Significance While many bacteria can sense the presence of a surface, the mechanical properties of different surfaces vary tremendously and can be as rigid as bone or as soft as mucus. We show that the pathogen Pseudomonas aeruginosa distinguishes surfaces by stiffness and transcriptionally tunes its virulence to surface rigidity. This connection between pathogenicity and mechanical properties of the infection site presents an interesting potential for clinical applications. The mechanism behind stiffness sensing relies on the retraction of external appendages called type IV pili that deform the surface. While this mechanism has interesting parallels to stiffness sensing in mammalian cells, our results suggest that stiffness sensing in much smaller bacterial cells relies on temporal sensing instead of spatial sensing strategies.

Bacteria which grow not on the featureless agar plates of the microbiology lab but in the real world must navigate topologies which are nontrivially complex, such as mazes or fractals. We show that chemosensitive motile E. coli can efficiently explore nontrivial mazes in times much shorter than a no-memory (Markovian) walk would predict, and can collectively escape from a fractal topology. The strategies used by the bacteria include individual power-law probability distribution function exploration, the launching of chemotactic collective waves with preferential branching at maze nodes and defeating of fractal pumping, and bet hedging in case the more risky attempts to find food fail.

Bacteria under external stress can reveal unexpected emergent phenotypes. We show that the intensely studied bacterium Escherichia coli can transform into long, highly motile helical filaments poized at a torsional buckling criticality when exposed to minimum inhibitory concentrations of several antibiotics. While the highly motile helices are physically either right- or left-handed, the motile helices always rotate with a right-handed angular velocity ω→, which points in the same direction as the translational velocity v→T of the helix. Furthermore, these helical cells do not swim by a “run and tumble” but rather synchronously flip their spin ω→ and thus translational velocity—backing up rather than tumbling. By increasing the translational persistence length, these dynamics give rise to an effective diffusion coefficient up to 20 times that of a normal E. coli cell. Finally, we propose an evolutionary mechanism for this phenotype’s emergence whereby the increased effective diffusivity provides a fitness advantage in allowing filamentous cells to more readily escape regions of high external stress.

The bacterium Myxoccocus xanthus produces multicellular protective droplets called fruiting bodies when starved. These structures form initially through the active dewetting of cells into surfacebound droplets, where substantial flows of the material are needed as the fruiting bodies grow and become round. These dynamics are followed by a primitive developmental process in which the fluid-like droplets of motile cells mature into mechanically-resilient mounds of non-motile spores that can resist significant mechanical perturbation from the external environment. To date, the mechanical properties of fruiting bodies and the changes in cellular behavior that lead to maturation have not been studied. We use atomic force microscopy to probe the rheology of droplets throughout their development and find that relaxation occurs on two time scales, ∼1 s and ∼100 s. We use a two-element Maxwell-Wiechert model to quantify the viscoelastic relaxation and find that at early developmental times, cellular motility is responsible for the flow of the material but that this flow ceases when cells stop moving and become nonmotile spores. Later in development there is a dramatic increase in the modulus of the droplet as cells sporulate and the fruiting body matures, resulting in a mostly elastic structure that can protect spores from harsh environmental insult.

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