandra Schambony13 and Doris Wedlich1*

Author Affiliations

1 Karlsruhe Institute of Technology, Campus South, Zoological Institute, Department of Cell and Developmental Biology, Fritz-Haber-Weg 4, Karlsruhe, 76131, Germany

2 Current Address: University of Freiburg, Institute of Biology I, Department of Developmental Biology, Hauptstr. 1, Freiburg, 79104, Germany

3 Current Address: University of Erlangen-Nuernberg, Biology Department, Developmental Biology, Staudtstr. 5, Erlangen, 91058, Germany

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BMC Developmental Biology 2011, 11:36  doi:10.1186/1471-213X-11-36

Published: 10 June 2011

Abstract

Background

Paraxial protocadherin (PAPC) plays a crucial role in morphogenetic movements during gastrulation and somitogenesis in mouse, zebrafish and Xenopus. PAPC influences cell-cell adhesion mediated by C-Cadherin. A putative direct adhesion activity of PAPC is discussed. PAPC also promotes cell elongation, tissue separation and coordinates cell mass movements. In these processes the signaling function of PAPC in activating RhoA/JNK and supporting Wnt-11/PCP by binding to frizzled 7 (fz7) is important.

Results

Here we demonstrate by loss of function experiments in Xenopus embryos that PAPC regulates another type of morphogenetic movement, the invagination of the ear placode. Knockdown of PAPC by antisense morpholinos results in deformation of the otic vesicle without altering otocyst marker expression. Depletion of PAPC could be rescued by full-length PAPC, constitutive active RhoA and by the closely related PCNS but not by classical cadherins. Also the cytoplasmic deletion mutant M-PAPC, which influences cell adhesion, does not rescue the PAPC knockdown. Interestingly, depletion of Wnt5a or Ror2 which are also expressed in the otocyst phenocopies the PAPC morphant phenotype.

Conclusions

PAPC signaling via RhoA and Wnt5a/Ror2 activity are required to keep cells aligned in apical-basal orientation during invagination of the ear placode. Since neither the cytoplasmic deletion mutant M-PAPC nor a classical cadherin is able to rescue loss of PAPC we suggest that the signaling function of the protocadherin rather than its role as modulator of cell-cell adhesion is required during invagination of the ear placode.