[Paper Review] Epithelial Tissue Growth Dynamics: Universal or Not?

Mahmood Mazarei, Jan Åström+2 more|arXiv (Cornell University)|Mar 29, 2022

Cellular Mechanics and Interactions4 citations

TL;DR

This study uses a kinetic division model for deformable cells to demonstrate that epithelial tissue growth dynamics are not universally governed by a single universality class. By varying cell-cell adhesion strength, the model reproduces both MBE-like scaling (weak adhesion) and KPZ-like scaling (strong adhesion), resolving the long-standing controversy over universality in interfacial roughness through mechanical and adhesive tuning of cellular interactions.

ABSTRACT

Universality of interfacial roughness in growing epithelial tissue has remained a controversial issue. Kardar-Parisi-Zhang (KPZ) and Molecular Beam Epitaxy (MBE) universality classes have been reported among other behaviors including total lack of universality. Here, we utilize a kinetic division model for deformable cells to investigate cell-colony scaling. With seemingly minor model changes, it can reproduce both KPZ- and MBE-like scaling in configurations that mimic the respective experiments. This result neutralizes the apparent scaling controversy. It can be speculated that this diversity in growth behavior is beneficial for efficient evolution and versatile growth dynamics.

Motivation & Objective

• To resolve the long-standing controversy over whether epithelial tissue growth follows universal scaling laws like KPZ or MBE.
• To investigate how mechanical and adhesive properties of cells influence interfacial roughness and scaling behavior in growing colonies.
• To determine whether observed differences in scaling exponents across experiments stem from intrinsic universality or model-specific parameters.
• To test the hypothesis that diverse growth dynamics arise from subtle changes in cell adhesion and mechanical interactions.

Proposed method

• A kinetic division model for deformable cells simulates radial and linear colony growth with tunable cell-cell adhesion strength.
• The model incorporates cell division, mechanical forces, and friction to mimic biological microenvironments.
• Scaling analysis is applied using the Family-Vicsek scaling relation to extract critical exponents β, α, and z from interface width and structure factor.
• The model is validated by comparing simulated scaling collapse with experimental data from Brú et al. (MBE-like) and Huergo et al. (KPZ-like).
• Systematic variation of adhesion strength, cell stiffness, friction, and division rules tests robustness of scaling behavior.
• Fractal dimension and velocity of the colony front are analyzed to assess morphological and kinetic consistency with experiments.

Experimental results

Research questions

• RQ1 Can a single cell-based model reproduce both MBE-like and KPZ-like scaling in epithelial tissue growth?
• RQ2 What mechanical or adhesive parameters determine whether a growing colony exhibits MBE or KPZ scaling?
• RQ3 Is the apparent conflict between experimental reports of KPZ vs. MBE universality due to model differences or biological variability?
• RQ4 How do changes in cell-cell adhesion strength affect the scaling exponents β, α, and z in radial and linear growth configurations?
• RQ5 To what extent is the scaling behavior robust to variations in cell-medium friction, intermembrane friction, and cell type heterogeneity?

Key findings

• With weak cell-cell adhesion, the model exhibits MBE-like scaling with global roughness exponent α_glob = 0.95 ± 0.04 and growth exponent β_weak = 0.40 ± 0.04.
• With strong adhesion, the model displays KPZ-like scaling, showing β_strong = 0.42 ± 0.06 and local roughness α_loc = 0.70 ± 0.01.
• The fractal dimension of the interface remains stable across conditions (1.13–1.26), consistent with experimental observations.
• Colony front velocity remains constant (v ≈ 4.24 for weak, v ≈ 2.15 for strong adhesion), supporting constant-velocity growth observed in experiments.
• Scaling behavior is robust to changes in cell-medium friction, intermembrane friction, division rules, and cell stiffness diversity.
• Digitized experimental data from Brú et al. and Huergo et al. show good agreement with simulated scaling collapse, validating the model’s predictive power.