Abstract: What determines whether an epithelial tissue behaves more like a solid or a fluid? This fundamental question connects statistical physics, soft matter, mechanics, and cell biology, and is central to dynamic biological processes such as embryonic development, wound healing, and cancer invasion.

In this seminar, I will address this question using epithelial cell monolayers in vitro as a model living material. A prevailing theoretical framework, based on vertex models, associates the solid-fluid behavior of confluent tissues with cell geometry, particularly the cell shape index. By systematically perturbing cell-cell adhesion, however, we find that epithelial monolayers become substantially more fluid without appreciable changes in cell shape, cell number density, cell-substrate traction, or junctional tension. These observations demonstrate a shape-independent route to tissue fluidization and point to an additional physical mechanism governing collective cell dynamics.

To understand this behavior, we consider the dual role of cell-cell adhesion. In addition to contributing to interfacial energetics, adhesion can generate dissipative resistance to cell-edge remodeling. Incorporating this dissipative “junctional drag” into an extended vertex-model framework quantitatively reproduces the experimentally observed shape-independent fluidization. The resulting picture reveals how the energetic and dissipative effects of adhesion can compete to regulate tissue fluidity.
 

These results suggest that the mechanics and dynamics of epithelial tissues cannot be understood from geometry alone. Instead, tissue fluidity emerges from an interplay between geometry and dissipation, providing broader connections to jamming, viscoelasticity, and collective dynamics in living active matter.

 

सभी का स्वागत है /All Are Welcome