|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
1 Department of Molecular Cell and Developmental Biology, University of California Los Angeles, Los Angeles, CA 90095, USA
2 Department of Zoology, University of Toronto, Toronto, Ontario M5S3G5, Canada
* These authors contributed equally to this work
Author for correspondence (e-mail: volkerh{at}mcdb.ucla.edu)
Accepted 22 May 2002
Dynamically regulated cell adhesion plays an important role during animal morphogenesis. Here we use the formation of the visual system in Drosophila embryos as a model system to investigate the function of the Drosophila classic cadherin, DE-cadherin, which is encoded by the shotgun (shg) gene. The visual system is derived from the optic placode which normally invaginates from the surface ectoderm of the embryo and gives rise to two separate structures, the larval eye (Bolwig’s organ) and the optic lobe. The optic placode dissociates and undergoes apoptotic cell death in the absence of DE-cadherin, whereas overexpression of DE-cadherin results in the failure of optic placode cells to invaginate and of Bolwig’s organ precursors to separate from the placode. These findings indicate that dynamically regulated levels of DE-cadherin are essential for normal optic placode development. It was shown previously that overexpression of DE-cadherin can disrupt Wingless signaling through titration of Armadillo out of the cytoplasm to the membrane. However, the observed defects are likely the consequence of altered DE-cadherin mediated adhesion rather than a result of compromising Wingless signaling, as overexpression of a DE-cadherin-
-catenin fusion protein, which lacks Armadillo binding sites, causes similar defects as DE-cadherin overexpression. We further studied the genetic interaction between DE-cadherin and the Drosophila EGF receptor homolog, EGFR. If EGFR function is eliminated, optic placode defects resemble those following DE-cadherin overexpression, which suggests that loss of EGFR results in an increased adhesion of optic placode cells. An interaction between EGFR and DE-cadherin is further supported by the finding that expression of a constitutively active EGFR enhances the phenotype of a weak shg mutation, whereas a mutation in rhomboid (rho) (an activator of the EGFR ligand Spitz) partially suppresses the shg mutant phenotype. Finally, EGFR can be co-immunoprecipitated with anti-DE-cadherin and anti-Armadillo antibodies from embryonic protein extracts. We propose that EGFR signaling plays a role in morphogenesis by modulating cell adhesion.
Key words: EGFR signaling, DE-cadherin, shotgun, Morphogenesis, Adhesion, Visual system, Drosophila melanogaster
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  Y. Haddad, W. Choi, and D. J. McConkey Delta-Crystallin Enhancer Binding Factor 1 Controls the Epithelial to Mesenchymal Transition Phenotype and Resistance to the Epidermal Growth Factor Receptor Inhibitor Erlotinib in Human Head and Neck Squamous Cell Carcinoma Lines Clin. Cancer Res., January 15, 2009; 15(2): 532 - 542. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. G. Sprecher, F. Pichaud, and C. Desplan Adult and larval photoreceptors use different mechanisms to specify the same Rhodopsin fates Genes & Dev., September 1, 2007; 21(17): 2182 - 2195. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Cela and M. Llimargas Egfr is essential for maintaining epithelial integrity during tracheal remodelling in Drosophila Development, August 15, 2006; 133(16): 3115 - 3125. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Blaser, S. Eisenbeiss, M. Neumann, M. Reichman-Fried, B. Thisse, C. Thisse, and E. Raz Transition from non-motile behaviour to directed migration during early PGC development in zebrafish J. Cell Sci., September 1, 2005; 118(17): 4027 - 4038. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Takahashi, F. Takahashi, K. Ui-Tei, T. Kojima, and K. Saigo Requirements of genetic interactions between Src42A, armadillo and shotgun, a gene encoding E-cadherin, for normal development in Drosophila Development, June 1, 2005; 132(11): 2547 - 2559. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Brumby, J. Secombe, J. Horsfield, M. Coombe, N. Amin, D. Coates, R. Saint, and H. Richardson A Genetic Screen for Dominant Modifiers of a cyclin E Hypomorphic Mutation Identifies Novel Regulators of S-Phase Entry in Drosophila Genetics, September 1, 2004; 168(1): 227 - 251. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Bazzoni and E. Dejana Endothelial Cell-to-Cell Junctions: Molecular Organization and Role in Vascular Homeostasis Physiol Rev, July 1, 2004; 84(3): 869 - 901. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. E. Brown and M. Freeman Egfr signalling defines a protective function for ommatidial orientation in the Drosophila eye Development, November 15, 2003; 130(22): 5401 - 5412. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Rintelen, E. Hafen, and K. Nairz The Drosophila dual-specificity ERK phosphatase DMKP3 cooperates with the ERK tyrosine phosphatase PTP-ER Development, August 1, 2003; 130(15): 3479 - 3490. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Gonzalez-Reyes Stem cells, niches and cadherins: a view from Drosophila J. Cell Sci., March 15, 2003; 116(6): 949 - 954. [Abstract] [Full Text] [PDF]
|
|
