Epithelium is the most common active matter in biology: it forms barriers, interfaces, and functional architectures of organs. Its ability to flow and remodel underlies embryonic morphogenesis, wound healing, and cancer progression. In previous work, including studies by neighboring groups, activity was typically described by a single universal mechanism—for instance, cell self-propulsion or effective active stress. However, in real tissues, forces are generated in multiple ways: actin cortex protrusions, polarized migration, contractility fluctuations, and mechanochemical feedback. Whether these mechanisms are equivalent at the tissue level remained an open question.
The authors used an active vertex model, where each cell is a polygon and its mechanical energy depends on area and perimeter. They introduced four classes of activity into this model: apolar motility (random forces at cell vertices), polar motility (coherent forces along the cell polarity direction), fluctuating contractility (random changes in cortex tension), and mechanochemical regulation (feedback between cell area and the Rho–ROCK–myosin signaling pathway). They simulated a tissue of about one thousand cells with open boundaries, starting from a rectangular shape, and tracked the transition to a rounded shape. They measured topological rearrangements (T1 and T2 transitions), mean squared displacement of cells, shape and area distributions, stress relaxation after shear, and spatial velocity correlations.
All four mechanisms fluidize the tissue and lead to a rounded morphology, but the paths differ. Apolar motility gives early and uniform T1 rearrangements; polar motility shows a delayed onset but then comparable speed; fluctuating contractility produces the slowest rearrangements; mechanochemical regulation shows a two-stage response with rapid accumulation of T1 after contraction waves form. For T2 transitions (cell extrusion), mechanochemical regulation stands out with explosive cell elimination, accelerating remodeling. Mean squared displacement distinguishes fluctuating contractility (cells are trapped in a cage), but does not separate the other three classes. Shape and area distributions divide the mechanisms into two groups: motility gives elongated cells with a wide spread of areas, while contractility gives isotropic cells with reduced mean area. Rheology: apolar and polar motility relax quickly, fluctuating contractility slower, and mechanochemical regulation shows damped oscillations with a peak in the spectrum. The key result is the spatial velocity correlations: apolar motility—short correlation without a negative tail; polar—longer but also monotonic; fluctuating contractility—short with a negative tail; mechanochemical regulation—the longest (about three cell diameters) with a pronounced negative tail. These signatures are robust to activity strength.
This work shows that epithelial fluidization is not a unique mechanical state but a common outcome of different force-generation pathways. It shifts the focus from specific models to understanding how the spatial organization of activity shapes tissue remodeling across scales. Unlike neighboring studies that consider one mechanism or compare two, here four classes are systematically compared in a unified computational framework, and a single observable—velocity correlations—is proposed that distinguishes all four mechanisms. This gives experimentalists a practical way to determine the dominant activity type from standard live microscopy without molecular reporters or mechanical perturbations.
A natural extension is to introduce finite persistence time of polarity to connect the model with self-propelled particle models. It is also important to consider mixed activity states, since living tissues rarely use a single mechanism in isolation. Incorporating interactions with the extracellular matrix and three-dimensional architecture will enhance applicability to development and pathology. The temporal organization of forces—their persistence and correlations—remains an unexplored dimension that could add new signatures.
The results are applicable in developmental biology, wound healing research, and cancer progression, where it is important to know which activity mechanism drives tissue remodeling. The velocity correlation method could be used in diagnostics and drug screening that affect cell mechanics.
Test predictions on living tissues with known activity mechanisms, such as MDCK monolayers with myosin inhibition or embryonic tissues with contraction waves. Develop algorithms for automatic extraction of correlation lengths from video data.
In tissue biology, an unresolved question is how cells coordinate their forces during morphogenesis and how disruptions in this coordination lead to disease. This work links microscopic force-generation mechanisms to macroscopic observables, bringing us closer to understanding the principles of epithelial self-organization.
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What the work does
The authors compared four classes of cell activity in the active vertex model of the epithelium: apolar and polar motility, fluctuating contractility, and mechanochemical regulation via Rho–ROCK–myosin. They showed that all mechanisms fluidize the tissue and lead to a round shape, but they differ in the dynamics of topological rearrangements, cell motility, distributions of shape and area, rheology, and spatial velocity correlations. The key result is that the velocity correlation length allows distinguishing the mechanisms from live-imaging data.
Where its strength is
A systematic comparison of four activity classes in a single model provides reference "fingerprints" for each mechanism, which can be used to identify the dominant activity type in experiments.
Where it could go next
Worth trying
Why this may matter
If the proposed method of identifying activity from velocity correlations is confirmed in experiments, it will provide a simple and non-invasive tool for diagnosing the mechanical state of the epithelium in health and disease, including morphogenesis and cancer progression.
Nearby works in our archive
The closest work in the archive sits at 0.65 by meaning — the usual level for our corpus.
as written by the authors arXiv:2608.14458v1
Cellular activity drives epithelial fluidization --- a widespread phenomenon observed during tissue development, remodeling, and repair both in vivo and in vitro. Yet the physical origins and spatial organization of active forces vary widely across biological systems and are often represented by a single generic mechanism in theoretical models. Here, using an active vertex model, we systematically compare four modes of epithelial activity spanning subcellular to tissue scales: apolar motility, polar motility, fluctuating contractility, and mechanochemical regulation. Although all four mechanisms drive the same global transition from a solid-like rectangular tissue to a fluid-like circular morphology, they reach this state through distinct pathways --- differing in the rates and topology of junctional rearrangements, cell elimination, and collective motion and leave distinguishable signatures in tissue architecture, cell dynamics, and mechanical relaxation. Among these observables, spatial velocity correlations directly capture the spatial organization of activity: their correlation length and functional form together resolve all four mechanisms. The robustness of these signatures across activity strengths suggests that spatial velocity correlations offer an experimentally accessible means of identifying the physical origin of epithelial activity from live-cell imaging alone.
The velocity correlation length in mechanochemical regulation reaches about three cell diameters, as if three neighboring cells moved in concert before their motions diverge.