scholarly journals Measurement of junctional tension in epithelial cells at the onset of primitive streak formation in the chick embryo via non-destructive optical manipulation

2018 ◽  
Author(s):  
Valentina Ferro ◽  
Manli Chuai ◽  
David McGloin ◽  
Cornelis Weijer
Keyword(s):  
Epithelial Cells ◽  
Cell Shape ◽  
Large Scale ◽  
Cell Sheet ◽  
Primitive Streak ◽  
Cell Junctions ◽  
Optical Manipulation ◽  
Cell Shape Changes ◽  
Non Destructive ◽  
Shape Changes

Oriented cell intercalations and cell shape changes are key determinants of large-scale epithelial cell sheet deformations occurring during gastrulation in many organisms. In several cases directional intercalation and cell shape changes have been shown to be associated with a planar cell polarity in the organisation of the actin-myosin cytoskeleton of epithelial cells. This polarised cytoskeletal organisation has been postulated to reflect the directional tension necessary to drive and orient directional cell intercalations. We have now further characterised and applied a recently introduced non-destructive optical manipulation technique to measure the tension in individual cell junctions in the epiblast of chick embryos in the early stages of primitive streak formation. We have measured junctional tension as a function of position and orientation. Junctional tension of mesendoderm cells, the tissue that drives the formation of the streak, is higher than tension of junctions of cells in other parts of the epiblast. Furthermore, in the mesendoderm junctional tension is higher in the direction of intercalation. The data are fitted best with a Maxwell model and we find that both junctional tension and relaxation time are dependent on myosin activity.

scholarly journals Direct laser manipulation reveals the mechanics of cell contacts in vivo

2015 ◽  
Vol 112 (5) ◽  
pp. 1416-1421 ◽  
Author(s):  
Kapil Bambardekar ◽  
Raphaël Clément ◽  
Olivier Blanc ◽  
Claire Chardès ◽  
Pierre-François Lenne
Keyword(s):  
Cell Shape ◽  
Constitutive Law ◽  
Cell Junctions ◽  
Scale Model ◽  
Tissue Morphogenesis ◽  
Cell Contacts ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Cell Cell

Cell-generated forces produce a variety of tissue movements and tissue shape changes. The cytoskeletal elements that underlie these dynamics act at cell–cell and cell–ECM contacts to apply local forces on adhesive structures. In epithelia, force imbalance at cell contacts induces cell shape changes, such as apical constriction or polarized junction remodeling, driving tissue morphogenesis. The dynamics of these processes are well-characterized; however, the mechanical basis of cell shape changes is largely unknown because of a lack of mechanical measurements in vivo. We have developed an approach combining optical tweezers with light-sheet microscopy to probe the mechanical properties of epithelial cell junctions in the early Drosophila embryo. We show that optical trapping can efficiently deform cell–cell interfaces and measure tension at cell junctions, which is on the order of 100 pN. We show that tension at cell junctions equilibrates over a few seconds, a short timescale compared with the contractile events that drive morphogenetic movements. We also show that tension increases along cell interfaces during early tissue morphogenesis and becomes anisotropic as cells intercalate during germ-band extension. By performing pull-and-release experiments, we identify time-dependent properties of junctional mechanics consistent with a simple viscoelastic model. Integrating this constitutive law into a tissue-scale model, we predict quantitatively how local deformations propagate throughout the tissue.

scholarly journals Mechanosensitive junction remodelling promotes robust epithelial morphogenesis

2019 ◽  
Author(s):  
Michael F. Staddon ◽  
Kate E. Cavanaugh ◽  
Edwin M. Munro ◽  
Margaret L. Gardel ◽  
Shiladitya Banerjee
Keyword(s):  
Cell Shape ◽  
Strain Relaxation ◽  
Cell Junctions ◽  
Elastic Behaviour ◽  
Model Parameters ◽  
Epithelial Junctions ◽  
Contractile Stress ◽  
Length Changes ◽  
Cell Shape Changes ◽  
Shape Changes

Morphogenesis of epithelial tissues requires tight spatiotemporal coordination of cell shape changes. In vivo, many tissue-scale shape changes are driven by pulsatile contractions of intercellular junctions, which are rectified to produce irreversible deformations. The functional role of this pulsatory ratchet and its mechanistic basis remain unknown. Here we combine theory and biophysical experiments to show that mechanosensitive tension remodelling of epithelial cell junctions promotes robust epithelial shape changes via ratcheting. Using optogenetic control of actomyosin contractility, we find that epithelial junctions show elastic behaviour under low contractile stress, returning to their original lengths after contraction, but undergo irreversible deformation under higher magnitudes of contractile stress. Existing vertex-based models for the epithelium are unable to capture these results, with cell junctions displaying purely elastic or fluid-like behaviours, depending on the choice of model parameters. To describe the experimental results, we propose a modified vertex model with two essential ingredients for junction mechanics: thresholded tension remodelling and continuous strain relaxation. First, a critical strain threshold for tension remodelling triggers irreversible junction length changes for sufficiently strong contractions, making the system robust to small fluctuations in contractile activity. Second, continuous strain relaxation allows for mechanical memory removal, enabling frequency-dependent modulation of cell shape changes via mechanical ratcheting. Taken together, the combination of mechanosensitive tension remodelling and junctional strain relaxation provides a robust mechanism for large-scale morphogenesis.

Real-time imaging of cell-cell adherens junctions reveals that Drosophila mesoderm invagination begins with two phases of apical constriction of cells

2001 ◽  
Vol 114 (3) ◽  
pp. 493-501 ◽  
Author(s):  
H. Oda ◽  
S. Tsukita
Keyword(s):  
Real Time ◽  
Cell Shape ◽  
Adherens Junctions ◽  
Cell Sheet ◽  
Apical Surface ◽  
Apical Constriction ◽  
Real Time Imaging ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Cell Cell

Invagination of the epithelial cell sheet of the prospective mesoderm in Drosophila gastrulation is a well-studied, relatively simple morphogenetic event that results from dynamic cell shape changes and cell movements. However, these cell behaviors have not been followed at a sufficiently short time resolution. We examined mesoderm invagination in living wild-type embryos by real-time imaging of fluorescently labeled cell-cell adherens junctions, which are located at the apical zones of cell-cell contact. Low-light fluorescence video microscopy directly visualized the onset and progression of invagination. In an initial period of approximately 2 minutes, cells around the ventral midline reduced their apical surface areas slowly in a rather synchronous manner. Next, the central and more lateral cells stochastically accelerated or initiated their apical constriction, giving rise to random arrangements of cells with small and relatively large apices. Thus, we found that mesoderm invagination began with slow synchronous and subsequent fast stochastic phases of cell apex constriction. Furthermore, we showed that the mesoderm invagination of folded gastrulation mutant embryos lacked the normal two constriction phases, and instead began with asynchronous, feeble cell shape changes. Our observations suggested that Folded gastrulation-mediated signaling enabled synchronous activation of the contractile cortex, causing competition among the individual mesodermal cells for apical constriction. Movies available on-line: http://www.biologists.com/JCS/movies/jcs2073.html

scholarly journals Myosin-II-mediated cell shape changes and cell intercalation contribute to primitive streak formation

2015 ◽  
Vol 17 (4) ◽  
pp. 397-408 ◽  
Author(s):  
Emil Rozbicki ◽  
Manli Chuai ◽  
Antti I. Karjalainen ◽  
Feifei Song ◽  
Helen M. Sang ◽  
...  
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Primitive Streak ◽  
Cell Shape Changes ◽  
Cell Intercalation ◽  
Shape Changes

scholarly journals Division of Labor among the α6β4 Integrin, β1 Integrins, and an E3 Laminin Receptor to Signal Morphogenesis and β-Casein Expression in Mammary Epithelial Cells

1999 ◽  
Vol 10 (9) ◽  
pp. 2817-2828 ◽  
Author(s):  
John Muschler ◽  
André Lochter ◽  
Calvin D. Roskelley ◽  
Peter Yurchenco ◽  
Mina J. Bissell
Keyword(s):  
Epithelial Cells ◽  
Cell Shape ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Laminin Receptor ◽  
Blocking Antibody ◽  
Α6β4 Integrin ◽  
Cell Shape Changes ◽  
Blocking Antibodies ◽  
Shape Changes

Contact of cultured mammary epithelial cells with the basement membrane protein laminin induces multiple responses, including cell shape changes, growth arrest, and, in the presence of prolactin, transcription of the milk protein β-casein. We sought to identify the specific laminin receptor(s) mediating the multiple cell responses to laminin. Using assays with clonal mammary epithelial cells, we reveal distinct functions for the α6β4 integrin, β1 integrins, and an E3 laminin receptor. Signals from laminin for β-casein expression were inhibited in the presence of function-blocking antibodies against both the α6 and β1 integrin subunits and by the laminin E3 fragment. The α6-blocking antibody perturbed signals mediated by the α6β4 integrin, and the β1-blocking antibody perturbed signals mediated by another integrin, the α subunit(s) of which remains to be determined. Neither α6- nor β1-blocking antibodies perturbed the cell shape changes resulting from cell exposure to laminin. However, the E3 laminin fragment and heparin both inhibited cell shape changes induced by laminin, thereby implicating an E3 laminin receptor in this function. These results elucidate the multiplicity of cell-extracellular matrix interactions required to integrate cell structure and signaling and ultimately permit normal cell function.

scholarly journals CDC42 and Rac1 control different actin-dependent processes in the Drosophila wing disc epithelium.

1995 ◽  
Vol 131 (1) ◽  
pp. 151-164 ◽  
Author(s):  
S Eaton ◽  
P Auvinen ◽  
L Luo ◽  
Y N Jan ◽  
K Simons
Keyword(s):  
Epithelial Cells ◽  
Cell Shape ◽  
Larval Instar ◽  
Cell Types ◽  
Wing Disc ◽  
Dominant Negative ◽  
The Third ◽  
Drosophila Wing ◽  
Cell Shape Changes ◽  
Shape Changes

Cdc42 and Rac1 are members of the rho family of small guanosinetriphosphatases and are required for a diverse set of cytoskeleton-membrane interactions in different cell types. Here we show that these two proteins contribute differently to the organization of epithelial cells in the Drosophila wing imaginal disc. Drac1 is required to assemble actin at adherens junctions. Failure of adherens junction actin assembly in Drac1 dominant-negative mutants is associated with increased cell death. Dcdc42, on the other hand, is required for processes that involve polarized cell shape changes during both pupal and larval development. In the third larval instar, Dcdc42 is required for apico-basal epithelial elongation. Whereas normal wing disc epithelial cells increase in height more than twofold during the third instar, cells that express a dominant-negative version of Dcdc42 remain short and are abnormally shaped. Dcdc42 localizes to both apical and basal regions of the cell during these events, and mediates elongation, at least in part, by effecting a reorganization of the basal actin cytoskeleton. These observations suggest that a common cdc42-based mechanism may govern polarized cell shape changes in a wide variety of cell types.

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