Collective epithelial migration mediated by the unbinding of hexatic defects
arXiv:2307.12956 · doi:10.7554/eLife.105397.1
Abstract
Collective cell migration in epithelia relies on cell intercalation: a local remodelling of the cellular network that allows neighbouring cells to swap their positions. Unlike foams and passive cellular fluid, in epithelial intercalation these rearrangements crucially depend on activity. During these processes, the local geometry of the network and the contractile forces generated therein conspire to produce a burst of remodelling events, which collectively give rise to a vortical flow at the mesoscopic length scale. In this article we formulate a continuum theory of the mechanism driving this process, built upon recent advances towards understanding the hexatic (i.e. fold ordered) structure of epithelial layers. Using a combination of active hydrodynamics and cell-resolved numerical simulations, we demonstrate that cell intercalation takes place via the unbinding of topological defects, naturally initiated by fluctuations and whose late-times dynamics is governed by the interplay between passive attractive forces and active self-propulsion. Our approach sheds light on the structure of the cellular forces driving collective migration in epithelia and provides an explanation of the observed extensile activity of in vitro epithelial layers.
References in corpus (17)
- Topological defect launches 3D mound in the active nematic sheet of neural progenitors
- Defect dynamics in active nematics
- Turbulent dynamics of epithelial cell cultures
- Anisotropy links cell shapes to tissue flow during convergent extension
- Taming active turbulence with patterned soft interfaces
- Discrete rearranging disordered patterns, part I: Robust statistical tools in two or three dimensions
- Solid-Liquid Transition of Deformable and Overlapping Active Particles
- Lattice Boltzmann Methods and Active Fluids
- Statistical Properties of Autonomous Flows in 2D Active Nematics
- Role of cell deformability in the two-dimensional melting of biological tissues
- Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues
- Mechanical basis and topological routes to cell elimination
- Chiral stresses in nematic cell monolayers
- Active T1 transitions in cellular networks
- Robust statistical properties of T1 transitions in confluent cell tissues
- Long-ranged order and flow alignment in sheared atic liquid crystals
- Hydrodynamic Enhancement of -atic Defect Dynamics