scholarly journals Eps15R and clathrin regulate EphB2-mediated cell repulsion

Traffic ◽  
2017 ◽  
Vol 19 (1) ◽  
pp. 44-57 ◽  
Author(s):  
Emma Evergren ◽  
Neville Cobbe ◽  
Harvey T. McMahon
Keyword(s):  
Cell Repulsion

scholarly journals Regulation of EphB2 activation and cell repulsion by feedback control of the MAPK pathway

2008 ◽  
Vol 183 (5) ◽  
pp. 933-947 ◽  
Author(s):  
Alexei Poliakov ◽  
Maria L. Cotrina ◽  
Andrea Pasini ◽  
David G. Wilkinson
Keyword(s):  
Feedback Loop ◽  
Fibroblast Growth Factor Receptor ◽  
Mapk Pathway ◽  
Tyrosine Phosphatase ◽  
Growth Factor Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Eph Receptor ◽  
Mitogen Activated Protein ◽  
Mediate Cell ◽  
Cell Repulsion

In this study, we investigated whether the ability of Eph receptor signaling to mediate cell repulsion is antagonized by fibroblast growth factor receptor (FGFR) activation that can promote cell invasion. We find that activation of FGFR1 in EphB2-expressing cells prevents segregation, repulsion, and collapse responses to ephrinB1 ligand. FGFR1 activation leads to increased phosphorylation of unstimulated EphB2, which we show is caused by down-regulation of the leukocyte common antigen–related tyrosine phosphatase receptor that dephosphorylates EphB2. In addition, FGFR1 signaling inhibits further phosphorylation of EphB2 upon stimulation with ephrinB1, and we show that this involves a requirement for the mitogen-activated protein kinase (MAPK) pathway. In the absence of activated FGFR1, EphB2 activates the MAPK pathway, which in turn promotes EphB2 activation in a positive feedback loop. However, after FGFR1 activation, the induction of Sprouty genes inhibits the MAPK pathway downstream of EphB2 and decreases cell repulsion and segregation. These findings reveal a novel feedback loop that promotes EphB2 activation and cell repulsion that is blocked by transcriptional targets of FGFR1.

scholarly journals Cell segregation and border sharpening by Eph receptor–ephrin-mediated heterotypic repulsion

2017 ◽  
Vol 14 (132) ◽  
pp. 20170338 ◽  
Author(s):  
Harriet B. Taylor ◽  
Anaïs Khuong ◽  
Zhonglin Wu ◽  
Qiling Xu ◽  
Rosalind Morley ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Adhesion ◽  
Computer Simulations ◽  
Contact Inhibition ◽  
Transient Increase ◽  
Cell Behaviour ◽  
Eph Receptor ◽  
Cell Segregation ◽  
Cell Repulsion

Eph receptor and ephrin signalling has a major role in cell segregation and border formation, and may act through regulation of cell adhesion, repulsion or tension. To elucidate roles of cell repulsion and adhesion, we combined experiments in cell culture assays with quantitations of cell behaviour which are used in computer simulations. Cells expressing EphB2, or kinase-inactive EphB2 (kiEphB2), segregate and form a sharp border with ephrinB1-expressing cells, and this is disrupted by knockdown of N-cadherin. Measurements of contact inhibition of locomotion reveal that EphB2-, kiEphB2- and ephrinB1-expressing cells have strong heterotypic and weak homotypic repulsion. EphB2 cells have a transient increase in migration after heterotypic activation, which underlies a shift in the EphB2–ephrinB1 border but is not required for segregation or border sharpening. Simulations with the measured values of cell behaviour reveal that heterotypic repulsion can account for cell segregation and border sharpening, and is more efficient than decreased heterotypic adhesion. By suppressing homotypic repulsion, N-cadherin creates a sufficient difference between heterotypic and homotypic repulsion, and enables homotypic cohesion, both of which are required to sharpen borders.

scholarly journals Formation of graded cell arrangement by cell repulsion

2001 ◽  
Vol 41 (supplement) ◽  
pp. S83
Author(s):  
H. Honda ◽  
A. Mochizuki
Keyword(s):  
Cell Arrangement ◽  
Cell Repulsion

scholarly journals Ephrin-B2-induced Cleavage of EphB2 Receptor Is Mediated by Matrix Metalloproteinases to Trigger Cell Repulsion

2008 ◽  
Vol 283 (43) ◽  
pp. 28969-28979 ◽  
Author(s):  
Kai-Ti Lin ◽  
Slawomir Sloniowski ◽  
Douglas W. Ethell ◽  
Iryna M. Ethell
Keyword(s):  
Matrix Metalloproteinases ◽  
Cell Repulsion

scholarly journals Synergy of cell–cell repulsion and vacuolation in a computational model of lumen formation

2014 ◽  
Vol 11 (92) ◽  
pp. 20131049 ◽  
Author(s):  
Sonja E. M. Boas ◽  
Roeland M. H. Merks
Keyword(s):  
Blood Perfusion ◽  
Formation Mechanisms ◽  
Cellular Potts Model ◽  
Lumen Formation ◽  
Agent Based ◽  
Small Vessels ◽  
Narrow Region ◽  
Vessel Development ◽  
Cell Repulsion ◽  
Cell Cell

A key step in blood vessel development (angiogenesis) is lumen formation: the hollowing of vessels for blood perfusion. Two alternative lumen formation mechanisms are suggested to function in different types of blood vessels. The vacuolation mechanism is suggested for lumen formation in small vessels by coalescence of intracellular vacuoles, a view that was extended to extracellular lumen formation by exocytosis of vacuoles. The cell–cell repulsion mechanism is suggested to initiate extracellular lumen formation in large vessels by active repulsion of adjacent cells, and active cell shape changes extend the lumen. We used an agent-based computer model, based on the cellular Potts model, to compare and study both mechanisms separately and combined. An extensive sensitivity analysis shows that each of the mechanisms on its own can produce lumens in a narrow region of parameter space. However, combining both mechanisms makes lumen formation much more robust to the values of the parameters, suggesting that the mechanisms may work synergistically and operate in parallel, rather than in different vessel types.

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