Julia Yeomans OBE FRS

Abstract:

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.

Abstract:

© 2021, The Author(s), under exclusive licence to Springer Nature Limited. In the version of this Letter originally published online, the author J. M. Yeomans was incorrectly affiliated with ‘Niels Bohr Institute, University of Copenhagen, Copenhagen, Denmark’, instead of ‘Rudolf Peierls Centre for Theoretical Physics, Clarendon Laboratory, University of Oxford, Oxford, UK’. This affiliation has now been added, and other footnotes renumbered accordingly, in all versions of the Letter.

Abstract:

We use analytic arguments and numerical solutions of the continuum, active nematohydrodynamic equations to study how friction alters the behaviour of active nematics. Concentrating on the case where there is nematic ordering in the passive limit, we show that, as the friction is increased, memory effects become more prominent and +1/2 topological defects leave increasingly persistent trails in the director field as they pass. The trails are preferential sites for defect formation and they tend to impose polar order on any new +1/2 defects. In the absence of noise and for high friction, it becomes very difficult to create defects, but trails formed by any defects present at the beginning of the simulations persist and organise into parallel arch-like patterns in the director field. We show aligned arches of equal width are approximate steady state solutions of the equations of motion which co-exist with the nematic state. We compare our results to other models in the literature, in particular dry systems with no hydrodynamics, where trails, arches and polar defect ordering have also been observed.

Abstract:

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 territory2,3,4,5, 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 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 crystals8,9,10,11,12,13, 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 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.