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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.

Competition is prevalent and could be harnessed as an alternative to antibiotics

Humans and many other hosts establish a diverse community of beneficial microbes anew each generation. The order and identity of incoming symbionts is critical for health, but what determines the success of the assembly process remains poorly understood. Here we develop ecological theory to identify factors important for microbial community assembly. Our method maps out all feasible pathways for the assembly of a given microbiome—with analogies to the mutational maps underlying fitness landscapes in evolutionary biology. Building these “assembly maps” reveals a tradeoff at the heart of the assembly process. Ecological dependencies between members of the microbiota make assembly predictable—and can provide metabolic benefits to the host—but these dependencies may also create barriers to assembly. This effect occurs because interdependent species can fail to establish when each relies on the other to colonize first. We support our predictions with published data from the assembly of the preterm infant microbiota, where we find that ecological dependence is associated with a predictable order of arrival. Our models also suggest that hosts can overcome barriers to assembly via mechanisms that either promote the uptake of multiple symbiont species in one step or feed early colonizers. This predicted importance of host feeding is supported by published data on the impacts of breast milk in the assembly of the human microbiome. We conclude that both microbe–microbe and host–microbe interactions are important for the trajectory of microbiome assembly.

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