Collective epithelial migration mediated by the unbinding of hexatic defects

TL;DR

This paper develops a continuum theory for collective epithelial migration, showing that cell intercalation occurs through defect unbinding driven by active forces, explaining observed cellular flow and force structures.

Contribution

It introduces a novel theoretical framework combining active hydrodynamics and defect dynamics to explain epithelial cell intercalation and migration.

Findings

Cell intercalation involves unbinding of topological defects.

Migration driven by a balance of passive forces and active self-propulsion.

Explains the extensile activity observed in epithelial layers.

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. $6-$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.