Cell intrinsic dynamics guide neuroblast ingression independent of tissue fluidity

David Green; Ermia Etemadi; Gonca Erdemci-Tandogan; Lauren Enright; Rodrigo Fernandez-Gonzalez; Ulrich Tepass

REVIEW 3 major objections 6 minor 4 references

Cell intrinsic dynamics guide neuroblast ingression independent of tissue fluidity

T0 review · 3 major / 6 minor · reviewed 2026-08-15 · deepseek-v4-flash

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Pith's one-line read Neuroblasts keep delaminating on schedule even when the surrounding germband tissue solidifies, and the paper attributes that robustness to cell-intrinsic myosin anisotropy and endocytosis-contractility coupling.

desk verdict The experimental robustness result is real and worth knowing, but the modeling rescue for zip-RNAi leaves the myosin-dependent tension at control levels, so the proposed endocytosis mechanism is not actually tested. read the letter →

arxiv 2608.02885 v1 pith:JQE4AA2K submitted 2026-08-03 physics.bio-ph

David Green , Ermia Etemadi , Lauren Enright , Rodrigo Fernandez-Gonzalez , Ulrich Tepass , Gonca Erdemci-Tandogan This is my paper · ORCID

classification physics.bio-ph MSC 92C1592C3792C10 PACS 87.17.Aa87.17.Ee

keywords neuroblastingressiongermbandextensiontissuefluidityvertexmodelDrosophilaembryogenesismyosinanisotropyendocytosis-contractilitycouplingcelldelamination

verification ladder T0 review T1 audit T2 compute T3 formal

The pith

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

The reading

The paper asks whether the large-scale tissue remodeling of germband extension mechanically controls the concurrent ingression of Drosophila neuroblasts. A computational vertex model, in which cells are represented as polygons and tissue fluidity is tuned by the time cells take to complete neighbor exchanges, predicted that solidifying the tissue should slow neuroblast apical constriction. Live imaging of embryos with disrupted myosin, including Krüppel mutants and maternal zipper RNAi, the latter reducing cell rearrangement rates by about 91%, showed that neuroblast ingression speed was largely unchanged. The paper concludes that neuroblasts carry cell-intrinsic machinery, anisotropic contractility plus endocytosis of the apical domain, that keeps ingression on schedule even in a solid-like tissue. If right, this identifies a design principle: spatially localized cellular events can be insulated from tissue-level mechanical variability.

What carries the argument

The load-bearing object is an anisotropic vertex model of the ventral epithelium, extended in two ways. First, cell neighbor exchanges (T1 transitions) carry a finite rearrangement time, so impaired intercalation directly raises tissue solidity rather than relying on cell shape alone; this is what lets the model reproduce the decoupling of cell shape from rearrangement rate seen in myosin-depleted embryos. Second, ingressing neuroblast edges carry a cell-specific line tension that either accumulates linearly or follows the endocytosis-contractility coupling system (Eq. 6), $\dot{\Gamma}^{NB} = \Delta\gamma_{NB} + \alpha\phi - \kappa\Gamma^{NB}$ and $\dot{\phi} = \beta\Gamma^{NB} - \lambda\phi$, where $\phi$ is endocytic activity. The coupling is the part that rescues normal ingression time in the zip-RNAi simulations, despite isotropic, strongly reduced myosin and near-complete tissue solidification.

What would settle it

Measure apical endocytic flux in S1 neuroblasts of zip-RNAi embryos, for example by counting internalized Crumbs or E-cadherin puncta over time: if flux is unchanged or lower than controls while ingression stays normal, the predicted endocytosis-contractility coupling is not operating, and the explanation fails.

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Extended reading notes

Core claim

During early embryogenesis the germband fluidizes as it extends, and S1 neuroblasts delaminate at the same time. A vertex model with finite T1 rearrangement delays predicted that reduced tissue fluidity raises the mechanical resistance to apical constriction and should slow ingression. In vivo, both Kr mutants and zip-RNAi embryos show strongly reduced tissue fluidity, with rearrangement rates falling by 50% and 91% respectively, yet the speed of neuroblast apical area loss is statistically unchanged, aside from a modest late-phase delay in Kr mutants. The authors explain this through cell-intrinsic mechanisms: the neuroblast's own anisotropic myosin distribution sets the pace of junction shrinkage, and progressive endocytic removal of apical membrane components effectively raises constriction efficiency, so the model with these two mechanisms restores normal ingression in solid-like tissue. The general claim is that developmental systems can achieve robustness by mechanically insulating a critical cellular event from tissue-scale changes.

Load-bearing premise

The load-bearing premise is that neuroblasts actually couple their endocytic removal of apical membrane to their contractility in the way the model assumes, with parameters set after the fact so the simulation reproduces normal ingression; the paper does not measure endocytic activity in neuroblasts when myosin is depleted, so if that coupling is absent the central mechanism collapses.

Editorial extensions

If this is right

First-wave neuroblast ingression does not require the germband to be fluid; even a 91% drop in cell rearrangement rate leaves ingression timing intact.
The isotropic version of neuroblast constriction is slower than the anisotropic one in the model, matching the late-phase delay seen in Kr mutants where planar myosin polarity is lost.
Apical membrane removal by endocytosis can substitute for much of the contractile force of myosin, so ingression speed is set by membrane turnover rather than by tissue resistance.
Cell-shape-alone measures of tissue fluidity are insufficient when myosin is perturbed; rearrangement kinetics must be included to predict mechanical state.
Overlap in space and time between two morphogenetic processes does not by itself imply mechanical coupling.

Reading between the lines

Editorial extensions of the paper, not claims the author makes directly.

If endocytic removal is the true rate-limiting engine, then acutely boosting apical endocytosis in wild-type neuroblasts should speed ingression beyond its normal pace, a prediction that follows from the coupling equations and could be tested by genetic or optogenetic activation of endocytosis.
The same insulation logic might apply to other single-cell delaminations, such as neural crest or sensory precursor ingression in vertebrates, where a cell removes its own apical surface while the surrounding epithelium is under large-scale strain.
The T1-delay modeling suggests that tissue fluidity should be reported as a kinetic quantity, not just a geometric one; reanalyzing existing solid-like versus fluid-like classifications with rearrangement-time data could reveal more cases where geometry and mechanics decouple.
The paper only tests the first wave of neuroblast ingression, which overlaps the fluidization phase; later waves occur in a fully extended, mechanically different germband, so the claimed independence is an open question there.

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Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, and a circularity audit.

Desk Editor's Note

read the letter

The thing to know about this paper is that the experiment is solid and the result is meaningful: NB ingression is essentially unchanged when tissue fluidity is severely reduced. That is a genuine observation, and the imaging work behind it is careful — the rearrangement rates, myosin quantifications, and the decoupling of cell shape from fluidity in zip-RNAi are all presented with enough detail to be checked. The paper also deserves credit for the initial model prediction being cleanly falsified by their own data; that is how science should work.

What is new here is the direct pairing of tissue-level fluidity measurements with single-cell ingression tracking in the same embryos, and the demonstration that a 91% drop in cell rearrangement rate does not slow NB delamination. That challenges the usual shape-based predictors of tissue mechanics and makes the paper worth reading for anyone working on morphogenesis or cell mechanics.

The soft spot is the explanatory model. The rescue of ingression in the zip-RNAi simulations relies on the endocytosis-contractility coupling model, but the parameters are picked after the fact to reproduce the observed normal ingression, and more concretely, the NB-specific tension accumulation rate Δγ_NB is kept at the control value of 0.06 per τ even though zip-RNAi reduces total myosin by 65%. If Δγ is meant to reflect myosin-driven tension, it should be scaled down to roughly 0.021. With that change, the steady-state tension drops substantially and the endocytosis coupling may not rescue ingression at all. The paper itself flags endocytic upregulation as untested, so the mechanism is currently a plausible hypothesis, not a demonstrated one. That does not undermine the phenomenological result — ingression really is robust — but it means the explanation is not yet supported.

A second, minor issue is that the endocytosis model is one of several possible explanations; without measuring endocytic activity in myosin-depleted NBs or varying the coupling parameters against data, the model is more illustrative than constrained.

Who should read it: developmental biologists and biophysicists interested in tissue mechanics and robustness. The experimental core deserves peer review. The modeling section needs revision — at minimum, re-running the rescue with a myosin-scaled Δγ and, ideally, testing the endocytosis prediction experimentally.

My recommendation: send it to review, but ask for the modeling issue to be addressed before acceptance. The observation stands; the mechanism needs work.

Referee Report

3 major / 6 minor

Summary. The paper combines an anisotropic vertex model with quantitative live imaging of Drosophila embryos to ask whether the tissue-level mechanics of germband extension (GBE) influence the concurrent ingression of neuroblasts (NBs). The model initially predicts that reducing tissue fluidity, via impaired cell rearrangements or changes in cell shape, should slow NB ingression by increasing mechanical resistance. Experiments in Kr mutants and zip-RNAi embryos show that tissue fluidity is dramatically reduced, yet NB ingression rates are largely unchanged. The authors then extend the model with cell-intrinsic myosin anisotropy and a coupled endocytosis-contractility system (Eq. 6) and report that these additions rescue normal NB ingression in simulations of solid-like tissues. The central conclusion is that NB ingression is mechanically insulated from tissue-level fluidity and is maintained by cell-intrinsic mechanisms.

Significance. If the central claim holds, the paper is significant: it provides a quantitative example of mechanical modularity in development, showing that a single-cell morphogenetic event can be insulated from a globally remodeling tissue, and it challenges shape-based predictors of tissue fluidity by reporting strong decoupling between cell geometry and rearrangement dynamics in myosin-depleted embryos. The experimental dataset is valuable and the use of an open-source vertex-model framework with T1 delays is a useful methodological contribution. However, the explanatory mechanism for the robustness is currently underdetermined: the endocytosis-contractility coupling is introduced after the experiments refuted the original model, its parameters are chosen to reproduce the observed normal ingression, and the model does not reduce the NB-specific myosin-driven tension accumulation rate in the zip-RNAi condition despite the measured 65% reduction in total myosin. The significance of the work for the journal's readership therefore depends on whether the modeling claim can be made non-circular and biophysically consistent.

major comments (3)

[Methods, Eq. (6); Fig. 7C–D] The zip-RNAi simulations that produce the endocytosis-contractility "rescue" keep the NB tension accumulation rate at Δγ_NB = 0.06 per τ, identical to control, even though Fig. 4G shows a 65% reduction in total myosin in zip-RNAi embryos. Because the steady-state effective tension in Eq. (6) is Γ* = Δγ/(κ − αβ/λ), scaling Δγ_NB to 0.35×0.06 ≈ 0.021 would lower Γ* from about 0.155 to about 0.054, which would almost certainly slow ingression. As written, the rescue in Fig. 7D may be an artifact of the unchanged Δγ_NB rather than a demonstration that endocytic coupling compensates for reduced myosin. The authors should either recompute the zip-RNAi simulations with Δγ_NB scaled by the measured myosin depletion, or provide a concrete justification for why maternal zip knockdown leaves NB-specific myosin tension accumulation unaffected, and then re-examine whether the coupled model still rescues ingression.
[Discussion, paragraph 5; Abstract] The endocytosis-contractility coupling is introduced only after the experiments refuted the original model prediction, and the parameters α, β, κ, λ are selected post hoc so that the coupled model reproduces the already-observed normal ingression in zip-RNAi embryos. The manuscript itself states in the Discussion that "Whether endocytic activity in NBs is upregulated in myosin compromised embryos... remains an important prediction to test." This makes the central explanatory claim unsupported by direct experimental evidence. The abstract and concluding statements present the mechanism as established ("cell-intrinsic mechanisms... maintain ingression kinetics"); they should be rephrased to present the endocytic coupling as a model-based hypothesis unless an independent experimental test is added.
[Results, Fig. 5D–E vs. Fig. 6D; calibration in Methods] The initial model prediction that zip-RNAi slows NB ingression is not an out-of-sample prediction, because the same experimental mutant phenotypes were used to calibrate the T1 delay and anisotropic line tension parameters before the NB ingression comparison. The later addition of new mechanisms then "rescues" the discrepancy. The modeling is best described as hypothesis generation, not as a test of a falsifiable prediction. The authors should state this status explicitly in the Results and Discussion, and should clarify that the Fig. 5 prediction is a model extrapolation whose calibration already includes the mutant tissue-level data.

minor comments (6)

[Methods, coupled-model parameters] The parameter list for the coupled model is garbled in the text (e.g., "\=0.4, ] =0.03, ^=0.045 and _ = 0.1"); please spell out α, β, κ, λ in a table or in clearly labeled equations so readers can verify the steady-state calculation.
[Fig. 2G, 3H, 4H] The "parameter-free prediction of transition" from Wang 2020 should be defined in the main text, and the term "corrected cell shape index" should be introduced with its formula, since the manuscript otherwise uses the ordinary shape index p0.
[Fig. 6B″] The Kr mutant shows a modest but significant delay in the late phase of ingression; the abstract's phrase "largely unaffected" should be accompanied by an explicit statement that this refers to overall ingression speed and that a late-phase exception exists in Kr mutants.
[Discussion, late constriction in zip-RNAi] The sentence noting that zip-RNAi "tended to have reduced constriction speed during late NB constriction, although differences from control embryos were not significant" deserves a brief comment on statistical power or effect size, so readers can distinguish a true null from an underpowered comparison.
[Methods, timescales] The characteristic time τ is defined in simulation units, but the manuscript reports T1 delays such as 9.5τ and 10^3τ without a clear mapping to experimental minutes; a statement of the calibration (even approximate) would help readers connect the model timescales to the imaging data.
[Fig. 7D and Movie S6] In Fig. 7D, the four simulation conditions are distinguished only by color; a small legend naming the model variant (linear anisotropic, linear isotropic, coupled isotropic) would make the comparison easier to follow without referring to the caption text.

Circularity Check

1 steps flagged · score 6.0 of 10

The zip-RNAi 'rescue' in Fig. 7C,D keeps the neuroblast tension accumulation rate at the control value despite a measured 65% myosin reduction, so the endocytosis-contractility rescue is built into the input rather than derived from the mechanism.

self definitional [Methods, 'Neuroblast tension dynamics' (Eq. 6) and 'Simulation implementation and parameters'; Fig. 7C,D]
"For zip-RNAi simulations, we dramatically increased the T1 delay to 10^3 τ ... and reduced the anisotropic line tension to γ0=0.05, corresponding to 25% of control levels to reflect severe myosin depletion (Fig. 4G). Other parameters are γ_NB(0)=0.1 and Δγ_NB=0.06 per τ. ... The coupled model parameters: γ_NB_end(0)=0.1, Δγ=0.06, φ(0)=0.0, κ=0.4, α=0.03, β=0.045 and λ=0.1."

The zip-RNAi simulation that produces the 'rescued' ingression in Fig. 7C,D keeps Δγ_NB = 0.06 per τ, the same tension accumulation rate as control, although the same paper measures 'a 65% reduction in total myosin' in zip-RNAi embryos (Fig. 4G). In Eq. 6, dγ_NB_end/dt = Δγ + αφ - κγ_NB_end, so the myosin-driven term is not depleted in the knockdown simulation; only the tissue-level T1 delay and anisotropic line tension γ0 are reduced. The normal ingression time is therefore inherited from the unchanged Δγ rather than produced by the endocytosis-contractility coupling. A biophysically consistent myosin depletion would scale Δγ to about 0.35 × 0.06 = 0.021, lowering the coupled steady-state tension T* = Δγ/(κ-αβ/λ) from ~0.155 to ~0.054; that case is not simulated.

full rationale

The experimental core of the paper is self-contained and not circular: live imaging shows that in zip-RNAi embryos cell rearrangement rates drop by 91% while neuroblast ingression speed is statistically unchanged, and that Kr mutants produce only a modest late-phase delay. These are independent observations. The vertex-model prediction that reduced fluidity should slow ingression is a genuine model output, and its falsification by the experiments is legitimate. The circularity is confined to the explanatory model for the zip-RNAi case: the 'endocytosis-contractility coupling' rescue simulation does not implement the measured myosin depletion in the neuroblast itself, because Δγ_NB remains at the control value of 0.06. Consequently, the normal ingression in Fig. 7C,D is guaranteed by the unchanged myosin-driven tension rate, and the coupling's purported role is not actually tested. The discussed alternative—that endocytosis might be upregulated—is explicitly listed as an untested prediction, reinforcing that the model's rescue is a post hoc construction rather than a derivation. Self-citations to prior work on T1 delays (ref. 36) and myosin anisotropy (ref. 35) are not load-bearing in a circular way, since those results are used as modeling ingredients calibrated against independent experimental measurements here. Overall, the central experimental phenomenon is robust and non-circular, but the central mechanistic explanation's model support reduces by construction, giving a partial circularity score of 6.

Assumptions & free parameters 6 free parameters · 8 assumptions · 2 invented entities

The central claim depends on a large number of calibrated model parameters. The tissue-level parameters (gamma0, T1 delay) are anchored to measurements of myosin depletion and rearrangement rates, but the endocytosis-contractility coupling parameters that enable the rescue prediction are chosen post hoc to match the observed normal ingression. The model thus contains a substantial fitting component, and the key mechanistic entity (endocytic activity phi) is not experimentally measured.

free parameters (6)

Anisotropic line tension strength gamma0 = 0.2 (control), 0.1 (Kr), 0.05 (zip-RNAi)
Set to 50% and 25% of control to reflect measured myosin depletion. This is a calibration to experimental myosin levels.
T1 cellular rearrangement delay = 9.5 tau (control, Kr), 103 tau (zip-RNAi)
zip-RNAi delay increased 10-fold to reproduce near-absence of T1 transitions. Calibrated to tissue rearrangement rates.
NB initial tension and accumulation rate = Gamma_NB(0)=0.1, Delta_gamma_NB=0.06 per tau
Control neuroblast constriction parameters; not independently measured.
Endocytosis-contractility coupling parameters = alpha=0.4, beta=0.03, kappa=0.045, lambda=0.1, phi(0)=0
Chosen so the coupled model reproduces normal ingression in zip-RNAi simulations. No experimental measurement of these rates.
Target shape index initial value and increase rate = p0=3.65, increase 0.00001 per timestep
Chosen to match observed shape index increase during GBE; calibration.
Area modulus, perimeter modulus, motility, effective temperature = K_A=1, K_P=1, mu=1, T=0.02 (simulation units)
Standard vertex model constants in dimensionless units, not fitted to biological data.

assumptions (8)

standard math Vertex model energy functional (Eq. 1) with area, perimeter, and line tension terms.
Standard confluent tissue vertex model from prior literature (Bi et al. 2015).
standard math Overdamped Brownian vertex dynamics (Eq. 7) with effective temperature.
Standard simulation scheme; effective temperature introduces stochastic fluctuations.
domain assumption T1 transition delay implementation.
Borrowed from Erdemci-Tandogan and Manning 2021; a finite rearrangement time acts as a kinetic brake.
domain assumption Tissue fluidity is related to T1 delay and cell shape index.
Based on prior solid-to-fluid transition frameworks (Bi et al. 2015, Wang et al. 2020).
domain assumption Progressive area reduction represents NB apical constriction.
Acknowledged simplification in Discussion: the model does not capture 3D morphology, pulsatility, or basal delamination.
ad hoc to paper Myosin depletion is represented by scaling gamma0 and T1 delay.
Calibrated to match tissue elongation and rearrangement phenotypes, not derived from first principles.
ad hoc to paper Endocytosis-contractility coupling ODE system (Eq. 6).
Introduced to explain the observed robustness; parameters chosen post hoc and endocytosis not measured.
domain assumption Wang 2020 solid-to-fluid prediction curve used as external benchmark.
Used to classify mutant tissue states relative to the predicted transition.

invented entities (2)

Endocytic activity variable phi
purpose: Dynamical variable in the coupled model that modulates effective NB tension through endocytic removal of apical membrane.
Introduced in Eq. 6; no direct measurement in this paper. Authors list upregulation in myosin-compromised embryos as an untested prediction.
Effective NB edge tension Gamma_NB_eff
purpose: Combines myosin-driven contractility and endocytic resistance removal into a single tension variable.
Modeling construct, not directly measurable; defined through Eq. 6.

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Pith. "Pith review of Cell intrinsic dynamics guide neuroblast ingression independent of tissue fluidity." pith.science (2026). https://pith.science/paper/JQE4AA2K

@misc{pith2026260802885,
  author       = {Pith},
  title        = {Pith review of: Cell intrinsic dynamics guide neuroblast ingression independent of tissue fluidity},
  year         = {2026},
  howpublished = {\url{https://pith.science/paper/JQE4AA2K}},
  note         = {Machine review of arXiv:2608.02885}
}

read the original abstract

Morphogenesis involves the coordination of multiple cellular processes that occur simultaneously within developing tissues. During early Drosophila embryogenesis, neuroblast (NB) ingression occurs concurrently with germ band extension (GBE), yet whether these processes interact mechanistically remains unclear. Here, we combine mathematical modelling with quantitative live imaging to investigate whether tissue-level mechanics during GBE influence NB ingression dynamics. Mathematical modelling predicted that reducing tissue fluidity through impaired cellular rearrangements should slow NB ingression by increasing mechanical resistance. Experimental analysis of mutants in which cell intercalation and GBE are disrupted revealed a dramatic reduction in tissue fluidity. However, NB ingression rates remained largely unaffected when tissue fluidity decreased. Incorporating cell-intrinsic myosin anisotropy and endocytosis-contractility coupling into our mathematical model rescued the rate of neuroblast ingression in solid-like tissues. Thus, our findings suggest that cell-intrinsic mechanisms, rather than tissue-level fluidity, maintain ingression kinetics. More broadly, these results illustrate how developmental systems can achieve robustness by insulating critical cellular events from tissue-level mechanical variability.

Figures

Figures reproduced from arXiv: 2608.02885 by the authors.

**Figure 2.** NB ingress in a fluid-like environment. (A) Schematic of Drosophila body axis elongation. The germband (grey) elongates along the head-to-tail body axis. (A’) Schematic of oriented rearrangement that occurs during GBE. (B) Stills from time-lapse video of the ventral epithelium (t=0, start of GBE). (membrane marker PH::mCherry). Anterior left, ventral down. Images were overlaid with polygonal segmentations used to qu… view at source ↗

**Figure 3.** Kr mutants moderately reduce tissue fluidity during GBE. (A) Representative stills from live imaging of ventral epithelium of stage 7-9 embryos (membrane marker PH::mCherry). Green line shows migration of a single cell at the onset of GBE (0min, red point) to 30 minutes later (blue point). (B-E) Quantification of tissue dynamics over time, aligned to the start of GBE in Kr mutants compared to wild-type (from [PITH_… view at source ↗

Figures from the paper (3 more)

**Figure 4.** Figure 4: zip-RNAi shows near-complete tissue solidification during GBE. (A) Representative stills from live imaging of ventral epithelium of stage 7-9 embryos (membrane marker Spider::GFP). Green line shows migration of a single cell at the onset of GBE (0min, red point) to 30 …

**Figure 5.** Figure 5: Extended model with cellular rearrangement delays recapitulates tissue dynamics [PITH_FULL_IMAGE:figures/full_fig_p032_5.png]

**Figure 7.** Figure 7: Cell-intrinsic mechanisms explain NB ingression dynamics in Kr and zip-RNAi conditions in the model. (A) NB area over time in simulations with control parameters (orange), Kr parameters with anisotropic NB constriction (red) and Kr parameters with isotropic NB constric…

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Works this paper leans on

4 extracted references · 4 canonical work pages

[5]

Y. Mao, S. A. Wickström, Mechanical state transitions in the regulation of tissue form and function. Nat Rev Mol Cell Biol 25, 654–670 (2024). 6. R. M. Herrera-Perez, K. E. Kasza, Biophysical control of the cell rearrangements and cell shape changes that build epithelial tissues. Current Opinion in Genetics & Development 51, 88–95 (2018). 7. L. Rustarazo-...

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S. Simões, Y. Oh, M. F. Z. Wang, R. Fernandez-Gonzalez, U. Tepass, Myosin II promotes the anisotropic loss of the apical domain during Drosophila neuroblast ingression. Journal of Cell Biology 216, 1387–1404 (2017). 36. G. Erdemci-Tandogan, M. L. Manning, Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues. ...

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S. Herszterg, A. Leibfried, F. Bosveld, C. Martin, Y. Bellaiche, Interplay between the Dividing Cell and Its Neighbors Regulates Adherens Junction Formation during Cytokinesis in Epithelial Tissue. Developmental Cell 24, 256–270 (2013). 51. H. Oda, S. Tsukita, Real-time imaging of cell-cell adherens junctions reveals that Drosophila mesoderm invagination ...

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Pith tools

Reviewed August 15, 2026 · model on record in the stance chip above.

[1] [5]

Y. Mao, S. A. Wickström, Mechanical state transitions in the regulation of tissue form and function. Nat Rev Mol Cell Biol 25, 654–670 (2024). 6. R. M. Herrera-Perez, K. E. Kasza, Biophysical control of the cell rearrangements and cell shape changes that build epithelial tissues. Current Opinion in Genetics & Development 51, 88–95 (2018). 7. L. Rustarazo-...

work page 2024

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K. D. Irvine, E. Wieschaus, Cell intercalation during Drosophila germband extension and its regulation by pair-rule segmentation genes. Development 120, 827–841 (1994). 21. J. A. Zallen, E. Wieschaus, Patterned Gene Expression Directs Bipolar Planar Polarity in Drosophila. Developmental Cell 6, 343–355 (2004). 22. C. Bertet, L. Sulak, T. Lecuit, Myosin-de...

work page 1994

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Simões, Y

S. Simões, Y. Oh, M. F. Z. Wang, R. Fernandez-Gonzalez, U. Tepass, Myosin II promotes the anisotropic loss of the apical domain during Drosophila neuroblast ingression. Journal of Cell Biology 216, 1387–1404 (2017). 36. G. Erdemci-Tandogan, M. L. Manning, Effect of cellular rearrangement time delays on the rheology of vertex models for confluent tissues. ...

work page 2017

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Herszterg, A

S. Herszterg, A. Leibfried, F. Bosveld, C. Martin, Y. Bellaiche, Interplay between the Dividing Cell and Its Neighbors Regulates Adherens Junction Formation during Cytokinesis in Epithelial Tissue. Developmental Cell 24, 256–270 (2013). 51. H. Oda, S. Tsukita, Real-time imaging of cell-cell adherens junctions reveals that Drosophila mesoderm invagination ...

work page 2013