arXiv subjects

Jan Rozman

Publications and source records attributed to Jan Rozman.

11 recordsLinked to original sources

arXiv2026

Active flows drive anchoring of nematics at rigid walls

Although confinement strongly influences flows in active materials, it remains unclear how active particles align at rigid boundaries when no thermodynamic anchoring is imposed. We address this question using continuum simulations of active nematics, together with analytical arguments based on a reduced near-wall description. In the flow-tumbling regime, extensile systems align parallel to the boundary, whereas contractile systems align perpendicular to it, consistent with active anchoring observed at active-passive interfaces. In the flow-aligning regime, the preferred orientation depends on the sign of activity and of the flow aligning parameter: either the shear-like flow generated near the wall selects the Leslie angle, or no unique alignment is established. These results provide a unified framework for activity-induced anchoring at rigid walls, demonstrating that boundary alignment in dense active matter can emerge solely from the interplay between self-generated flows and orientational dynamics.

cond-mat.soft↗

arXiv2025

Why Extensile and Contractile Tissues Could be Hard to Tell Apart

Active nematic models explain the topological defects and flow patterns observed in epithelial tissues, but the nature of active stress-whether it is extensile or contractile, a key parameter of the theory-is not well established experimentally. Individual cells are contractile, yet tissue-level behavior often resembles extensile nematics. To address this discrepancy, we use a continuum theory with two-tensor order parameters that distinguishes cell shape from active stress. We show that correlating cell shape and flow, whether in coherent flows in channels, near topological defects, or at rigid boundaries, cannot unambiguously determine the type of active stress. Our results demonstrate that simultaneous measurements of stress and cell shape are essential to fully interpret experiments investigating the nature of the physical forces acting within epithelial cell layers.

cond-mat.soft↗

arXiv2025

Junctional-Fluctuation-Mediated Fluidisation of Multi-Phase Field Epithelial Monolayers

We analyse a multi-phase field model for an epithelial monolayer with pairwise adhesions between neighbouring cells following an Ornstein-Uhlenbeck process, representing the stochastic turnover of junctional molecular motors. These fluctuations in junctional adhesion result in rearrangements in the tissue, fluidising it and producing diffusive cell motion. Similar junctional fluctuations have proven a very useful tool in the vertex model literature, and we hope they will be equally helpful to the multi-phase field model approach. Moreover, we observe that the cells' effective diffusion coefficient depends non-monotonically on the persistence time of the fluctuations, confirming results previously observed in the vertex model.

cond-mat.soft↗

arXiv2025

Spontaneous Hole Formation in Cell Monolayers Emerges from Collective Cell Motion

Although cell monolayers typically remain confluent, they can spontaneously develop persistent holes as a result of collective cellular motion. Recent studies on MDCK monolayers cultured on soft substrates have revealed that cells can align to create regions of local nematic order, and topological defects that generate localised mechanical stresses which can spontaneously trigger hole formation. To investigate this process, we develop a continuum multi-phase field model that incorporates internal dissipation and active dipolar forces that drive cell shape anisotropy. Our simulations show that reducing substrate friction enhances cell-cell velocity correlations. In this low-friction regime, topological defects give rise to spiral flow patterns that concentrate stress and can trigger hole formation. We further demonstrate that the number and stability of the holes, whether they close or persist, depends on both substrate friction and cellular activity. These findings underscore the critical role of collective cell dynamics in maintaining tissue integrity.

cond-mat.soft↗

arXiv2024

Cell Sorting in an Active Nematic Vertex Model

We study a mixture of extensile and contractile cells using a vertex model extended to include active nematic stresses. The two cell populations phase separate over time. While phase separation strengthens monotonically with an increasing magnitude of contractile activity, the dependence on extensile activity is non-monotonic, so that sufficiently high values reduce the extent of sorting. We interpret this by showing that extensile activity renders the system motile, enabling cells to undergo neighbour exchanges. Contractile cells that come into contact as a result are then more likely to stay connected due to an effective attraction arising from contractile activity.

cond-mat.soft↗

arXiv2024

Cell-level modelling of homeostasis in confined epithelial monolayers

Tissue homeostasis, the biological process of maintaining a steady state in tissue via control of cell proliferation, death, and metabolic function, is essential for the development, growth, maintenance, and proper function of living organisms. Disruptions to this process can lead to serious diseases and even death. In this study, we use the vertex model for the cell-level description of tissue mechanics to investigate the impact of the tissue microenvironment and local mechanical properties of cells on homeostasis in confined epithelial tissues. We find a dynamic steady state, where the balance between cell divisions and removals sustains homeostasis. By characterising homeostasis in terms of cell count, tissue area, and the cells' neighbour count distribution, we identify the factors that govern regulated and ordered tissue growth. This work, therefore, sheds light on the mechanisms underlying tissue homeostasis and highlights the importance of mechanics in the control of biological processes such as tissue development and disease pathology.

physics.bio-ph↗

arXiv2024

Basolateral mechanics prevents rigidity transition in epithelial monolayers

The mechanics of epithelial tissues, which is governed by forces generated in various cell domains, is often investigated using two-dimensional models that account for the apically-positioned actomyosin structures but neglect basolateral mechanics. We employ a more detailed three-dimensional model to study how lateral surface tensions affect the structure and rigidity of such tissues. We find that cells are apicobasally asymmetric, with one side appearing more ordered than the other depending on cell target perimeter. In contrast to the 2D model, which predicts a rigidity transition at large target perimeters, tissues in the 3D model remain solid-like across all parameter space.

cond-mat.soft↗

arXiv2023

Vertex model with internal dissipation enables sustained flows

Complex tissue flows in epithelia are driven by intra- and inter-cellular processes that generate, maintain, and coordinate mechanical forces. There has been growing evidence that cell shape anisotropy, manifested as nematic order, plays an important role in this process. Here we extend an active nematic vertex model by replacing substrate friction with internal viscous dissipation, dominant in epithelia not supported by a substrate or the extracellular matrix, which are found in many early-stage embryos. When coupled to cell shape anisotropy, the internal viscous dissipation allows for long-range velocity correlations and thus enables the spontaneous emergence of flows with a large degree of spatiotemporal organisation. We demonstrate sustained flow in epithelial sheets confined to a channel, providing a link between the cell-level vertex model of tissue dynamics and continuum active nematics, whose behaviour in a channel is theoretically understood and experimentally realisable. Our findings also show a simple mechanism that could account for collective cell migration correlated over distances large compared to the cell size, as observed during morphogenesis.

cond-mat.soft↗

arXiv2022

Shape-tension coupling produces nematic order in an epithelium vertex model

We study the vertex model for epithelial tissue mechanics extended to include coupling between the cell shapes and tensions in cell-cell junctions. This coupling represents an active force which drives the system out of equilibrium and leads to the formation of nematic order interspersed with prominent, long-lived $+1$ defects. The defects in the nematic ordering are coupled to the shape of the cell tiling, affecting cell areas and coordinations. This intricate interplay between cell shape, size, and coordination provides a possible mechanism by which tissues could spontaneously develop long-range polarity through local mechanical forces without resorting to long-range chemical patterning.

cond-mat.soft↗

arXiv2021

Morphologies of compressed active epithelial monolayers

Using a three-dimensional active vertex model, we numerically study the shapes of strained unsupported epithelial monolayers subject to active junctional noise due to stochastic binding and unbinding of myosin. We find that while uniaxial, biaxial, and isotropic in-plane compressive strains do lead to the formation of longitudinal, herringbone-pattern, and labyrinthine folds, respectively, the villus morphology characteristic of, e.g., the small intestine appears only if junctional tension fluctuations are strong enough to fluidize the tissue. Moreover, the fluidized epithelium features villi even in absence of compressive strain provided that the apico-basal differential tension is large enough. We analyze several details of the different epithelial forms including the role of strain rate and the modulation of tissue thickness across folds. Our results show that nontrivial morphologies can form even in unsupported, non-patterned epithelia.

cond-mat.soft↗

arXiv2020

Collective Cell Mechanics of Small-Organoid Morphologies

The study of organoids, artificially grown cell aggregates with the functionality and small-scale anatomy of real organs, is one of the most active areas of research in biology and biophysics, yet the basic physical origins of their different morphologies remain poorly understood. Here we propose a mechanistic theory of small-organoid morphologies. Using a 3D surface-tension-based vertex model, we reproduce the characteristic shapes, ranging from branched and budded structures to invaginated shapes. We find that the formation of branched morphologies relies strongly on junctional activity, enabling temporary aggregations of topological defects in cell packing. To elucidate our numerical results, we develop an effective elasticity theory, which allows one to estimate the apico-basal polarity from the organoid-scale modulation of cell height. Our work provides a generic interpretation of the observed small-organoid morphologies, highlighting the role of physical factors such as the differential surface tension, cell rearrangements, and tissue growth.

physics.bio-ph↗