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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.

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.

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

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.

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.

Cells often navigate through confined spaces. Now it is shown that cells retain a mechanical memory of previous confinement events, which makes them more efficient at migrating through narrow microenvironments.

An end-to-end machine learning approach that can learn which mechanisms determine cell fate and competition from a large time-lapse microscopy dataset is developed. The approach makes use of a probabilistic autoencoder to learn an interpretable representation of the organization of cells, and provides cell fate predictions that can be tested in drug screening experiments.

Cells typically migrate toward stiffer substrates via durotaxis, relying on focal adhesions. Here, the authors show that confined cells can migrate up friction gradients without focal adhesions, revealing a mode of directed migration called frictiotaxis.

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.

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.

Stiffness topography with sharp atomic force microscopy tips can be used to generate nanoscale cross-sections of nuclear pore complexes, and suggests that the selective barrier in the complexes consists of a crosslinked network of nuclear pore proteins.

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.

Cells migrating within a collective naturally have restricted access to their surroundings. Experiments on micropatterned substrates now show that this confinement can regulate epithelial migration—governing cell morphology, forces and velocity.

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.

Cellular mechanical forces are regulated by Rho GTPases. Here the authors develop an optogenetic system to control the spatiotemporal activity of RhoA, and show that directing a RhoA activator to the plasma membrane causes contraction and YAP nuclear localization, whereas directing it to the mitochondria causes relaxation.

Cell metabolism must adapt to the energy needs of migrating cells. This study finds that fast amoeboid migrating cells harbor high AMPK activity, which controls both mitochondrial dynamics and cytoskeletal remodeling, enabling reduced energy needs.

Sample processing for biological imaging experiments involves elaborate protocols with low reproducibility and throughput. Here the authors develop an open-source system called NanoJ-Fluidics, composed of off-the-shelf Lego components and an ImageJ-based controller to achieve automated fixation, labelling and imaging of cells.

Atomic force microscopy indentation measurements of cells cultured on soft substrates may result in an underestimation of cell stiffness. A model has now been developed that takes this soft substrate effect into account, revealing that cortical cell stiffness is largely independent of substrate mechanics.

Sahai and colleagues report that YAP is required for the establishment and function of cancer-associated fibroblasts. They propose that matrix stiffening promotes Src-mediated activation of YAP in fibroblasts, which is necessary for the cancer-associated fibroblast phenotype and further promotes matrix stiffening in a positive feedback loop.

The authors investigate the effects of varying strain rates on the response of epithelial cells

Bergert et al. use theoretical modelling and cell-based experiments to show that adhesion-independent cell migration is powered by nonspecific substrate friction, with smaller forces exerted compared with those of focal-adhesion-dependent movement.

Stiffening of the mesoderm owing to an accumulation of cells triggers collective migration of neural crest cells during morphogenesis.

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