Active instability and nonlinear dynamics of cell-cell junctions

TL;DR

This paper models active cell-cell junctions as dynamic force dipoles, revealing how their nonlinear elastic responses and collective behaviors can lead to tissue morphogenesis through instabilities and oscillations.

Contribution

It introduces a mechanical model capturing active junction dynamics, instability mechanisms, and collective oscillations, advancing understanding of tissue morphogenesis.

Findings

Junction instability can trigger cell intercalations.

Nonlinear elastic responses stabilize collapse via limit cycles or condensation.

Active junction networks exhibit collective oscillations and topological transitions.

Abstract

Active cell-junction remodeling is important for tissue morphogenesis, yet its underlying physics is not understood. We study a mechanical model that describes junctions as dynamic active force dipoles. Their instability can trigger cell intercalations by a critical collapse. Nonlinearities in tissue's elastic response can stabilize the collapse either by a limit cycle or condensation of junction lengths at cusps of the energy landscape. Furthermore, active junction networks undergo collective instability to drive active in-plane ordering or develop a limit cycle of collective oscillations, which extends over regions of the energy landscape corresponding to distinct network topologies.