Epithelial colonies in vitro elongate through collective effects

Comelles, Jordi; Ss, Soumya; Lu, Linjie; Maout, Emilie Le; Anvitha, S; Salbreux, Guillaume; Jülicher, Frank; Inamdar, Mandar M.; Riveline, Daniel

doi:10.7554/elife.57730

Cited by 40 publications

(38 citation statements)

References 65 publications

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“…In line with earlier predictions from models of active liquid crystals [74], recent experiments on epithelial cells (MDCK) have shown that the self-propulsion of comet-like defects are correlated with the protrusion formation and elongation of initially circular cell colonies (Fig. 3d) [75]. Under cellular confinement, topological defects have been identified in cellular monolayers as pumps of cellular flows.…”

Section: Biological Functions Of Active Nematics In Tissuessupporting

confidence: 84%

Physics of liquid crystals in cell biology

Doostmohammadi¹,

Ladoux²

2021

Preprint

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Section: Biological Functions Of Active Nematics In Tissuessupporting

confidence: 84%

Physics of liquid crystals in cell biology

Doostmohammadi¹,

Ladoux²

2021

Preprint

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“…To identify the origins of the pulsatile collective flow, we ran numerical simulations of the tissue flow based on a vertex model [28]. In our model, cells were assigned a polarity vector that evolved over time according to a local alignment rule and a polarity diffusion.…”

Section: Numerical Simulations To Model Tissue Pulsatile Flowsmentioning

confidence: 99%

Pulsations and flows in tissues: two collective dynamics with simple cellular rules

Thiagarajan

Bhat

Salbreux

et al. 2020

Preprint

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Epithelial cells flows are observed both in vivo and in vitro and are essential for morphogenesis. Here, we show that pulsatile flows involving local contraction and expansion of a tissue can arise in vitro in an epithelial monolayer of Madine Darby Canine Kidney (MDCK) cells. The strength of pulsation can be modulated through friction heterogeneity by observing the monolayer dynamics on micro-contact printed fibronectin grids with dimensions matching the length-scale of spontaneous oscillations. We also report pulsations by inducing wound closure in domains of similar size with micro-fabricated pillars. In contrast, strongly coherent flows can be induced by adding and washing out acto-myosin cytoskeleton inhibitors. To gain insight into the associated cellular mechanisms, we fluorescently label actin and myosin. We find that lamellipodia align with the direction of the flow, and tissue-scale myosin gradients arise during pulsations in wound-healing experiments. Pulsations and flows are recapitulated in silico by a vertex model with cell motility and polarisation dynamics. The nature of collective movements depends on the interplay between velocity alignment and random diffusion of cell polarisation. When they are comparable, a significant pulsatile flow emerges, whereas the tissue undergoes long-range flows when alignment dominates. We conjecture that the interplay between lamellipodial motile activity and cell polarization, with a possible additional role for tissue-scale myosin gradients, is at the origin of the pulsatile nature of the collective flow. Altogether, our study reveals that monolayer dynamics is dictated by simple rules of interaction at cellular levels which could be involved in morphogenesis.

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“…In this theoretical paper, we perform a systematic study of the role of bond tension fluctuations on the rheological properties of cellular networks. Our analysis is guided by a two-dimensional vertex model, which has been shown to provide a remarkable agreement with experimental data in the case of Drosophila wing morphogenesis [2] and for other confluent monolayers [6,[21][22][23]. To quantify the dynamical deformations of the cell network and relate them to cellular processes, we use a shear decomposition based on a triangulation of the cell network [24].…”

Section: Introductionmentioning

confidence: 95%

Nonlinear rheology of cellular networks

Duclut¹,

Paijmans²,

Inamdar³

et al. 2021

Preprint

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Morphogenesis depends crucially on the complex rheological properties of cell tissues and on their ability to maintain mechanical integrity while rearranging at long times. In this paper, we study the rheology of polygonal cellular networks described by a vertex model in the presence of fluctuations. We use a triangulation method to decompose shear into cell shape changes and cell rearrangements. Considering the steady-state stress under constant shear, we observe nonlinear shear-thinning behavior at all magnitudes of the fluctuations, and an even stronger nonlinear regime at lower values of the fluctuations. We successfully capture this nonlinear rheology by a mean-field model that describes the tissue in terms of cell elongation and cell rearrangements. We furthermore introduce anisotropic active stresses in the vertex model and analyze their effect on rheology. We include this anisotropy in the meanfield model and show that it recapitulates the behavior observed in the simulations. Our work clarifies how tissue rheology is related to stochastic cell rearrangements and provides a simple biophysical model to describe biological tissues. Further, it highlights the importance of nonlinearities when discussing tissue mechanics.

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Epithelial colonies in vitro elongate through collective effects

Cited by 40 publications

References 65 publications

Physics of liquid crystals in cell biology

Physics of liquid crystals in cell biology

Pulsations and flows in tissues: two collective dynamics with simple cellular rules

Nonlinear rheology of cellular networks

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