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How bacterial chemotaxis is performed is much better understood than why. Traditionally, chemotaxis has been understood as a foraging strategy by which bacteria enhance their uptake of nutrients and energy, yet it has remained puzzling why certain less nutritious compounds are strong chemoattractants and vice versa. Recently, we have gained increased understanding of alternative ecological roles of chemotaxis, such as navigational guidance in colony expansion, localization of hosts or symbiotic partners and contribution to microbial diversity by the generation of spatial segregation in bacterial communities. Although bacterial chemotaxis has been observed in a wide range of environmental settings, insights into the phenomenon are mostly based on laboratory studies of model organisms. In this Review, we highlight how observing individual and collective migratory behaviour of bacteria in different settings informs the quantification of trade-offs, including between chemotaxis and growth. We argue that systematically mapping when and where bacteria are motile, in particular by transgenerational bacterial tracking in dynamic environments and in situ approaches from guts to oceans, will open the door to understanding the rich interplay between metabolism and growth and the contribution of chemotaxis to microbial life.Chemotaxis is one of the best studied bacterial behaviours, but the underlying mechanisms are much better understood than the reasons and consequences of chemotaxis. In this Review, Keegstra et al. discuss the costs and benefits both for individual bacteria and whole populations.

Bacteria have developed a large array of motility mechanisms to exploit available resources and environments. These mechanisms can be broadly classified into swimming in aqueous media and movement over solid surfaces. Swimming motility involves either the rotation of rigid helical filaments through the external medium or gyration of the cell body in response to the rotation of internal filaments. On surfaces, bacteria swarm collectively in a thin layer of fluid powered by the rotation of rigid helical filaments, they twitch by assembling and disassembling type IV pili, they glide by driving adhesins along tracks fixed to the cell surface and, finally, non-motile cells slide over surfaces in response to outward forces due to colony growth. Recent technological advances, especially in cryo-electron microscopy, have greatly improved our knowledge of the molecular machinery that powers the various forms of bacterial motility. In this Review, we describe the current understanding of the physical and molecular mechanisms that allow bacteria to move around.In this Review, Wadhwa and Berg explore the most common bacterial motility mechanisms and summarize the current understanding of the molecular machines that enable bacteria to swim in aqueous media and move on solid surfaces.

In embryonic development or tumour evolution, cells often migrate collectively within confining tracks defined by their microenvironment1,2. In some of these situations, the displacements within a cell strand are antiparallel3, giving rise to shear flows. However, the mechanisms underlying these spontaneous flows remain poorly understood. Here, we show that an ensemble of spindle-shaped cells plated in a well-defined stripe spontaneously develops a shear flow whose characteristics depend on the width of the stripe. On wide stripes, the cells self-organize in a nematic phase with a director at a well-defined angle with the stripe’s direction, and develop a shear flow close to the stripe’s edges. However, on stripes narrower than a critical width, the cells perfectly align with the stripe’s direction and the net flow vanishes. A hydrodynamic active gel theory provides an understanding of these observations and identifies the transition between the non-flowing phase oriented along the stripe and the tilted phase exhibiting shear flow as a Fréedericksz transition driven by the activity of the cells. This physical theory is grounded in the active nature of the cells and based on symmetries and conservation laws, providing a generic mechanism to interpret in vivo antiparallel cell displacements.

The soil bacterium Myxococcus xanthus lives in densely packed groups that form dynamic three-dimensional patterns in response to environmental changes, such as droplet-like fruiting bodies during starvation1. The development of these multicellular structures begins with the sequential formation of cell layers in a process that is poorly understood2. Here, using confocal three-dimensional imaging, we find that motile, rod-shaped M. xanthus cells are densely packed and aligned in each layer, forming an active nematic liquid crystal. Cell alignment is nearly perfect throughout the population except at point defects that carry half-integer topological charge. We observe that new cell layers preferentially form at the position of +1/2 defects, whereas holes preferentially open at −1/2 defects. To explain these findings, we model the bacterial colony as an extensile active nematic fluid with anisotropic friction. In agreement with our experimental measurements, this model predicts an influx of cells towards the +1/2 defects and an outflux of cells from the −1/2 defects. Our results suggest that cell motility and mechanical cell–cell interactions are sufficient to promote the formation of cell layers at topological defects, thereby seeding fruiting bodies in colonies of M. xanthus.Topological defects in active nematic systems such as epithelial tissues and neural progenitor cells can be associated with biological functions. Here, the authors show that defects can play a role in the layer formation of the soil bacterium Myxococcus xanthus.

Bacteria commonly live attached to surfaces in dense collectives containing billions of cells1. While it is known that motility allows these groups to expand en masse into new territory2–5, how bacteria collectively move across surfaces under such tightly packed conditions remains poorly understood. Here we combine experiments, cell tracking and individual-based modelling to study the pathogen Pseudomonas aeruginosa as it collectively migrates across surfaces using grappling-hook-like pili3,6,7. We show that the fast-moving cells of a hyperpilated mutant are overtaken and outcompeted by the slower-moving wild type at high cell densities. Using theory developed to study liquid crystals8–13, we demonstrate that this effect is mediated by the physics of topological defects, points where cells with different orientations meet one another. Our analyses reveal that when defects with topological charge +1/2 collide with one another, the fast-moving mutant cells rotate to point vertically and become trapped. By moving more slowly, wild-type cells avoid this trapping mechanism and generate collective behaviour that results in faster migration. In this way, the physics of liquid crystals explains how slow bacteria can outcompete faster cells in the race for new territory.Bacteria are able to move as vast, dense collectives. Here the authors show that slow movement is key to this collective behaviour because faster bacteria cause topological defects to collide together and trap cells in place.

Actomyosin machinery endows cells with contractility at a single-cell level. However, within a monolayer, cells can be contractile or extensile based on the direction of pushing or pulling forces exerted by their neighbours or on the substrate. It has been shown that a monolayer of fibroblasts behaves as a contractile system while epithelial or neural progentior monolayers behave as an extensile system. Through a combination of cell culture experiments and in silico modelling, we reveal the mechanism behind this switch in extensile to contractile as the weakening of intercellular contacts. This switch promotes the build-up of tension at the cell–substrate interface through an increase in actin stress fibres and traction forces. This is accompanied by mechanotransductive changes in vinculin and YAP activation. We further show that contractile and extensile differences in cell activity sort cells in mixtures, uncovering a generic mechanism for pattern formation during cell competition, and morphogenesis. It is now revealed, using cell cultures and in silico models, that weakening intercellular contacts is a fundamental process essential for switching from extensile to contractile tissue behaviour.

The directed migration of cell collectives is essential in various physiological processes, such as epiboly, intestinal epithelial turnover, and convergent extension during morphogenesis, as well as during pathological events such as wound healing and cancer metastasis. Collective cell migration leads to the emergence of coordinated movements over multiple cells. Our current understanding emphasizes that these movements are mainly driven by large-scale transmission of signals through adherens junctions. In this study, we show that collective movements of epithelial cells can be triggered by polarity signals at the single-cell level through the establishment of coordinated lamellipodial protrusions. We designed a minimalistic model system to generate one-dimensional epithelial trains confined in ring-shaped patterns that recapitulate rotational movements observed in vitro in cellular monolayers and in vivo in genital or follicular cell rotation. Using our system, we demonstrated that cells follow coordinated rotational movements after establishing directed Rac1-dependent polarity over the entire monolayer. Our experimental and numerical approaches show that the maintenance of coordinated migration requires the acquisition of a front–rear polarity within each single cell but does not require the maintenance of cell–cell junctions. Taken together, these unexpected findings demonstrate that collective cell dynamics in closed environments as observed in multiple in vitro and in vivo situations can arise from single-cell behaviour through a sustained memory of cell polarity. Collective cell migration is usually attributed to large-scale transmission of signals through cell junctions. Here, the authors confine cells into a ring-shaped pattern and show that collective cell migration can arise at the single-cell level.

Control of the structure and function of three-dimensional multicellular tissues depends critically on the spatial and temporal coordination of cellular physical properties, yet the organizational principles that govern these events and their disruption in disease remain poorly understood. Using a multicellular mammary cancer organoid model, we map here the spatial and temporal evolution of positions, motions and physical characteristics of individual cells in three dimensions. Compared with cells in the organoid core, cells at the organoid periphery and the invasive front are found to be systematically softer, larger and more dynamic. These mechanical changes are shown to arise from supracellular fluid flow through gap junctions, the suppression of which delays the transition to an invasive phenotype. These findings highlight the role of spatiotemporal coordination of cellular physical properties in tissue organization and disease progression. A platform for probing the mechanics and migratory dynamics of a growing model breast cancer reveals that cells at the invasive edge are faster, softer and larger than those in the core. Eliminating the softer cells delays the transition to invasion.

Spindle-shaped cells readily form nematic structures marked by topological defects. When confined, the defect distribution is independent of the domain size, activity and type of cell, lending a stability not found in non-cellular active nematics. Most spindle-shaped cells (including smooth muscles and sarcomas) organize in vivo into well-aligned ‘nematic’ domains 1 , 2 , 3 , creating intrinsic topological defects that may be used to probe the behaviour of these active nematic systems. Active non-cellular nematics have been shown to be dominated by activity, yielding complex chaotic flows 4 , 5 . However, the regime in which live spindle-shaped cells operate, and the importance of cell–substrate friction in particular, remains largely unexplored. Using in vitro experiments, we show that these active cellular nematics operate in a regime in which activity is effectively damped by friction, and that the interaction between defects is controlled by the system’s elastic nematic energy. Due to the activity of the cells, these defects behave as self-propelled particles and pairwise annihilate until all displacements freeze as cell crowding increases 6 , 7 . When confined in mesoscopic circular domains, the system evolves towards two identical +1/2 disclinations facing each other. The most likely reduced positions of these defects are independent of the size of the disk, the cells’ activity or even the cell type, but are well described by equilibrium liquid crystal theory. These cell-based systems thus operate in a regime more stable than other active nematics, which may be necessary for their biological function.

Diverse processes—e.g. bioremediation, biofertilization, and microbial drug delivery—rely on bacterial migration in disordered, three-dimensional (3D) porous media. However, how pore-scale confinement alters bacterial motility is unknown due to the opacity of typical 3D media. As a result, models of migration are limited and often employ ad hoc assumptions. Here we reveal that the paradigm of run-and-tumble motility is dramatically altered in a porous medium. By directly visualizing individual Escherichia coli , we find that the cells are intermittently and transiently trapped as they navigate the pore space, exhibiting diffusive behavior at long time scales. The trapping durations and the lengths of “hops” between traps are broadly distributed, reminiscent of transport in diverse other disordered systems; nevertheless, we show that these quantities can together predict the long-time bacterial translational diffusivity. Our work thus provides a revised picture of bacterial motility in complex media and yields principles for predicting cellular migration. Many bacteria swim with run-and-tumble motion in unconfined fluid. Here the authors report that confinement of these bacteria in a 3D porous medium changes this motion into hopping and trapping, in which the cells are intermittently and transiently trapped as they navigate the pore space.