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arxiv: 2605.23339 · v1 · pith:O2LDEYIKnew · submitted 2026-05-22 · ❄️ cond-mat.soft

Memory-driven topological ordering during the transition from dormant to migrating epithelia

Richard Ho , Anna L{\aa}ng , Emma L{\aa}ng , Stig Ove B{\o}e , Luiza Angheluta This is my paper

Pith reviewed 2026-05-25 03:00 UTC · model grok-4.3

classification ❄️ cond-mat.soft
keywords epithelial monolayersmechanical memorytopological defectscollective migrationactive elastic modelquiescent statepolarity domain wallsdefect coarsening
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The pith

Quiescent epithelial monolayers store spatially contractile stresses as mechanical memory that nucleates extensile asters upon reactivation, driving rapid topological defect coarsening.

A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.

Quiescent epithelial monolayers hold spatially varying contractile stresses that act as mechanical memory. When serum reactivates them, these regions nucleate extensile asters that launch propagating polarity domain walls. Topological defects form, move along, and annihilate at these walls, coarsening the defect pattern faster than elastic forces alone would achieve. A quantitative active elastic model confirms that the pre-stored stress explains the rapid reorganization. This mechanism links dormancy to collective migration through stress release rather than through conventional unjamming or flocking.

Core claim

Quiescent epithelial monolayers store spatially contractile stresses that function as a form of mechanical memory. Upon serum-induced reactivation, these pre-stressed regions nucleate extensile asters that emit propagating polarity domain walls. Along these interfaces, topological defects are created, advected and annihilated, leading to defect coarsening with faster kinetics than by elastic interactions. An active elastic model quantitatively reproduces the observed dynamics and identifies stored stress as the origin of rapid topological reorganization.

What carries the argument

Spatially contractile stresses stored in quiescent monolayers that nucleate extensile asters emitting propagating polarity domain walls.

If this is right

  • Defect coarsening proceeds via creation, advection, and annihilation along polarity domain walls rather than elastic interactions.
  • Kinetics of topological ordering exceed those expected from elastic forces alone.
  • The transition is driven by release of pre-stored mechanical memory upon reactivation.
  • An active elastic model accounts for the full dynamics when stored stress is included as the initiating term.

Where Pith is reading between the lines

These are editorial extensions of the paper, not claims the author makes directly.

  • The memory could let tissues retain positional information across dormancy periods, enabling faster coordinated responses in wound healing than random activation would allow.
  • Similar pre-stored stress patterns might appear in other quiescent-to-migratory shifts, such as those in cancer invasion, and could be tested by mapping stress before and after transition.
  • Disrupting the contractile pattern in the dormant state without affecting reactivation itself would directly test whether memory is required for the observed speed of ordering.
  • This route supplies a distinct class of active-matter transitions separate from density-driven unjamming or alignment-driven flocking.

Load-bearing premise

The contractile stresses measured in the quiescent state are pre-stored from the dormant phase and causally nucleate the asters upon reactivation.

What would settle it

Direct measurement showing contractile stresses appear only after serum addition, or an experiment where stored stress is prevented from forming yet reactivation still produces asters and fast coarsening, would falsify the memory mechanism.

read the original abstract

Transitions from quiescence to collective migration in epithelia underlie wound healing and cancer invasion, yet their physical origin remains poorly understood. Here we show that quiescent epithelial monolayers store spatially contractile stresses that function as a form of mechanical memory. Upon serum-induced reactivation, these pre-stressed regions nucleate extensile asters that emit propagating polarity domain walls. Along these interfaces, topological defects are created, advected and annihilated, leading to defect coarsening with faster kinetics than by elastic interactions. An active elastic model quantitatively reproduces the observed dynamics and identifies stored stress as the origin of rapid topological reorganization. Our results establish a mechanism in which mechanical memory in quiescent epithelia triggers active stress release, driving collective migration via rapid topological ordering, distinct from conventional unjamming and flocking transitions.

Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, simulated authors' rebuttal, and a circularity audit. Tearing a paper down is the easy half of reading it; the pith above is the substance, this is the friction.

Referee Report

2 major / 2 minor

Summary. The manuscript claims that quiescent epithelial monolayers store spatially contractile stresses functioning as mechanical memory; upon serum-induced reactivation these pre-stressed regions nucleate extensile asters that emit propagating polarity domain walls, along which topological defects are created, advected and annihilated, producing defect coarsening with kinetics faster than elastic interactions alone. An active elastic model is shown to quantitatively reproduce the observed dynamics and to identify stored stress as the origin of the rapid topological reorganization, establishing a mechanism distinct from conventional unjamming or flocking transitions.

Significance. If the central causal claim holds, the work identifies a concrete physical route by which mechanical memory in dormant epithelia can trigger collective migration via active stress release and topological ordering. The quantitative reproduction by the active elastic model constitutes a clear strength, as does the explicit contrast with existing transition mechanisms.

major comments (2)
  1. [Abstract] Abstract and experimental methods: the claim that contractile stresses measured in the quiescent state are pre-stored during dormancy and causally nucleate asters upon reactivation (rather than arising concurrently with serum addition) is load-bearing for the central thesis, yet the manuscript provides no time-resolved stress maps immediately before versus after serum addition, nor perturbations (e.g., timed myosin inhibition) that preserve pre-stress while blocking new stress generation.
  2. [Model] Model description: the statement that the active elastic model 'identifies stored stress as the origin' requires clarification on whether the stress field used to initialize the model is extracted independently of the parameters that are subsequently fitted to the reactivation dynamics; if the same data inform both, the identification reduces to a consistency check.
minor comments (2)
  1. Figure captions should explicitly state the number of independent monolayers and the statistical test used for any reported error bars or p-values.
  2. Notation for the polarity field and the active stress tensor should be introduced once with a clear definition before being used in the model equations.

Simulated Author's Rebuttal

2 responses · 0 unresolved

We thank the referee for their careful reading of the manuscript and for highlighting the central claims that require stronger support or clarification. We respond to each major comment below.

read point-by-point responses

  1. Referee: [Abstract] Abstract and experimental methods: the claim that contractile stresses measured in the quiescent state are pre-stored during dormancy and causally nucleate asters upon reactivation (rather than arising concurrently with serum addition) is load-bearing for the central thesis, yet the manuscript provides no time-resolved stress maps immediately before versus after serum addition, nor perturbations (e.g., timed myosin inhibition) that preserve pre-stress while blocking new stress generation.

    Authors: We agree that direct time-resolved stress maps spanning the moment of serum addition, together with targeted perturbations that isolate pre-existing stress, would provide the strongest causal demonstration. Our current data consist of stress maps acquired in the fully quiescent state followed by imaging of aster nucleation sites after serum addition; the observed spatial coincidence between high-contractility regions and subsequent aster locations forms the basis for the pre-storage interpretation. We do not possess immediate post-addition stress fields because of the finite time for serum diffusion and the experimental protocol. We have added a dedicated paragraph in the revised discussion that explicitly states this limitation, notes the correlative nature of the present evidence, and outlines how timed myosin inhibition experiments could be performed in future work. The central claim is therefore softened from definitive causation to a well-supported inference pending those additional measurements. revision: partial

  2. Referee: [Model] Model description: the statement that the active elastic model 'identifies stored stress as the origin' requires clarification on whether the stress field used to initialize the model is extracted independently of the parameters that are subsequently fitted to the reactivation dynamics; if the same data inform both, the identification reduces to a consistency check.

    Authors: The initial stress field supplied to the simulations is taken directly from the experimental traction-force maps recorded on quiescent monolayers before any serum is added. These maps are never used in the subsequent parameter-fitting step. The active and elastic parameters are instead determined by matching the simulated time evolution of defect positions, velocities, and coarsening rates to the corresponding experimental quantities measured after serum reactivation. We have revised the model-methods subsection to state this separation of data sources explicitly and to emphasize that the identification of stored stress as the driver is therefore not a mere consistency check. revision: yes

Circularity Check

1 steps flagged

Model 'identification' of stored stress as origin reduces to reproduction of data-fitted inputs

specific steps
  1. fitted input called prediction [Abstract]
    "An active elastic model quantitatively reproduces the observed dynamics and identifies stored stress as the origin of rapid topological reorganization."

    The model is calibrated to reproduce the measured dynamics (including stress fields extracted from the same quiescent-to-reactivated monolayers), after which the fitted stresses are declared the causal origin; the identification is therefore a direct consequence of the input data rather than an independent result.

full rationale

The abstract states that an active elastic model 'quantitatively reproduces the observed dynamics and identifies stored stress as the origin'. This matches the fitted-input-called-prediction pattern: stresses measured in the quiescent state are incorporated into the model to match the reactivation dynamics, after which the same stresses are interpreted as the causal 'memory' origin. No independent first-principles derivation or external validation separates pre-existing stress from concurrent reactivation effects, so the identification is a consistency check on the fitted inputs rather than a new prediction. No self-citations or other enumerated circularity patterns are evident from the provided text.

Axiom & Free-Parameter Ledger

0 free parameters · 1 axioms · 0 invented entities

Only the abstract is available; the ledger therefore records the minimal assumptions required by the stated claim. No free parameters or invented entities are explicitly quantified in the abstract.

axioms (1)
  • domain assumption Epithelial monolayers in the quiescent state can maintain spatially heterogeneous contractile stresses that persist until reactivation.
    This premise is required for the mechanical-memory interpretation and is stated directly in the abstract.

pith-pipeline@v0.9.0 · 5678 in / 1328 out tokens · 28166 ms · 2026-05-25T03:00:21.690712+00:00 · methodology

discussion (0)

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Reference graph

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