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First published online 3 August 2004
doi: 10.1242/jcs.01298
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Research Article |

1 Developmental Biology Unit, Department of Molecular Biomedical Research, Flanders Interuniversity Institute for Biotechnology (VIB) - Ghent University, Technologiepark 927, B-9052 Ghent, Belgium
2 Molecular Cell Biology Unit, Department of Molecular Biomedical Research, Flanders Interuniversity Institute for Biotechnology (VIB) - Ghent University, Technologiepark 927, B-9052 Ghent, Belgium
3 Department of Biochemistry and Molecular Biology, Program in Genes and Development, University of Texas, M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA
Author for correspondence (e-mail: kris.vleminckx{at}dmbr.ugent.be)
Accepted 28 April 2004
During Xenopus development, p120 transcripts are enriched in highly morphogenetic tissues. We addressed the developmental function of p120 by knockdown experiments and by expressing E-cadherin mutants unable to bind p120. This resulted in defective eye formation and provoked malformations in the craniofacial cartilage structures, derivatives of the cranial neural crest cells. Closer inspection showed that p120 depletion impaired evagination of the optic vesicles and migration of cranial neural crest cells from the neural tube into the branchial arches. These morphogenetic processes were also affected by p120-uncoupled cadherins or E-cadherin containing a deletion of the juxtamembrane domain. Irrespective of the manipulation that caused the malformations, coexpression of dominant-negative forms of either Rac1 or LIM kinase rescued the phenotypes. Wild-type RhoA and constitutively active Rho kinase caused partial rescue. Our results indicate that, in contrast to invertebrates, p120 is an essential factor for vertebrate development and an adequate balance between cadherin activity and cytoskeletal condition is critical for correct morphogenetic movements.
Key words: Embryogenesis, Cadherins, Catenins, Rho GTPases, Xenopus
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