Contributor info: Dr Jens Elgeti

Chenyun Yao, Jens Elgeti

SciPost Phys. 19, 097 (2025) · published 15 October 2025 | Toggle abstract · pdf

Ever since the ground breaking work of Trepat et al. in 2009, we know that cell colonies growing on a substrate can be under tensile mechanical stress. The origin of tension has so far been attributed to cellular motility forces being oriented outward of the colony. Works in the field mainly revolve around how this orientation of the forces can be explained, ranging from velocity alignment to self-sorting due to self-propulsion. In this work, we demonstrate that tension in growing colonies can also be explained without cellular motility forces! Using a combination of well established tissue growth simulation technique and analytical modelling, we show how tension can arise as a consequence of simple mechanics of growing tissues. Combining these models with a minimalistic motility model shows how colonies can expand while under even larger tension. Furthermore, our results and analytical models provide novel analysis procedures to identify the underlying mechanics.

Johannes C. Krämer, Edouard Hannezo, Gerhard Gompper, Jens Elgeti

SciPost Phys. 16, 097 (2024) · published 8 April 2024 | Toggle abstract · pdf

The homeostasis of epithelial tissue relies on a balance between the self-renewal of stem cell populations, cellular differentiation, and loss. Although this balance needs to be tightly regulated to avoid pathologies, such as tumor growth, the regulatory mechanisms, both cell-intrinsic and collective, which ensure tissue steady-state are still poorly understood. Here, we develop a computational model that incorporates basic assumptions of stem cell renewal into distinct populations and mechanical interactions between cells. We find that the model generates unexpected dynamic features: stem cells repel each other in the bulk tissue and are thus found rather isolated, as in a number of in vivo contexts. By mapping the system onto a gas of passive Brownian particles with effective repulsive interactions, that arise from the generated flows of differentiated cells, we show that we can quantitatively describe such stem cell distribution in tissues. The interaction potential between a pair of stem cells decays exponentially with a characteristic length that spans several cell sizes, corresponding to the volume of cells generated per stem cell division. Our findings may help understanding the dynamics of normal and cancerous epithelial tissues.