Motility-Driven Viscoelastic Control of Tissue Morphology in Presomitic Mesoderm

TL;DR

This study develops a vertex-based model to understand how cell motility influences tissue viscoelasticity, revealing mechanisms of mechanical memory and patterning in embryonic tissues.

Contribution

It introduces a quantitative framework linking cell motility to tissue-scale viscoelastic behavior and morphogenesis, validated by experimental data.

Findings

Motility shifts tissue behavior between elastic and viscous regimes.

Tissues act as mechanical filters for spatially patterned forces.

Localized motility hotspots induce sustained tissue deformations.

Abstract

Embryonic tissues deform across broad spatial and temporal scales and relax stress through active rearrangements. A quantitative link between cell-scale activity, spatial forcing, and emergent tissue-scale mechanics remains incomplete. Here, we use a vertex-based tissue model with active force fluctuations to study how motility controls viscoelastic response. After validation against experimental presomitic mesoderm relaxation dynamics, we extract intrinsic mechanical timescales using stress relaxation and oscillatory shear. The model captures motility-dependent shifts between elastic and viscous behavior and the coexistence of fast relaxation with long-lived residual stress. When subjected to spatially patterned, temporally pulsed forcing, tissues behave as mechanical filters: long-wavelength inputs are accumulated, whereas short-wavelength, cell-scale perturbations are rapidly erased, largely independent of motility. Simulations with localized motility hotspots, motivated by spatially confined FGF signaling reported in vertebrate limb development, produce sustained protrusive tissue deformations consistent with experimentally observed early bud-like morphologies. Together, these results establish a minimal framework linking motility-driven activity to wavelength-selective mechanical memory and emergent tissue patterning.