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Much of our understanding of the role of actin in cell migration is based on studies of cells moving across two-dimensional surfaces. Wilson et al.show that cells crawling in three dimensions through a narrow channel form two functionally distinct actin networks at the leading edge.

Tissue monolayers avoid rupture at large tensile stresses through a strain-stiffening process governed by intermediate keratin filaments.

Evidence has been found that a biological tissue might behave like a liquid crystal. Even more remarkably, topological defects in this liquid-crystal system seem to influence cell behaviour. A materials physicist and a biologist discuss what the findings mean for researchers in their fields. See Letter p.212

Cracks in stretched epithelial tissue are caused by a build-up of hydraulic pressure beneath the cells when the tissue is unloaded.

Stress relaxation in cell monolayers shows remarkable similarities with that of single cells, suggesting the rheology of epithelial tissues is mediated by the actomyosin cortex—with dynamics reminiscent of those on a cellular level.

Cao et al. show that SPIN90 enhances formation of Arp2/3-mediated unbranched filaments and promotes a formin-based cortex by recruiting mDia1 or forming a ternary SPIN90–Arp2/3–mDia1 complex.

Epithelial tissues behave as pre-tensed viscoelastic sheets that can buffer against compression and rapidly recover from buckling. Epithelial mechanical properties define a tissue-intrinsic buckling threshold that dictates the compressive strain above which tissue folds become permanent.

N-WASP activates Arp2/3-mediated actin nucleation. N-WASP is now shown to stabilize and organize the actin cytoskeleton at cell–cell junctions through its interaction with the actin-binding protein WIRE.

Yap and colleagues demonstrate that E-cadherin-based cell–cell junctions exhibit distinct patterns of apical and lateral contractility. They show that N-WASP-dependent stabilization of F-actin mediates increased apical junctional tension, and that modulation of intra-junctional tension differences can promote extrusion of cells from monolayers.

The interior of the cell is organized with the help of dynamic structures that condense like droplets. A timing strategy ensures that cells maintain healthy function by avoiding uncontrolled growth of these condensates.

It has been suggested that the cytoplasm of living cells can be described as a porous elastic meshwork bathed in an interstitial fluid. Microindentation tests now show that intracellular water redistribution plays a fundamental role in cellular rheology and that at physiologically relevant timescales cellular responses to mechanical stresses are consistent with such a poroelastic model.

Cellular deformations are largely driven by contractile forces generated by myosin motors in the submembraneous actin cortex. Here we show that these forces are controlled not simply by cortical myosin levels, but rather by myosins spatial arrangement, specifically the extent of their overlap with cortical actin.

Membrane blebs are considered to be a hallmark of apoptosis; however, blebs are also observed in healthy cells during cytokinesis and cell motility. What are the potential mechanisms by which blebbing can be polarized and translated into movement? And what are the advantages of blebbing motility?

In vitro models of actin organization show the formation of vortices, asters and stars. Here Fritzsche et al. show that such actin structures form in living cells in a manner dependent on the Arp2/3 complex but not myosin, and such structures influence membrane architecture but not cortex elasticity.

Stress fibres form a fully integrated meshwork with the submembranous contractile actin cortex that generates and propagates traction forces across the entire cell.

Cortical tension is thought to be generated by myosin II, and little is known about the role of actin network properties. Chugh et al. demonstrate that actin cortex thickness, determined by actin filament length, influences cortical tension.

Yolland et al. demonstrate persistent flow of the actin flow behind the leading edge and its impact on cell directionality during migration.

The physical properties of the extracellular environment — in terms of confinement, rigidity, surface topology and adhesion-ligand density — can have profound effects on the migration strategy and migration velocity of cells in differentin vivocontexts.

This protocol uses fluorescence recovery after photobleaching (FRAP) to dissect the reaction dynamics leading to protein turnover in macromolecular complexes in living cells.