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Differential cell adhesion and cortex tension are thought to drive cell sorting by controlling cell-cell contact formation. Here, we show that cell adhesion and cortex tension have different mechanical functions in controlling progenitor cell-cell contact formation and sorting during zebrafish gastrulation. Cortex tension controls cell-cell contact expansion by modulating interfacial tension at the contact. By contrast, adhesion has little direct function in contact expansion, but instead is needed to mechanically couple the cortices of adhering cells at their contacts, allowing cortex tension to control contact expansion. The coupling function of adhesion is mediated by E-cadherin and limited by the mechanical anchoring of E-cadherin to the cortex. Thus, cell adhesion provides the mechanical scaffold for cell cortex tension to drive cell sorting during gastrulation.

Blebs are spherical membrane protrusions often observed during cell migration, cell spreading, cytokinesis, and apoptosis, both in cultured cells and in vivo. Bleb expansion is thought to be driven by the contractile actomyosin cortex, which generates hydrostatic pressure in the cytoplasm and can thus drive herniations of the plasma membrane. However, the role of cortical tension in bleb formation has not been directly tested, and despite the importance of blebbing, little is known about the mechanisms of bleb growth. In order to explore the link between cortical tension and bleb expansion, we induced bleb formation on cells with different tensions. Blebs were nucleated in a controlled manner by laser ablation of the cortex, mimicking endogenous bleb nucleation. Cortical tension was modified by treatments affecting the level of myosin activity or proteins regulating actin turnover. We show that there is a critical tension below which blebs cannot expand. Above this threshold, the maximal size of a bleb strongly depends on tension, and this dependence can be fitted with a model of the cortex as an active elastic material. Together, our observations and model allow us to relate bleb shape parameters to the underlying cellular mechanics and provide insights as to how bleb formation can be biochemically regulated during cell motility.T he cell cortex is a thin meshwork of actin filaments, myosin, and associated proteins that lies beneath the plasma membrane (1). Because of the presence of active myosin motors, which slide filaments with respect to one another in the network, the cortex is under tension. As a result, the cortex exerts pressure on the cytoplasm and can actively contract, driving cell deformations (2).Blebs are spherical membrane protrusions that commonly occur at the cortex during cytokinesis, cell spreading, virus uptake, and apoptosis (3-7). Moreover, increasing evidence points to an essential role for blebs as leading edge protrusions during cell migration in three-dimensional environments, particularly during embryonic development and tumor-cell dissemination (8-11; reviewed in refs. 7, 12). Despite the importance of blebbing, very little is known about the mechanisms of bleb growth.The life cycle of a bleb can be subdivided into three phases (7, 13). First, a bleb is nucleated, either by local detachment of the cortex from the plasma membrane or by local rupture of the cortex. In the subsequent growth phase, a membrane bulge, initially devoid of cortex, expands from the nucleation site. Finally, the cortex gradually reassembles at the bleb membrane, leading to bleb retraction.Bleb formation is often correlated with high myosin II activity, and myosin II inhibition prevents blebbing (6,7,10,14). For that reason, and because of their round shape and rapid expansion, blebs are commonly believed to be a direct mechanical consequence of the hydrostatic pressure exerted on the cytoplasm by the contractile cortex, which would drive bleb growth from places of local cortex weakening without any further r...

How tissue shape emerges from the collective mechanical properties and behavior of individual cells is not understood. We combine experiment and theory to study this problem in the developing wing epithelium of Drosophila. At pupal stages, the wing-hinge contraction contributes to anisotropic tissue flows that reshape the wing blade. Here, we quantitatively account for this wing-blade shape change on the basis of cell divisions, cell rearrangements and cell shape changes. We show that cells both generate and respond to epithelial stresses during this process, and that the nature of this interplay specifies the pattern of junctional network remodeling that changes wing shape. We show that patterned constraints exerted on the tissue by the extracellular matrix are key to force the tissue into the right shape. We present a continuum mechanical model that quantitatively describes the relationship between epithelial stresses and cell dynamics, and how their interplay reshapes the wing.DOI: http://dx.doi.org/10.7554/eLife.07090.001