Flocking transitions in confluent tissues

Giavazzi, Fabio; Paoluzzi, Matteo; Macchi, Marta; Bi, Dapeng; Scita, Giorgio; Manning, M. Lisa; Cerbino, Roberto; Marchetti, M. Cristina

doi:10.1039/c8sm00126j

Cited by 151 publications

(180 citation statements)

References 57 publications

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“…Another important question is whether a coupling between cell shape and cell motility could give rise to our observations, instead of tissue drag. Previous simulations using a similar model showed that cells tend to elongate slightly in the direction perpendicular to the direction of cell motility [53]. This effect is not dominant here, as the cell shape changes are not the same anteriorly (where cells are elongated parallel to the direction of motion) and posteriorly (where cells are elongated perpendicular to the direction of motion).…”

Section: Discussionmentioning

confidence: 60%

Tissue Flow Induces Cell Shape Changes During Organogenesis

Erdemci-Tandogan

Clark

Amack

et al. 2018

Biophysical Journal

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In embryonic development, cell shape changes are essential for building functional organs, but in many cases the mechanisms that precisely regulate these changes remain unknown. We propose that fluid-like drag forces generated by the motion of an organ through surrounding tissue could generate changes to its structure that are important for its function. To test this hypothesis, we study the zebrafish left-right organizer, Kupffer's vesicle (KV), using experiments and mathematical modeling. During development, monociliated cells that comprise the KV undergo region-specific shape changes along the anterior-posterior axis that are critical for KV function: anterior cells become long and thin, while posterior cells become short and squat. Here, we develop a mathematical vertex-like model for cell shapes, which incorporates both tissue rheology and cell motility, and constrain the model parameters using previously published rheological data for the zebrafish tailbud [Serwane et al.] as well as our own measurements of the KV speed. We find that drag forces due to dynamics of cells surrounding the KV could be sufficient to drive KV cell shape changes during KV development. More broadly, these results suggest that cell shape changes could be driven by dynamic forces not typically considered in models or experiments.

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Section: Discussionmentioning

confidence: 60%

Tissue Flow Induces Cell Shape Changes During Organogenesis

Erdemci-Tandogan

Clark

Amack

et al. 2018

Biophysical Journal

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“…Other studies have focused on the onset of collective motion, showing that cell-autonomous polarity-velocity alignment ( Fig. 5c and Section 2.4.1) gives rise to emergent cell-cell alignment, which leads to coherent rotations [114] and flocking [68,108,115]. Altogether, SPV models predict four distinct phases: solid, liquid, solid flock, and liquid flock (Fig.…”

Section: Collective Phenomenamentioning

confidence: 90%

“…b, Cells are parametrized by an area Ai and a perimeter Pi, and experience a self-propulsion force Ta pi (orange) and an interaction force F int i = − ∇ r i F (dashed black), which give the resultant force (black). Adapted from[108] with permission from The Royal Society of Chemistry. c, Polarity-velocity alignment with a time-scale τ .…”

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confidence: 99%

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Physical Models of Collective Cell Migration

Alert

Trepat

2020

Annu. Rev. Condens. Matter Phys.

286

269

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Collective cell migration is a key driver of embryonic development, wound healing, and some types of cancer invasion. Here we provide a physical perspective of the mechanisms underlying collective cell migration. We begin with a catalogue of the cell-cell and cell-substrate interactions that govern cell migration, which we classify into positional and orientational interactions. We then review the physical models that have been developed to explain how these interactions give rise to collective cellular movement. These models span the sub-cellular to the supracellular scales, and they include lattice models, phase fields models, active network models, particle models, and continuum models. For each type of model, we discuss its formulation, its limitations, and the main emergent phenomena that it has successfully explained. These phenomena include flocking and fluid-solid transitions, as well as wetting, fingering, and mechanical waves in spreading epithelial monolayers. We close by outlining remaining challenges and future directions in the physics of collective cell migration.

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“…RAB5A further promotes millimetres-scale, ballistic locomotion of multicellular streams by augmenting the extension of oriented and persistent RAC1-driven, protrusions 31 . These effects combine to endow monolayers with a flocking fluid mode of motion, which is explained in numerical simulations in terms of large scale coordinated migration and local unjamming, driven by an increased capability of each individual cell to align its velocity to the one of the surrounding group 31-33 . Molecularly, impairing endocytosis, macropinocytosis or increasing fluid efflux abrogated RAB5A-induced collective motility, suggesting that perturbations of trafficking processes impacting on different signalling and biomechanical pathways are necessary for the JUT.…”

Section: Introductionmentioning

confidence: 99%

Unjamming overcomes kinetic and proliferation arrest in terminally differentiated cells and promotes collective motility of carcinoma

Palamidessi

Malinverno

Frittoli

et al. 2018

Preprint

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29During wound repair, branching morphogenesis and carcinoma dissemination, cellular 30 rearrangements are fostered by a solid-to-liquid transition known as unjamming. The biomolecular 31 machinery behind unjamming, its physiological and clinical relevance remain, however, a mystery. 32Here, we combine biophysical and biochemical analysis to study unjamming in a variety of epithelial 33 2D and 3D collectives: monolayers, differentiated normal mammary cysts, spheroid models of breast 34 ductal carcinoma in situ (DCIS), and ex vivo slices of orthotopically-implanted DCIS. In all cases, 35 elevation of the small GTPase RAB5A sparks unjamming by promoting non-clathrin-dependent 36 internalization of epidermal growth factor receptor that leads to hyper-activation of endosomally-37 confined ERK1/2 and phosphorylation of the actin nucleator WAVE2. Physically, activation of this 38 pathway causes highly coordinated flocking of the cells, with striking rotational motion in 3D that 39 eventually leads to matrix remodelling and collective invasiveness of otherwise jammed carcinoma. 40The identified endo-ERK1/2 pathway provides an effective switch for unjamming through flocking 41 to promote epithelial tissues morphogenesis and carcinoma invasion and dissemination. 42 43 Introduction 44Collective motility, a widely recognized mode of migration during embryogenesis, wound repair 45 and cancer 1, 2 , refers to the process of many cells migrating as a cohesive group with a high degree of 46 coordination between neighbouring cells. A complex network of biochemical and physical 47 interactions governs cellular and multicellular motility 2-5 . How cellular and supra-cellular 48 biomechanics and biochemical wiring are integrated and impact onto each other remains, however, 49 largely unexplored. 50An emerging framework to interpret these interactions in unifying principles is the notion of cell 51 jamming 6-8 . During tissue growth, cells are rather free to move around, as in a fluid. As density rises, 52 the motion of each cell is constrained by the crowding due to its neighbours. At a critical density, 53 motility ceases and collectives rigidify undergoing a liquid (unjammed)-to-solid (jammed) 54 transition 6-8 , herein referred to as UJT. This transition, which depends on a variety of biophysical 55 parameters such as cell shape variance 9 , intercellular adhesion, cortical tension and single cell 56 motility, is thought to ensure proper development of barrier properties in epithelial tissues, but also 57 to act as a tumour suppressive mechanism 6-8, 10 . The reverse jamming-to-unjamming transition (JUT) 58 might, instead, represent a complementary gateway to epithelial cell migration, enabling tissues to 59 escape the caging imposed by the crowded cellular landscape of mature epithelia 6, 10-12 . Indeed, 60whereas Epithelial-to-Mesenchymal Transition (EMT) has emerged as the overarching mechanism 61 enabling the dissemination of single tumour cells 13, 14 , invasion by epithelial malignancies 62 (carcinomas) frequently involves...

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Flocking transitions in confluent tissues

Cited by 151 publications

References 57 publications

Tissue Flow Induces Cell Shape Changes During Organogenesis

Tissue Flow Induces Cell Shape Changes During Organogenesis

Physical Models of Collective Cell Migration

Unjamming overcomes kinetic and proliferation arrest in terminally differentiated cells and promotes collective motility of carcinoma

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