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Published online 5 April 2004. doi:10.1083/jcb.200307109
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 1, 87-98
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Article

 Vertebrate development requires ARVCF and p120 catenins and their interplay with RhoA and Rac

Xiang Fang1, Hong Ji1, Si-Wan Kim1, Jae-Il Park1,2, Travis G. Vaught1,2, Panos Z. Anastasiadis3, Malgorzata Ciesiolka4, and Pierre D. McCrea1,2

1 Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030
2 Program in Genes and Development, University of Texas Graduate School of Biomedical Science, Houston, TX 77025
3 Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, TX 77555
4 Department of Molecular Biomedical Research, Ghent University, B-9000 Ghent, Belgium

Address correspondence to P.D. McCrea, Dept. of Biochemistry and Molecular Biology, Box 117, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030-4095. Tel.: (713) 792-8979. Fax: (713) 791-9478. email: pmccrea{at}odin.mdacc.tmc.edu

Using an animal model system and depletion-rescue strategies, we have addressed the requirement and functions of armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) and p120 catenins in early vertebrate embryogenesis. We find that xARVCF and Xp120 are essential to development given that depletion of either results in disrupted gastrulation and axial elongation, which are specific phenotypes based on self-rescue analysis and further criteria. Exogenous xARVCF or Xp120 cross-rescued depletion of the other, and each depletion was additionally rescued with (carefully titrated) dominant-negative RhoA or dominant-active Rac. Although xARVCF or Xp120 depletion did not appear to reduce the adhesive function of C-cadherin in standard cell reaggregation and additional assays, C-cadherin levels were somewhat reduced after xARVCF or Xp120 depletion, and rescue analysis using partial or full-length C-cadherin constructs suggested contributory effects on altered adhesion and signaling functions. This work indicates the required functions of both p120 and ARVCF in vertebrate embryogenesis and their shared functional interplay with RhoA, Rac, and cadherin in a developmental context.

Key Words: GTPase; actin cytoskeleton; cell adhesion; cell motility; morphogenesis

The online version of this article includes supplemental material.

P.Z. Anastasiadis's present address is Mayo Clinic, Jacksonville, FL 32224.

Abbreviations used in this paper: ARVCF, armadillo repeat gene deleted in velo-cardio-facial syndrome; DA, dominant-active; DN, dominant-negative; EC, ectodomain; GDI, guanine nucleotide dissociation inhibitor; GEF, guanine nucleotide exchange factor; JMR, juxtamembrane; MO, morpholino oligonucleotide.


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