Spatial regulation of Dia and Myosin-II by RhoGEF2 controls initiation of E-cadherin endocytosis during epithelial morphogenesis

2011 ◽  
Vol 13 (5) ◽  
pp. 529-540 ◽  
Author(s):  
Romain Levayer ◽  
Anne Pelissier-Monier ◽  
Thomas Lecuit
Keyword(s):  
Myosin Ii ◽  
Epithelial Morphogenesis ◽  
Spatial Regulation ◽  
E Cadherin

scholarly journals Distinct contributions of tensile and shear stress on E-cadherin levels during morphogenesis

2018 ◽  
Author(s):  
Girish R. Kale ◽  
Xingbo Yang ◽  
Jean-Marc Philippe ◽  
Madhav Mani ◽  
Pierre-François Lenne ◽  
...  
Keyword(s):  
Myosin Ii ◽  
Epithelial Morphogenesis ◽  
Shear Stresses ◽  
Mechanical Forces ◽  
Mechanical Tension ◽  
Tensile Forces ◽  
Axis Elongation ◽  
Persistent Cell ◽  
Adhesive Forces ◽  
E Cadherin

AbstractDuring epithelial morphogenesis, cell contacts (junctions) are constantly remodeled by mechanical forces that work against adhesive forces. E-cadherin complexes play a pivotal role in this process by providing persistent cell adhesion and by transmitting mechanical tension. In this context, it is unclear how mechanical forces affect E-cadherin adhesion and junction dynamics.During Drosophila embryo axis elongation, Myosin-II activity in the apico-medial and junctional cortex generates mechanical forces to drive junction remodeling. Here we report that the ratio between Vinculin and E-cadherin intensities acts as a ratiometric readout for these mechanical forces (load) at E-cadherin complexes. Medial Myosin-II loads E-cadherin complexes on all junctions, exerts tensile forces, and increases levels of E-cadherin. Junctional Myosin-II, on the other hand, biases the distribution of load between junctions of the same cell, exerts shear forces, and decreases the levels of E-cadherin. This work suggests distinct effects of tensile versus shear stresses on E-cadherin adhesion.

Mutant cadherin affects epithelial morphogenesis and invasion, but not transformation

2001 ◽  
Vol 114 (6) ◽  
pp. 1237-1246 ◽  
Author(s):  
M.L. Troxell ◽  
D.J. Loftus ◽  
W.J. Nelson ◽  
J.A. Marrs
Keyword(s):  
Tumor Progression ◽  
Mdck Cells ◽  
Collagen Gel ◽  
Collagen Matrix ◽  
Soft Agar ◽  
Epithelial Morphogenesis ◽  
Adhesion System ◽  
Severe Impairment ◽  
Hepatocyte Growth ◽  
E Cadherin

MDCK cells were engineered to reversibly express mutant E-cadherin protein with a large extracellular deletion. Mutant cadherin overexpression reduced the expression of endogenous E- and K-cadherins in MDCK cells to negligible levels, resulting in decreased cell adhesion. Despite severe impairment of the cadherin adhesion system, cells overexpressing mutant E-cadherin formed fluid-filled cysts in collagen gel cultures and responded to hepatocyte growth factor/scatter factor (HGF/SF) that induced cellular extension formation with a frequency similar to that of control cysts. However, cells were shed from cyst walls into the lumen and into the collagen matrix prior to and during HGF/SF induced tubule extension. Despite the propensity for cell dissociation, MDCK cells lacking cadherin adhesion molecules were not capable of anchorage-independent growth in soft agar and cell proliferation rate was not affected. Thus, cadherin loss does not induce transformation, despite inducing an invasive phenotype, a later stage of tumor progression. These experiments are especially relevant to tumor progression in cells with altered E-cadherin expression, particularly tumor samples with identified E-cadherin extracellular domain genomic mutations.

scholarly journals HGF Converts ErbB2/Neu Epithelial Morphogenesis to Cell Invasion

2005 ◽  
Vol 16 (2) ◽  
pp. 550-561 ◽  
Author(s):  
Hanane Khoury ◽  
Monica A. Naujokas ◽  
Dongmei Zuo ◽  
Veena Sangwan ◽  
Melanie M. Frigault ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Invasion ◽  
Single Cells ◽  
Epithelial Morphogenesis ◽  
Cell Junctions ◽  
Junction Protein ◽  
Hepatocyte Growth ◽  
E Cadherin ◽  
Cell Cell

Activation of the hepatocyte growth factor receptor Met induces a morphogenic response and stimulates the formation of branching tubules by Madin-Darby canine kidney (MDCK) epithelial cells in three-dimensional cultures. A constitutively activated ErbB2/Neu receptor, NeuNT, promotes a similar invasive morphogenic program in MDCK cells. Because both receptors are expressed in breast epithelia, are associated with poor prognosis, and hepatocyte growth factor (HGF) is expressed in stroma, we examined the consequence of cooperation between these signals. We show that HGF disrupts NeuNT-induced epithelial morphogenesis, stimulating the breakdown of cell-cell junctions, dispersal, and invasion of single cells. This correlates with a decrease in junctional proteins claudin-1 and E-cadherin, in addition to the internalization of the tight junction protein ZO-1. HGF-induced invasion of NT-expressing cells is abrogated by pretreatment with a pharmacological inhibitor of the mitogen-activated protein kinase kinase (MEK) pathway, which restores E-cadherin and ZO-1 at cell-cell junctions, establishing the involvement of MEK-dependent pathways in this process. These results demonstrate that physiological signals downstream from the HGF/Met receptor synergize with ErbB2/Neu to enhance the malignant phenotype, promoting the breakdown of cell-cell junctions and enhanced cell invasion. This is particularly important for cancers where ErbB2/Neu is overexpressed and HGF is a physiological growth factor found in the stroma.

Supplementary Figure 5, (f) of the paper Feedback regulation through myosin II confers robustness on RhoA signalling at E-cadherin junctions.

UQ eSpace ◽  
2016 ◽  
Author(s):  
Rashmi Priya ◽  
Guillermo Gomez ◽  
Srikanth Budnar ◽  
Rukhmani (Suzie) Verma ◽  
Hayley Cox ◽  
...  
Keyword(s):  
Myosin Ii ◽  
Feedback Regulation ◽  
E Cadherin

Supplementary Figure 5, (c) of the paper Feedback regulation through myosin II confers robustness on RhoA signalling at E-cadherin junctions.

UQ eSpace ◽  
2016 ◽  
Author(s):  
Rashmi Priya ◽  
Guillermo Gomez ◽  
Srikanth Budnar ◽  
Rukhmani (Suzie) Verma ◽  
Hayley Cox ◽  
...  
Keyword(s):  
Myosin Ii ◽  
Feedback Regulation ◽  
E Cadherin

Supplementary Figure 4, (h) of the paper Feedback regulation through myosin II confers robustness on RhoA signalling at E-cadherin junctions.

UQ eSpace ◽  
2016 ◽  
Author(s):  
Rashmi Priya ◽  
Guillermo Gomez ◽  
Srikanth Budnar ◽  
Rukhmani (Suzie) Verma ◽  
Hayley Cox ◽  
...  
Keyword(s):  
Myosin Ii ◽  
Feedback Regulation ◽  
E Cadherin

Supplementary Figure 3, (d) of the paper Feedback regulation through myosin II confers robustness on RhoA signalling at E-cadherin junctions.

UQ eSpace ◽  
2016 ◽  
Author(s):  
Rashmi Priya ◽  
Guillermo Gomez ◽  
Srikanth Budnar ◽  
Rukhmani (Suzie) Verma ◽  
Hayley Cox ◽  
...  
Keyword(s):  
Myosin Ii ◽  
Feedback Regulation ◽  
E Cadherin
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