[Paper Review] Defect-mediated morphogenesis

Ludwig A. Hoffmann, Livio Nicola Carenza+2 more|arXiv (Cornell University)|May 31, 2021

Micro and Nano Robotics48 references4 citations

TL;DR

This paper proposes that topological defects in active polar liquid crystals act as organizing centers for tissue morphogenesis by mediating instability-driven protrusion formation through elastic force focusing and active flow renormalization of surface tension. Using linear stability analysis and computational fluid dynamics, it demonstrates that disclinations trigger buckling instabilities in confined cell layers, leading to complex morphodynamic behaviors such as oscillations, droplet nucleation, and active turbulence.

ABSTRACT

Growing experimental evidence indicates that topological defects could serve as organizing centers in the morphogenesis of tissues. In this article 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 confined cell layers 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 post-transitional 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.

Motivation & Objective

• To explain how topological defects organize tissue morphogenesis in developing epithelia.
• To identify the physical mechanisms underlying defect-driven instability in confined active cell layers.
• To quantify the role of elastic forces and active flows in shaping tissue deformations.
• To characterize post-buckling morphodynamic phenomena such as oscillations and turbulence in active surfaces.

Proposed method

• Employed linear stability analysis to study the onset of instabilities in confined active polar liquid crystals.
• Applied computational fluid dynamics simulations to model the nonlinear evolution of morphological instabilities.
• Integrated buckling theory with active matter physics to describe elastic force focusing near topological defects.
• Tracked the renormalization of surface tension due to active flows in the presence of disclinations.
• Analyzed the transition from linear instability to complex post-transitional dynamics in the system.
• Modeled the emergence of oscillatory deformations, droplet nucleation, and active turbulence as collective phenomena.

Experimental results

Research questions

• RQ1 How do topological defects induce morphological instabilities in confined active cell layers?
• RQ2 What is the role of elastic force focusing in defect-mediated tissue deformation?
• RQ3 How does active flow renormalize surface tension to promote protrusion formation?
• RQ4 What complex morphodynamic processes emerge in the post-buckling regime of active surfaces?
• RQ5 To what extent can defect-mediated instabilities explain experimental observations in tissue morphogenesis?

Key findings

• Topological defects in active polar liquid crystals act as organizing centers for tissue morphogenesis by triggering localized buckling instabilities.
• The instability arises from the focusing of elastic forces near disclinations and the renormalization of surface tension by active flows.
• Linear stability analysis confirms that confined cell layers become unstable in the presence of disclinations, leading to protrusion formation.
• Post-transitional dynamics include oscillatory deformations, droplet nucleation, and active turbulence, indicating rich morphological complexity.
• The model quantitatively explains recent experimental observations of tissue shape changes driven by defects.
• The framework provides a general mechanism for active surface dynamics beyond biological tissues, applicable to active matter systems.