Theory of defect-mediated morphogenesis

TL;DR

This paper presents a quantitative theory explaining how topological defects in active polar liquid crystals can organize tissue morphogenesis, linking defect dynamics to tissue shape changes through buckling and active flow interactions.

Contribution

It introduces a novel theoretical framework combining stability analysis and fluid dynamics to explain defect-driven tissue morphogenesis.

Findings

Active layers become unstable and form protrusions near disclinations.

Elastic forces focused by defects influence surface tension and morphology.

Complex morphodynamical behaviors like oscillations and turbulence are observed.

Abstract

Growing experimental evidence indicates that topological defects could serve as organizing centers in the morphogenesis of tissues. Here, we provide a quantitative explanation for this phenomenon, rooted in the buckling theory of deformable active polar liquid crystals. Using a combination of linear stability analysis and computational fluid dynamics, we demonstrate that active layers, such as confined cell monolayers, are unstable to the formation of protrusions in the presence of disclinations. The instability originates from an interplay between the focusing of the elastic forces, mediated by defects, and the renormalization of the system's surface tension by the active flow. The posttransitional regime is also characterized by several complex morphodynamical processes, such as oscillatory deformations, droplet nucleation, and active turbulence. Our findings offer an explanation of recent observations on tissue morphogenesis and shed light on the dynamics of active surfaces in general.