Bacteria commonly live attached to surfaces in very dense collectives containing billions of cells 1 . While it is known that motility allows these groups to expand en masse into new territory [2][3][4][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 pili 3,6,7 . 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 crystals [8][9][10][11][12][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, allowing them to collectively migrate faster. Our work demonstrates that the physics of liquid crystals explains why slow bacteria can outcompete fast moving cells when competing for new territory.

3D-printing networks of droplets connected by interface bilayers are a powerful platform to build synthetic tissues in which functionality relies on precisely ordered structures. However, the structural precision and consistency in assembling these structures is currently limited, which restricts intricate designs and the complexity of functions performed by synthetic tissues. Here, we report that the equilibrium contact angle (θ DIB) between a pair of droplets is a key parameter that dictates the tessellation and precise positioning of hundreds of picolitresized droplets within 3D-printed, multi-layer networks. When θ DIB approximates the geometrically-derived critical angle (θ c) of 35.3°, the resulting networks of droplets arrange in regular hexagonal close-packed (hcp) lattices with the least fraction of defects. With this improved control over droplet packing, we can 3D-print functional synthetic tissues with single-droplet-wide conductive pathways. Our new insights into 3D droplet packing permit the fabrication of complex synthetic tissues, where precisely positioned compartments perform coordinated tasks.

Bacteria often live in diverse communities where the spatial arrangement of strains and species is considered critical for their ecology. However, a test of this hypothesis requires manipulation at the fine scales at which spatial structure naturally occurs. Here we develop a droplet-based printing method to arrange bacterial genotypes across a sub-millimetre array. We print strains of the gut bacterium Escherichia coli that naturally compete with one another using protein toxins. Our experiments reveal that toxin-producing strains largely eliminate susceptible non-producers when genotypes are well-mixed. However, printing strains side-by-side creates an ecological refuge where susceptible strains can persist in large numbers. Moving to competitions between toxin producers reveals that spatial structure can make the difference between one strain winning and mutual destruction. Finally, we print different potential barriers between competing strains to understand how ecological refuges form, which shows that cells closest to a toxin producer mop up the toxin and protect their clonemates. Our work provides a method to generate customised bacterial communities with defined spatial distributions, and reveals that micron-scale changes in these distributions can drive major shifts in ecology.