scholarly journals Mtlinteracts with members of Egfr signaling and cell adhesion genes in the Drosophila eye

Fly ◽  
2011 ◽  
Vol 5 (2) ◽  
pp. 88-101 ◽  
Author(s):  
Verónica Muñoz-Soriano ◽  
Yaiza Belacortu ◽  
Fabrice C. Durupt ◽  
Silvia Muñoz-Descalzo ◽  
Nuria Paricio
Keyword(s):  
Cell Adhesion ◽  
Egfr Signaling ◽  
Drosophila Eye

scholarly journals Notch Controls Cell Adhesion in the Drosophila Eye

PLoS Genetics ◽  
2014 ◽  
Vol 10 (1) ◽  
pp. e1004087 ◽  
Author(s):  
Sujin Bao
Keyword(s):  
Cell Adhesion ◽  
Drosophila Eye

Interaction between EGFR signaling and DE-cadherin during nervous system morphogenesis

Development ◽  
2002 ◽  
Vol 129 (17) ◽  
pp. 3983-3994 ◽  
Author(s):  
Karin Dumstrei ◽  
Fay Wang ◽  
Diana Shy ◽  
Ulrich Tepass ◽  
Volker Hartenstein
Keyword(s):  
Cell Adhesion ◽  
Visual System ◽  
Egf Receptor ◽  
Genetic Interaction ◽  
Apoptotic Cell ◽  
Egfr Signaling ◽  
Surface Ectoderm ◽  
Egfr Ligand ◽  
Wingless Signaling ◽  
Bolwig's Organ

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-α-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.

The cell adhesion molecule Echinoid defines a new pathway that antagonizes the Drosophila EGF receptor signaling pathway

Development ◽  
2001 ◽  
Vol 128 (4) ◽  
pp. 591-601 ◽  
Author(s):  
J. Bai ◽  
W. Chiu ◽  
J. Wang ◽  
T. Tzeng ◽  
N. Perrimon ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Egf Receptor ◽  
Ectopic Expression ◽  
Growth Factor Receptor ◽  
Photoreceptor Cells ◽  
Egfr Signaling ◽  
Eye Disc ◽  
Cone Cells

Photoreceptor and cone cells in the Drosophila eye are recruited following activation of the epidermal growth factor receptor (EGFR) pathway. We have identified echinoid (ed) as a novel putative cell adhesion molecule that negatively regulates EGFR signaling. The ed mutant phenotype is associated with extra photoreceptor and cone cells. Conversely, ectopic expression of ed in the eye leads to a reduction in the number of photoreceptor cells. ed expression is independent of EGFR signaling and ED is localized to the plasma membrane of every cells throughout the eye disc. We present evidence that ed acts nonautonomously to generate extra R7 cells by a mechanism that is sina-independent but upstream of Tramtrack (TTK88). Together, our results support a model whereby ED defines an independent pathway that antagonizes EGFR signaling by regulating the activity, but not the level, of the TTK88 transcriptional repressor.

Dsg2 via Src-mediated transactivation shapes EGFR signaling towards cell adhesion

2018 ◽  
Vol 75 (22) ◽  
pp. 4251-4268 ◽  
Author(s):  
Hanna Ungewiß ◽  
Vera Rötzer ◽  
Michael Meir ◽  
Christina Fey ◽  
Markus Diefenbacher ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Egfr Signaling

scholarly journals Reggies/flotillins regulate E-cadherin–mediated cell contact formation by affecting EGFR trafficking

2012 ◽  
Vol 23 (10) ◽  
pp. 1812-1825 ◽  
Author(s):  
Gonzalo P. Solis ◽  
Yvonne Schrock ◽  
Nikola Hülsbusch ◽  
Marianne Wiechers ◽  
Helmut Plattner ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Membrane Trafficking ◽  
Tyrosine Kinases ◽  
Growth Factor Receptor ◽  
Cellular Prion Protein ◽  
Cell Contact ◽  
Egfr Signaling ◽  
A431 Cells ◽  
Epidermal Growth ◽  
E Cadherin

The reggie/flotillin proteins are implicated in membrane trafficking and, together with the cellular prion protein (PrP), in the recruitment of E-cadherin to cell contact sites. Here, we demonstrate that reggies, as well as PrP down-regulation, in epithelial A431 cells cause overlapping processes and abnormal formation of adherens junctions (AJs). This defect in cell adhesion results from reggie effects on Src tyrosine kinases and epidermal growth factor receptor (EGFR): loss of reggies reduces Src activation and EGFR phosphorylation at residues targeted by Src and c-cbl and leads to increased surface exposure of EGFR by blocking its internalization. The prolonged EGFR signaling at the plasma membrane enhances cell motility and macropinocytosis, by which junction-associated E-cadherin is internalized and recycled back to AJs. Accordingly, blockage of EGFR signaling or macropinocytosis in reggie-deficient cells restores normal AJ formation. Thus, by promoting EGFR internalization, reggies restrict the EGFR signaling involved in E-cadherin macropinocytosis and recycling and regulate AJ formation and dynamics and thereby cell adhesion.

scholarly journals Perturbing Nuclear Transport in Drosophila Eye Imaginal Discs Causes Specific Cell Adhesion and Axon Guidance Defects

2001 ◽  
Vol 240 (2) ◽  
pp. 315-325 ◽  
Author(s):  
Justin P. Kumar ◽  
Gavin S. Wilkie ◽  
Hildegard Tekotte ◽  
Kevin Moses ◽  
Ilan Davis
Keyword(s):  
Cell Adhesion ◽  
Axon Guidance ◽  
Nuclear Transport ◽  
Imaginal Discs ◽  
Specific Cell ◽  
Drosophila Eye

scholarly journals Split ends antagonizes the Notch and potentiates the EGFR signaling pathways during Drosophila eye development

2007 ◽  
Vol 124 (9-10) ◽  
pp. 792-806 ◽  
Author(s):  
David B. Doroquez ◽  
Terry L. Orr-Weaver ◽  
Ilaria Rebay
Keyword(s):  
Signaling Pathways ◽  
Eye Development ◽  
Egfr Signaling ◽  
Drosophila Eye ◽  
Split Ends
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