Collective migration and cell jamming in asthma, cancer and development

Park, Jin‐Ah; Atia, Lior; Mitchel, Joseph F.; Fredberg, Jeffrey J.; Butler, James P.

doi:10.1242/jcs.187922

Cited by 149 publications

(178 citation statements)

References 85 publications

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“…Here we identified that a physical boundary is sufficient to trigger differentials of cellular forces and deformations, and that jamming is sufficient to control the dynamics of those differentials. Our findings thus raise the possibility that rather than being solely controlled by genetic clocks and travelling waves of biochemical nature, tissue segregation and patterning during development and homeostasis is controlled by cell jamming 57 .…”

mentioning

confidence: 87%

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

et al. 2017

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For an organism to develop and maintain homeostasis, cell types with distinct functions must often be separated by physical boundaries. The formation and maintenance of such boundaries are commonly attributed to local mechanisms restricted to the cells lining the boundary. Here we show that, besides these local subcellular mechanisms, the formation and maintenance of tissue boundaries involves long-lived, long-ranged mechanical events. We analyzed the formation of repulsive epithelial boundaries between two epithelial monolayers, one expressing the receptor tyrosine kinase EphB2 and one expressing its ligand ephrinB1. Upon contact, both monolayers exhibited oscillatory patterns of traction forces and intercellular stresses that spanned several cell rows and tended to pull cell-matrix adhesions away from the boundary. With time, monolayers jammed and supracellular force patterns became long-lived, thereby permanently sustaining tissue segregation. Jamming was paralleled by the emergence of deformation waves that propagated away from the boundary. This phenomenon was not specific to EphB2/ephrinB1 repulsion but was also present during the formation of boundaries with an inert interface and during fusion of homotypic epithelial layers. Our findings thus unveil a global physical mechanism that sustains tissue separation independently of the biochemical and mechanical features of the local tissue boundary.

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confidence: 87%

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

et al. 2017

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“…Dynamic cell -cell junctions enable cells to change position relative to their neighbors or as multicellular groups; they are relevant during morphogenesis and phases of tissue activation, for example, in response to injury or inflammation (Collins and Nelson 2015). By regulating junction "fluidity," the ag-gregate state and dynamics of cells can change remarkably and, accordingly, alter collective functions (Collins and Nelson 2015;Park et al 2016).…”

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confidence: 99%

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Friedl

Mayor

2017

Cold Spring Harb Perspect Biol

299

253

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Collective cell migration critically depends on cell -cell interactions coupled to a dynamic actin cytoskeleton. Important cell-cell adhesion receptor systems implicated in controlling collective movements include cadherins, immunoglobulin superfamily members (L1CAM, NCAM, ALCAM), Ephrin/Eph receptors, Slit/Robo, connexins and integrins, and an adaptive array of intracellular adapter and signaling proteins. Depending on molecular composition and signaling context, cell -cell junctions adapt their shape and stability, and this gradual junction plasticity enables different types of collective cell movements such as epithelial sheet and cluster migration, branching morphogenesis and sprouting, collective network migration, as well as coordinated individual-cell migration and streaming. Thereby, plasticity of cell -cell junction composition and turnover defines the type of collective movements in epithelial, mesenchymal, neuronal, and immune cells, and defines migration coordination, anchorage, and cell dissociation. We here review cell -cell adhesion systems and their functions in different types of collective cell migration as key regulators of collective plasticity.

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“…There are increasing recognition that this non-local cooperative process can be explained by the concept of jamming which have been proposed at the soft matter physics. Similarly to close-packed inert particulate matter, the increase or decrease in cell-cell adhesion would promote jamming or unjamming transition in the confluent living cellular layer2728. In the context of jamming transition, we found that HGF interfered with the jamming of the cell collectives and promoted the expansion of a confluent layer by changing the cell-cell adhesive stresses and kinematic behaviors, consistently with the cellular “unjamming”.…”

Section: Discussionmentioning

confidence: 63%

Homogenizing cellular tension by hepatocyte growth factor in expanding epithelial monolayer

Jang

Notbohm

Gweon

et al. 2017

Sci Rep

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Hepatocyte growth factor (HGF) induces cell migration and scattering by mechanisms that are thought to tip a local balance of competing physical forces; cell-to-cell and cell-to-substrate forces. In this local process, HGF is known to attenuate local cadherin-dependent adhesion forces for cell-cell junction development and enhance local integrin-dependent contractile forces for pulling neighboring cells apart. Here we use an expanding island of confluent Madin-Darby canine kidney (MDCK) cells as a model system to quantify the collective cell migration. In the absence of HGF, cell trajectories are highly tortuous whereas in the presence of HGF, they become far less so, resembling free expansion of a gas. At the level of cell-to-cell junctions, HGF attenuates the linkage of stress fibers to cell-to-cell junctions with concomitant decrease in intercellular stress. At the level of cell-to-substrate junctions, HGF augments the linkage of stress fibers to cell-to-substrate junctions with no apparent effect on traction. Together, HGF induces both structural changes in the actin-bound junctional protein complex and physical forces spanning multicellular clusters, which further promotes the expansion of confluent cellular layer.

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Collective migration and cell jamming in asthma, cancer and development

Cited by 149 publications

References 85 publications

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Homogenizing cellular tension by hepatocyte growth factor in expanding epithelial monolayer

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