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Solid-to-solid transition in dense assemblies of elongated cells

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Shao-Zhen Lin, Jean-François Rupprecht

Soft Condensed Matter · Submitted 25 Jun 2026 · 58 references

Pith's verdict: The paper shows that switching cell elongation to an autonomous elastic anisotropy in the vertex model produces a solid-to-solid transition instead of fluidization, and the distinction holds up as the load-bearing change.

T0 · AI review

How this review was made: An AI referee (grok-4.3) read the paper on June 26, 2026 and answered a fixed list of questions about it. T0 is the starting level every paper gets. The levels describe how deeply Pith has checked the paper, never the authors.

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arXiv ID2606.26726 (version 1)
Pith IDQH6GZ4XQ, Pith's permanent record of this paper and its review
CitationJean-Fran\c{c}ois Rupprecht, Shao-Zhen Lin. "Solid-to-solid transition in dense assemblies of elongated cells." arXiv:2606.26726 (2026). https://pith.science/paper/QH6GZ4XQ
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The paper

The paper claims

Cell elongation from intrinsic shape preference drives a solid-to-solid transition rather than fluidization.

The reading

The paper models dense cell assemblies where elongation arises from an internal elastic drive toward anisotropic shapes instead of an imposed target shape index. This change produces a transition from an ordered isotropic solid to a disordered anisotropic solid. Both phases retain finite yield stress and shear rigidity, unlike the fluidization seen in conventional models. The result separates cell morphology from tissue mechanical state.

What carries the argument

The intrinsic passive elastic preference for anisotropic cell shape, which generates elongation autonomously and reverses the expected rheological response compared to standard target shape index control.

Extended reading notes

Core claim

When cell elongation is generated by an autonomous, passive elastic preference for anisotropic shape rather than by an imposed target shape index, the tissue undergoes a solid-to-solid transition from an ordered isotropic solid to a disordered anisotropic solid. Finite yield stress and shear rigidity persist across the transition.

Load-bearing premise

Cell elongation must emerge from an internal elastic bias for anisotropic shapes rather than from an externally set target shape index.

Original abstract

Cell shapes in confluent tissues range from nearly isotropic epithelial morphologies to highly elongated endothelial ones. In standard vertex models, tissue rigidity is controlled by a target shape index; increasing this index drives cell elongation and ultimate tissue fluidization. Here, we consider the case where cell elongation emerges autonomously by assigning an intrinsic, passive elastic preference for anisotropic shape. This distinction reverses the usual expectation: cell elongation does not fluidize the tissue, but drives a solid-to-solid transition from an ordered isotropic solid to a disordered anisotropic solid, with finite yield stress and shear rigidity on either side of the transition. These results decouple cell shape from tissue rheology and caution against inferring fluid-like mechanics from elongated cell morphologies alone.

Figures
Figure 1. FIG. 1. Vertex model with cell elongation elasticity (CEE).
Figure 2. FIG. 2. Autonomous cell elongation drives a solid-to-solid
Figure 3. FIG. 3. First-order phase transition on increasing
Figure 4. FIG. 4. Schematic of the CEE-mediated tissue solidification

Figures reproduced from arXiv:2606.26726 by the authors.

References

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Each citing sentence is taken from the citing paper's LaTeX source and typed by Pith's classifier. A label appears at probability 0.8 or more (0.95 for support), a contest at 0.7 or more; the quoted words are the citing authors'. How each label was checked · JSON

What it cites

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