Bacteria solve the problem of crowding by moving slowly

Abstract

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.

Mechanotaxis directs Pseudomonas aeruginosa twitching motility

“…S1A). These observations could explain the patterns observed at the edge of larger colonies (14,24). In summary, by controlling reversal rates upon collision, Chp-dependent mechanosensing can optimize P. aeruginosa collective motility.…”

Swarming bacteria undergo localized dynamic phase transition to form stress-induced biofilms

“…The biophysical transition that we report here would suggest that this happens once the ageing swarm cannot be driven anymore to within the putative MIPS region by the external stressor. It would be useful to explore this further within the general framework of biophysical models for cluster formation ( Be’er et al, 2020 ; Worlitzer et al, 2020 ), 3D architecture formation ( Partridge et al, 2018 ) and motility-induced buckling within a bacterial swarm ( Meacock et al, 2020 ; Takatori and Mandadapu, 2003 ). Another important question lies in the interplay between biophysical and molecular mechanisms regulating stress-induced biofilm development.…”

Activity pulses induce spontaneous flow reversals in viscoelastic environments

“…The cross-talk between the mechanical micro-environment of living matter and this intrinsic ability of living systems to actively generate self-sustained motion governs pattern formation and self-organization in important biological processes including collective transport of sperm cells in confined tubes [8], shaping bacterial biofilms [9,10], tissue regeneration [11] and sculpting organ development [12]. Not only does the mechanical micro-environment provide geometrical constraints for active materials [13], but it is also often endowed with viscoelastic properties that allow for time-dependent responses to activity-induced stresses and deformations [2,14].…”