pith. sign in

arxiv: 2509.04316 · v1 · submitted 2025-09-04 · ❄️ cond-mat.soft · physics.bio-ph· q-bio.TO

Control of lumen morphology by lateral and basal cell surfaces

Pith reviewed 2026-05-18 19:08 UTC · model grok-4.3

classification ❄️ cond-mat.soft physics.bio-phq-bio.TO
keywords lumen morphologyepithelial cystsvertex modelcell contractilitytight junctionsMDCK cystsshape instabilityapical surface
0
0 comments X

The pith

Epithelial cysts stabilize lumen shape by boosting lateral contractility after apical perturbations.

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

The paper examines how fluid-filled lumina in MDCK cysts maintain their morphology through mechanical forces acting on different parts of the cell surfaces. When tight junction perturbations trigger apical surface instability, the cells adjust not only pressure and apical tension but also increase lateral and basal tensions. A mean-field three-dimensional vertex model matches the observed shape changes and shows that the rise in lateral contractility functions as a direct cellular countermeasure to restore stability. This coordinated adjustment across all surfaces, rather than apical control alone, determines the final lumen form. The finding matters because it explains a basic mechanical strategy tissues use to preserve architecture during development and repair.

Core claim

Cysts respond to tight junction perturbations by modulating their lateral and basal tensions in addition to pressure and apical belt tension. The mean-field three-dimensional vertex model reproduces the experimental shape instability quantitatively. This reveals that the observed increase of lateral contractility is a cellular response that counters the instability, showing how regulation of the mechanics of all cell surfaces conspires to control lumen morphology.

What carries the argument

The mean-field three-dimensional vertex model that incorporates uniform modulations of pressure together with apical, lateral, and basal tensions to match observed cyst shapes.

If this is right

  • Lumen morphology results from coordinated tension changes at apical, lateral, and basal surfaces rather than apical mechanics alone.
  • The rise in lateral contractility directly counters apical instability to preserve cyst shape.
  • Mean-field vertex models suffice to predict the instability using only measured tension modulations.
  • Regulation of all cell-surface mechanics is required for proper control of enclosed lumen geometry.

Where Pith is reading between the lines

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

  • Similar tension-based stabilization may operate in other epithelial tubes or vesicles where lumen pressure varies.
  • Disrupting lateral contractility pathways could produce predictable shape defects useful for testing in organoid models.
  • The uniform-cell assumption suggests that population-level tension measurements can guide predictions even without single-cell resolution.

Load-bearing premise

The mean-field three-dimensional vertex model with uniform cell properties and tension modulations can quantitatively reproduce the experimental shape instability without additional unmodeled factors such as cell-to-cell variability.

What would settle it

Direct measurement showing that preventing the increase in lateral contractility still allows stable lumen shapes, or that the vertex model fails to predict shapes once lateral tension changes are blocked, would falsify the central claim.

Figures

Figures reproduced from arXiv: 2509.04316 by Alf Honigmann, Chandraniva Guha Ray, Markus Mukenhirn, Pierre A. Haas.

Figure 2
Figure 2. Figure 2: FIG. 2. Experimental quantification of contractility and adhesion across all cell surfaces wild-type (WT), ZO-KO, and CLDN-KO MDCK-II [PITH_FULL_IMAGE:figures/full_fig_p003_2.png] view at source ↗
Figure 3
Figure 3. Figure 3: FIG. 3. Mean-field model of the instability of lumen morphology. (a) Geometry of a spherical lumen of radius [PITH_FULL_IMAGE:figures/full_fig_p005_3.png] view at source ↗
Figure 5
Figure 5. Figure 5: FIG. 5. Additional model predictions. (a) At zero pressure ( [PITH_FULL_IMAGE:figures/full_fig_p009_5.png] view at source ↗
read the original abstract

Across development, the morphology of fluid-filled lumina enclosed by epithelial tissues arises from an interplay of lumen pressure, mechanics of the cell cortex, and cell-cell adhesion. Here, we explore the mechanical basis for the control of this interplay using the shape space of MDCK cysts and the instability of their apical surfaces under tight junction perturbations [Mukenhirn et al., Dev. Cell 59, 2886 (2024)]. We discover that the cysts respond to these perturbations by significantly modulating their lateral and basal tensions, in addition to the known modulations of pressure and apical belt tension. We develop a mean-field three-dimensional vertex model of these cysts that reproduces the experimental shape instability quantitatively. This reveals that the observed increase of lateral contractility is a cellular response that counters the instability. Our work thus shows how regulation of the mechanics of all cell surfaces conspires to control lumen morphology.

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 examines how MDCK cysts control lumen morphology through coordinated mechanics of apical, lateral, and basal cell surfaces. Using tight-junction perturbations, the authors measure changes in lumen pressure, apical belt tension, and lateral/basal tensions. They introduce a mean-field three-dimensional vertex model that is reported to reproduce the observed apical-surface instability quantitatively, leading to the conclusion that the measured increase in lateral contractility functions as a cellular response that stabilizes lumen shape.

Significance. If the quantitative reproduction is robust, the work provides evidence that epithelial lumen morphology is controlled by the joint regulation of all three cell-surface classes rather than apical tension and pressure alone. The experimental observation of tension modulation supplies independent grounding, and the modeling framework offers a concrete way to test how changes in lateral contractility counteract shape instabilities. This advances understanding of multi-surface mechanical feedback in tissue morphogenesis.

major comments (2)
  1. [Model section] Model section (around the description of the mean-field 3D vertex model): The claim that the model reproduces the experimental shape instability quantitatively is central to attributing the lateral-tension increase as a counteracting response. However, the manuscript does not report the specific numerical values of the lateral and basal tensions employed, the fitting procedure used to match shapes, or quantitative agreement metrics (e.g., RMS deviation or overlap scores between simulated and observed cyst cross-sections). Without these, it is not possible to determine whether the lateral-tension increase is required or whether other parameter combinations could produce equivalent instability thresholds.
  2. [Results section] Results section discussing model-experiment comparison: The mean-field assumption of uniform cell properties and tensions is used throughout. No test is presented of how cell-to-cell variability in tension or adhesion would shift the instability threshold or allow alternative combinations of apical, lateral, and basal parameters to match the same shapes. If heterogeneity alters the critical tension values, the necessity of the observed lateral-contractility increase could be reduced, weakening the attribution of a specific counteracting response.
minor comments (2)
  1. [Figure legends] Figure legends for the model outputs should explicitly state which parameters are taken directly from experiment and which are adjusted to achieve the reported quantitative match.
  2. [Abstract and main text] The abstract states that the model reproduces the instability 'quantitatively,' but the main text does not define the precise meaning of this term (e.g., within a stated tolerance on curvature or volume). Clarifying this definition would strengthen the central claim.

Simulated Author's Rebuttal

2 responses · 0 unresolved

We thank the referee for the constructive comments, which help clarify the presentation of our modeling results. We address each major point below and will revise the manuscript to incorporate additional details where feasible.

read point-by-point responses
  1. Referee: [Model section] Model section (around the description of the mean-field 3D vertex model): The claim that the model reproduces the experimental shape instability quantitatively is central to attributing the lateral-tension increase as a counteracting response. However, the manuscript does not report the specific numerical values of the lateral and basal tensions employed, the fitting procedure used to match shapes, or quantitative agreement metrics (e.g., RMS deviation or overlap scores between simulated and observed cyst cross-sections). Without these, it is not possible to determine whether the lateral-tension increase is required or whether other parameter combinations could produce equivalent instability thresholds.

    Authors: We agree that explicit reporting of these details is necessary for full evaluation of the model's robustness. In the revised manuscript we will add the specific numerical values of the lateral and basal tensions (obtained from experimental measurements and used in the simulations), a description of the fitting procedure employed to match cyst cross-sections, and quantitative agreement metrics including RMS deviation and overlap scores between simulated and experimental shapes. These additions will confirm that the observed increase in lateral contractility is required to reproduce the instability threshold. revision: yes

  2. Referee: [Results section] Results section discussing model-experiment comparison: The mean-field assumption of uniform cell properties and tensions is used throughout. No test is presented of how cell-to-cell variability in tension or adhesion would shift the instability threshold or allow alternative combinations of apical, lateral, and basal parameters to match the same shapes. If heterogeneity alters the critical tension values, the necessity of the observed lateral-contractility increase could be reduced, weakening the attribution of a specific counteracting response.

    Authors: The mean-field model is intended to represent average mechanical behavior consistent with our population-level experimental measurements of tension modulation. While we did not perform explicit simulations with cell-to-cell variability, such heterogeneity would be expected to broaden rather than eliminate the instability threshold, preserving the requirement for elevated lateral contractility to stabilize lumen shape. In the revision we will add a discussion of this limitation together with a qualitative assessment of how variability might influence the critical parameters. revision: partial

Circularity Check

0 steps flagged

No significant circularity: experimental tension measurements provide independent input to the vertex model

full rationale

The paper first reports experimental discovery of modulated lateral and basal tensions in response to tight-junction perturbations. These measured values are then supplied to a mean-field 3D vertex model whose output is compared against the observed shape instability. Because the tension parameters originate from direct measurement rather than being tuned to force agreement with the instability data, and because the prior citation [Mukenhirn et al.] supplies only the perturbation protocol rather than the present mechanical interpretation, the derivation chain remains self-contained and does not reduce to its own inputs by construction. The quantitative match therefore constitutes a genuine test rather than a tautology.

Axiom & Free-Parameter Ledger

1 free parameters · 1 axioms · 0 invented entities

Only the abstract is available, so the ledger is based on stated elements: the vertex model is assumed to capture cell mechanics, and tension values are adjusted to match data.

free parameters (1)
  • lateral and basal tension values
    Tensions on lateral and basal surfaces are modulated in the model to reproduce the experimental instability; specific values are not given in the abstract but are central to the quantitative match.
axioms (1)
  • domain assumption The mean-field 3D vertex model accurately represents the mechanical behavior of MDCK cyst cells under tight junction perturbation.
    Invoked when stating that the model reproduces the shape instability quantitatively.

pith-pipeline@v0.9.0 · 5695 in / 1282 out tokens · 34714 ms · 2026-05-18T19:08:26.192246+00:00 · methodology

discussion (0)

Sign in with ORCID, Apple, or X to comment. Anyone can read and Pith papers without signing in.

Reference graph

Works this paper leans on

59 extracted references · 59 canonical work pages

  1. [1]

    (3) is replaced with 𝑒cell = 𝛤a 𝐴 + 𝛤b(π𝑋2) + 𝛤ℓ [π(𝑅𝑋 − 𝑟𝑥 )] + 𝛬(2π𝑥) = const

    Energy of the cyst With these geometric results and the assumption of single- cell apical area conservation, Eq. (3) is replaced with 𝑒cell = 𝛤a 𝐴 + 𝛤b(π𝑋2) + 𝛤ℓ [π(𝑅𝑋 − 𝑟𝑥 )] + 𝛬(2π𝑥) = const. + 4π𝛤b 𝑁 𝑅2 + 2π𝛤ℓ√ 𝑁 𝑅2 − 𝑟2 + 4π𝛬√ 𝑁 𝑥, (10) using Eqs. (1). On discarding the constant single-cell apical area and substituting into the expression for the enth...

  2. [2]

    (13a), 𝑟 = 𝑟∗ ≡ √ 𝑁/2

    Stability analysis If 𝑑 = 0, then, from Eq. (13a), 𝑟 = 𝑟∗ ≡ √ 𝑁/2. For 𝑑 ≠ 0, Eq. (13a) implies that 𝑟 < 𝑟 ∗. We analyse the stability of the apical surfaces by expanding the energy close to 𝑑 = 0, i.e., for 𝑠 ≡ 𝑟∗ − 𝑟 ≪ 1. This leads to 𝐸 = 𝐸0 ∓ 𝐸1𝑠1/2 + 𝐸2𝑠 + 𝑂𝑠3/2 , (14) in which 𝐸1 = 𝑁5/12 4√ 𝑁 + 8𝑣 1/3 n 𝑝 𝑁√ 𝑁 + 8𝑣 1/3 − 2 √ 𝑁 𝛾 − 4 o , (15a) 𝐸2 = 𝑁...

  3. [3]

    Now 𝐸1 ≷ 0 ⇐ ⇒ 𝛱 − 2𝐺 − 4 ≷ 0, (17a) 𝐸2 ≷ 0 ⇐ ⇒ 𝛱 − 4𝐿 + 2𝛼𝐺 − 4𝛽 ≷ 0, (17b) where, from Eqs

    Phase diagram of lumen morphology The phase diagram of the instability thus depends on the signs of 𝐸1 and 𝐸2. Now 𝐸1 ≷ 0 ⇐ ⇒ 𝛱 − 2𝐺 − 4 ≷ 0, (17a) 𝐸2 ≷ 0 ⇐ ⇒ 𝛱 − 4𝐿 + 2𝛼𝐺 − 4𝛽 ≷ 0, (17b) where, from Eqs. (15), 𝛱 = 𝑝 𝑁√ 𝑁 + 8𝑣 1/3, 𝐺 = √ 𝑁 𝛾, 𝐿 = √ 𝑁 + 8𝑣 1/3 𝑁1/6 𝜆, (18) and 𝛼 = √ 𝑁 +8𝑣 1/3 𝑁1/6 ( 1 − 1 𝑁√ 𝑁 +8𝑣 1/3 √ 𝑁 + 1√ 𝑁 +8𝑣 ) , (19a) 𝛽 = 1 + 1√ 𝑁√...

  4. [4]

    small” cysts to bend into the lumen, while those of “large

    Mechanisms of lumen morphology Equation (17b) and Fig. 3(k) show that higher values of 𝛱 −4𝐿+2𝛼𝐺 favour stability. Thus, high𝛱 or 𝐺 are stabilising and high 𝐿 is destabilising. Indeed, at high 𝐿 (i.e., high belt tension), the apical belt contracts, so the apical surface must buckle to maintain constant area. This contraction reduces the radius of the lume...

  5. [5]

    [43] using CRISPR/Cas9, and the Claudin quin-KO (CLDN-KO) MDCK-II cell line was obtained from the Furuse lab [45]

    MDCK cell culture and maintenance Madin–Darby Canine Kidney-II (MDCK) cell lines with tight junction perturbations used for this study were as follows: the ZO1/2 knockout MDCK-II (ZO-KO) cell line was gener- ated by Beutelet al. [43] using CRISPR/Cas9, and the Claudin quin-KO (CLDN-KO) MDCK-II cell line was obtained from the Furuse lab [45]. Myosin II was...

  6. [6]

    Briefly, MDCK monolayers were dissociated and embedded in 50% Matrigel (Corning, USA)

    3D culture of MDCK cysts MDCK cysts were cultured following established protocols. Briefly, MDCK monolayers were dissociated and embedded in 50% Matrigel (Corning, USA). Cells were maintained for 5 days before immunofluorescence staining

  7. [7]

    Immunofluorescence staining Cells were seeded onto glass coverslips and cultured until they reached the desired confluence. They were then fixed with 4% paraformaldehyde for 15 minutes at room temper- ature, permeabilised with 0.1% Triton X-100 for 15 min- utes, and blocked with 5% bovine serum albumin (BSA) for 1 hour. Primary antibodies against Vinculin...

  8. [8]

    intensity

    Analysis of experimental images Apical junctional myosin in 2D monolayers was quanti- fied using previously published data [16]. In this dataset, endogenous myosin IIa tagged with mNeonGreen was imaged in MDCK-II WT and mutant monolayers. To quantify api- cal belt myosin, the average fluorescence intensity at apical cell–cell junctions was measured and co...

  9. [9]

    4(e), for the WT and the two perturbations, ZO-KO and CLDN-KO

    Estimation of model parameters These measurements allow us to estimate or constrain the three model parameters𝛱 , 𝐺, and 𝐿, and the two parameters𝛼 and 𝛽 that define the slopes of the planes in the phase diagram in Fig. 4(e), for the WT and the two perturbations, ZO-KO and CLDN-KO. a. Estimation of tensions We begin by estimating the surface and line tens...

  10. [10]

    Lubarsky and M

    B. Lubarsky and M. A. Krasnow, Tube morphogenesis: Making and shaping biological tubes, Cell 112, 19 (2003)

  11. [11]

    D. J. Andrew and A. J. Ewald, Morphogenesis of epithelial tubes: Insights into tube formation, elongation, and elaboration, Dev. Biol. 341, 34 (2010)

  12. [12]

    Datta, D

    A. Datta, D. M. Bryant, and K. E. Mostov, Molecular regulation of lumen morphogenesis, Curr. Biol. 21, R126 (2011)

  13. [13]

    Sigurbj ¨ornsd´ottir, R

    S. Sigurbj ¨ornsd´ottir, R. Mathew, and M. Leptin, Molecular mechanisms of de novo lumen formation, Nat. Rev. Mol. Cell Bio. 15, 665 (2014)

  14. [14]

    Navis and M

    A. Navis and M. Bagnat, Developing pressures: fluid forces driving morphogenesis, Curr. Opin. Gen. Dev. 32, 24 (2015)

  15. [15]

    Navis and C

    A. Navis and C. M. Nelson, Pulling together: Tissue-generated forces that drive lumen morphogenesis, Semin. Cell Dev. Biol. 55, 139 (2016)

  16. [16]

    Camelo and S

    C. Camelo and S. Luschnig, Cells into tubes: Molecular and physical principles underlying lumen formation in tubular or- gans, Curr. Top. Dev. Biol.143, 37 (2021)

  17. [17]

    Torres-S ´anchez, M

    A. Torres-S ´anchez, M. Kerr Winter, and G. Salbreux, Tissue hydraulics: Physics of lumen formation and interaction, Cells Dev. 168, 203724 (2021)

  18. [18]

    M. J. Bovyn and P. A. Haas, Shaping epithelial lumina under pressure, Biochem. Soc. Trans. 52, 331 (2024)

  19. [19]

    E. Gin, E. M. Tanaka, and L. Brusch, A model for cyst lumen expansion and size regulation via fluid secretion, J. Theor. Biol. 264, 1077 (2010)

  20. [20]

    Dasgupta, K

    S. Dasgupta, K. Gupta, Y. Zhang, V. Viasnoff, and J. Prost, Physics of lumen growth, Proc. Natl. Acad. Sci. USA115, E4751 (2018)

  21. [21]

    Duclut, N

    C. Duclut, N. Sarkar, J. Prost, and F. J¨ ulicher, Fluid pumping and active flexoelectricity can promote lumen nucleation in cell assemblies, Proc. Natl. Acad. Sci. USA 116, 19264 (2019)

  22. [22]

    C. G. Vasquez, V. T. Vachharajani, C. Garzon-Coral, and A. R. Dunn, Physical basis for the determination of lumen shape in a simple epithelium, Nat. Commun. 12, 5608 (2021)

  23. [23]

    Duclut, J

    C. Duclut, J. Prost, and F. J¨ ulicher, Hydraulic and electric control of cell spheroids, Proc. Natl. Acad. Sci. USA118, e2021972118 (2021)

  24. [24]

    Le Verge-Serandour and H

    M. Le Verge-Serandour and H. Turlier, A hydro-osmotic coars- ening theory of biological cavity formation, PLoS Comput. Biol. 17, 1 (2021)

  25. [25]

    Mukenhirn, C.-H

    M. Mukenhirn, C.-H. Wang, T. Guyomar, M. J. Bovyn, M. F. Staddon, R. E. van der Veen, R. Maraspini, L. Lu, C. Martin- Lemaitre, M. Sano, M. Lehmann, T. Hiraiwa, D. Riveline, and A. Honigmann, Tight junctions control lumen morphology via hydrostatic pressure and junctional tension, Dev. Cell 59, 2866 (2024)

  26. [26]

    B. H. Lee, K. Fuji, H. Petzold, P. Seymour, S. Yennek, C. Schewin, A. Lewis, D. Riveline, T. Hiraiwa, M. Sano, and A. Grapin-Botton, Control of lumen geometry and topology by the interplay between pressure and cell proliferation rate in pancreatic organoids, bioRxiv:2024.05.29.596462 (2024)

  27. [27]

    de Gennes, F

    P.-G. de Gennes, F. Brochard-Wyart, and D. Qu ´er´e, Capillar- ity and wetting phenomena: Drops, bubbles, pearls, waves (Springer, New York, NY, 2003) Chap. 1, pp. 1–31

  28. [28]

    Farhadifar, J.-C

    R. Farhadifar, J.-C. R ¨oper, B. Aigouy, S. Eaton, and F. J¨ ulicher, The influence of cell mechanics, cell-cell interactions, and pro- liferation on epithelial packing, Curr. Biol. 17, 2095 (2007)

  29. [29]

    D. B. Staple, R. Farhadifar, J.-C. R ¨oper, B. Aigouy, S. Eaton, and F. J¨ ulicher, Mechanics and remodelling of cell packings in epithelia, Eur. Phys. J. E 33, 117 (2010)

  30. [30]

    A. G. Fletcher, M. Osterfield, R. E. Baker, and S. Y. Shvartsman, Vertex models of epithelial morphogenesis, Biophys. J. 106, 2291 (2014)

  31. [31]

    A. G. Fletcher, F. Cooper, and R. E. Baker, Mechanocellular models of epithelial morphogenesis, Phil. Trans. Roy. Soc. B 372, 20150519 (2016). 13

  32. [32]

    S. Alt, P. Ganguly, and G. Salbreux, Vertex models: from cell mechanics to tissue morphogenesis, Phil. Trans. Roy. Soc. B 372, 20150520 (2017)

  33. [33]

    Honda, M

    H. Honda, M. Tanemura, and T. Nagai, A three-dimensional ver- tex dynamics cell model of space-filling polyhedra simulating cell behavior in a cell aggregate, J. Theor. Biol.226, 439 (2004)

  34. [34]

    Hannezo, J

    E. Hannezo, J. Prost, and J.-F. Joanny, Theory of epithelial sheet morphology in three dimensions, Proc. Natl. Acad. Sci. USA 111, 27 (2014)

  35. [35]

    P. C. Sanematsu, G. Erdemci-Tandogan, H. Patel, E. M. Retzlaff, J. D. Amack, and M. L. Manning, 3D viscoelastic drag forces contribute to cell shape changes during organogenesis in the zebrafish embryo, Cells Dev.168, 203718 (2021)

  36. [36]

    P. Sahu, J. M. Schwarz, and M. L. Manning, Geometric signa- tures of tissue surface tension in a three-dimensional model of confluent tissue, New J. Phys.23, 093043 (2021)

  37. [37]

    Zhang and J

    T. Zhang and J. M. Schwarz, Topologically-protected interior for three-dimensional confluent cellular collectives, Phys. Rev. Res. 4, 043148 (2022)

  38. [38]

    Villeneuve, A

    C. Villeneuve, A. Hashmi, I. Ylivinkka, E. Lawson-Keister, Y. A. Miroshnikova, C. P ´erez-Gonz´alez, S.-M. Myllym ¨aki, F. Bertillot, B. Yadav, T. Zhang, D. Matic Vignjevic, M. L. Mikkola, M. L. Manning, and S. A. Wickstr ¨om, Mechanical forces across compartments coordinate cell shape and fate tran- sitions to generate tissue architecture, Nat. Cell Biol...

  39. [39]

    Ma ˆıtre, H

    J.-L. Ma ˆıtre, H. Berthoumieux, S. F. G. Krens, G. Salbreux, F. J¨ ulicher, E. Paluch, and C.-P. Heisenberg, Adhesion functions in cell sorting by mechanically coupling the cortices of adhering cells, Science 338, 253 (2012)

  40. [40]

    J. A. McAteer, A. P. Evan, E. E. Vance, and K. D. Gardner, MDCK cysts: An in vitro model of epithelial cyst formation and growth, J. Tiss. Cult. Meth. 10, 245 (1986)

  41. [41]

    Montesano, G

    R. Montesano, G. Schaller, and L. Orci, Induction of epithe- lial tubular morphogenesis in vitro by fibroblast-derived soluble factors, Cell 66, 697 (1991)

  42. [42]

    L. E. O’Brien, M. M. P. Zegers, and K. E. Mostov, Building epithelial architecture: insights from three-dimensional culture models, Nat. Rev. Mol. Cell Biol.3, 531 (2002)

  43. [43]

    C. E. Buckley and D. St Johnston, Apical–basal polarity and the control of epithelial form and function, Nat. Rev. Mol. Cell Biol. 23, 559 (2022)

  44. [44]

    Otani and M

    T. Otani and M. Furuse, Tight junction structure and function revisited, Trends Cell Biol. 30, 805 (2020)

  45. [45]

    Miyoshi and Y

    J. Miyoshi and Y. Takai, Structural and functional associations of apical junctions with cytoskeleton, Biochim. Biophys. Acta 1778, 670 (2008)

  46. [46]

    Mangeol, D

    P. Mangeol, D. Massey-Harroche, M. Sebbagh, F. Richard, A. L. Bivic, and P.-F. Lenne, The zonula adherens matura redefines the apical junction of intestinal epithelia, Proc. Natl. Acad. Sci. USA 121, e2316722121 (2024)

  47. [47]

    W. Yu, A. Datta, P. Leroy, L. E. O’Brien, G. Mak, T.-S. Jou, K. S. Matlin, K. E. Mostov, and M. M. Zegers, β1-Integrin orients epithelial polarity via Rac1 and laminin, Mol. Biol. Cell 16, 433 (2005)

  48. [48]

    L. E. O’Brien, T.-S. Jou, A. L. Pollack, Q. Zhang, S. H. Hansen, P. Yurchenco, and K. E. Mostov, Rac1 orientates epithelial apical polarity through effects on basolateral laminin assembly, Nat. Cell Biol. 3, 831 (2001)

  49. [49]

    Maraspini, C.-H

    R. Maraspini, C.-H. Wang, and A. Honigmann, Optimization of 2D and 3D cell culture to study membrane organization with STED microscopy, J. Phys. D53, 014001 (2019)

  50. [50]

    R ¨oper, D

    K. R ¨oper, D. Corbeil, and W. B. Huttner, Retention of prominin in microvilli reveals distinct cholesterol-based lipid micro- domains in the apical plasma membrane, Nat. Cell Biol. 2, 582 (2000)

  51. [51]

    Schindelin, I

    J. Schindelin, I. Arganda-Carreras, E. Frise, V. Kaynig, M. Lon- gair, T. Pietzsch, S. Preibisch, C. Rueden, S. Saalfeld, B. Schmid, J.-Y. Tinevez, D. J. White, V. Hartenstein, K. Eliceiri, P. Toman- cak, and A. Cardona, Fiji: an open-source platform for biological-image analysis, Nat. Methods 9, 676 (2012)

  52. [52]

    Beutel, R

    O. Beutel, R. Maraspini, K. Pombo-Garc´ıa, C. Martin-Lemaitre, and A. Honigmann, Phase separation of Zonula occludens pro- teins drives formation of tight junctions, Cell 179, 923 (2019)

  53. [53]

    S. Le, M. Yu, and J. Yan, Direct single-molecule quantifica- tion reveals unexpectedly high mechanical stability of vinculin– talin/α-catenin linkages, Sci. Adv.5, eaav2720 (2019)

  54. [54]

    Otani, T

    T. Otani, T. P. Nguyen, S. Tokuda, K. Sugihara, T. Sugawara, K. Furuse, T. Miura, K. Ebnet, and M. Furuse, Claudins and JAM-A coordinately regulate tight junction formation and ep- ithelial polarity, J. Cell Biol. 218, 3372 (2019)

  55. [55]

    Guyomar, L

    T. Guyomar, L. Lu, T. Hiraiwa, and D. Riveline, Asymmetry of acto-myosin cortices as active fluids shape cells in organoids, bioRxiv:2024.08.22.609097 (2024)

  56. [56]

    Fischer-Friedrich, Y

    E. Fischer-Friedrich, Y. Toyoda, C. J. Cattin, D. J. M¨ uller, A. A. Hyman, and F. J¨ ulicher, Rheology of the active cell cortex in mitosis, Biophys. J. 111, 589 (2016)

  57. [57]

    Kamalesh, N

    K. Kamalesh, N. Scher, T. Biton, E. D. Schejter, B.-Z. Shilo, and O. Avinoam, Exocytosis by vesicle crumpling maintains apical membrane homeostasis during exocrine secretion, Dev. Cell56, 1603 (2021)

  58. [58]

    Sim ˜oes, G

    S. Sim ˜oes, G. Lerchbaumer, M. Pellikka, P. Giannatou, T. Lam, D. Kim, J. Yu, D. ter Stal, K. Al Kakouni, R. Fernandez- Gonzalez, and U. Tepass, Crumbs complex–directed apical membrane dynamics in epithelial cell ingression, J. Cell Biol. 221, e202108076 (2022)

  59. [59]

    Data are available at zenodo:17055495