Actin-based force generation and cell adhesion in tissue morphogenesis

2021 ◽  
Vol 31 (10) ◽  
pp. R667-R680
Author(s):  
D. Nathaniel Clarke ◽  
Adam C. Martin
2014 ◽  
Vol 106 (2) ◽  
pp. 789a
Author(s):  
Jeffrey van Haren ◽  
Torsten Wittmann

2020 ◽  
Vol 31 (16) ◽  
pp. 1663-1674 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin

Cell divisions can either promote or inhibit tissue morphogenesis. In contractile epithelia, mitotic entry disrupts medioapical myosin activation and reverses apical constriction. We found that different spatiotemporal patterns of mitotic entry and the resultant changes in force generation at the tissue level dictate distinct tissue shape outcomes.


2008 ◽  
Vol 214 (3) ◽  
pp. 218-232 ◽  
Author(s):  
Craig R. Magie ◽  
Mark Q. Martindale

2016 ◽  
Vol 113 (51) ◽  
pp. 14621-14626 ◽  
Author(s):  
Bart Smeets ◽  
Ricard Alert ◽  
Jiří Pešek ◽  
Ignacio Pagonabarraga ◽  
Herman Ramon ◽  
...  

Cells in tissues can organize into a broad spectrum of structures according to their function. Drastic changes of organization, such as epithelial–mesenchymal transitions or the formation of spheroidal aggregates, are often associated either to tissue morphogenesis or to cancer progression. Here, we study the organization of cell colonies by means of simulations of self-propelled particles with generic cell-like interactions. The interplay between cell softness, cell–cell adhesion, and contact inhibition of locomotion (CIL) yields structures and collective dynamics observed in several existing tissue phenotypes. These include regular distributions of cells, dynamic cell clusters, gel-like networks, collectively migrating monolayers, and 3D aggregates. We give analytical predictions for transitions between noncohesive, cohesive, and 3D cell arrangements. We explicitly show how CIL yields an effective repulsion that promotes cell dispersal, thereby hindering the formation of cohesive tissues. Yet, in continuous monolayers, CIL leads to collective cell motion, ensures tensile intercellular stresses, and opposes cell extrusion. Thus, our work highlights the prominent role of CIL in determining the emergent structures and dynamics of cell colonies.


2006 ◽  
Vol 20 (23) ◽  
pp. 3199-3214 ◽  
Author(s):  
J. M. Halbleib ◽  
W. J. Nelson

2021 ◽  
Author(s):  
Luka Sheppard ◽  
Ulrich Tepass

Abstractα-catenin couples the cadherin-catenin complex to the actin cytoskeleton. The mechanosensitive α-catenin M region undergoes conformational changes upon application of force to recruit binding partners. Here, we took advantage to the tension landscape in the Drosophila embryo to define three different states of α-catenin mechanosensing in support of cell adhesion. Low, medium, and high tension contacts showed α-catenin M region-dependent low, medium, and high levels of Vinculin and Ajuba recruitment. In contrast, Afadin/Canoe acts in parallel to α-catenin at bicellular low and medium tension junctions, but requires an interaction with α-catenin for its tension-sensitive enrichment at high-tension tricellular junctions. Individual M region domains make complex contributions to cell adhesion through their impact on binding partner recruitment, and redundancies with the function of Afadin/Canoe. Our data argue that α-catenin and its interaction partners are part of a cooperative and partially redundant, mechanoresponsive network that supports AJs remodelling during morphogenesis.


2017 ◽  
Author(s):  
R Clément ◽  
C. Collinet ◽  
B. Dehapiot ◽  
T. Lecuit ◽  
P.-F. Lenne

Tissue morphogenesis relies on the production of active cellular forces. Understanding how such forces are mechanically converted into cell shape changes is essential to our understanding of morphogenesis. Here we use Myosin II pulsatile activity during Drosophila embryogenesis to study how transient forces generate irreversible cell shape changes. Analyzing the dynamics of junction shortening and elongation resulting from Myosin II pulses, we find that long pulses yield less reversible deformations, typically a signature of dissipative mechanics. This is consistent with a simple viscoelastic description, which we use to model individual shortening and elongation events. The model predicts that dissipation typically occurs on the minute timescale, a timescale commensurate with that of force generation by Myosin II pulses. We test this estimate by applying time-controlled forces on junctions with optical tweezers. Our results argue that active junctional deformation is stabilized by dissipation. Hence, tissue morphogenesis requires coordination between force generation and dissipation.


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