Directional cell migration through cell–cell interaction on polyelectrolyte multilayers with swelling gradients

Biophysical mechanisms underlying collective cell migration of eukaryotic cells have been studied extensively in recent years. One mechanism that induces cells to correlate their motions is contact inhibition of locomotion, by which cells migrating away from the contact site. Here, we report that tail-following behavior at the contact site, termed contact following locomotion (CFL), can induce a non-trivial collective behavior in migrating cells. We show the emergence of a traveling band showing polar order in a mutant Dictyostelium cell that lacks chemotactic activity. We find that CFL is the cell–cell interaction underlying this phenomenon, enabling a theoretical description of how this traveling band forms. We further show that the polar order phase consists of subpopulations that exhibit characteristic transversal motions with respect to the direction of band propagation. These findings describe a novel mechanism of collective cell migration involving cell–cell interactions capable of inducing traveling band with polar order.

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N-cadherin-Presented Slit Repulsive-Cues Direct Collective Schwann cell Migration

10.1101/549030 ◽

2019 ◽

Author(s):

Julian J.A Hoving ◽

Elizabeth Harford-Wright ◽

Patrick Wingfield-Digby ◽

Anne-Laure Cattin ◽

Mariana Campana ◽

...

Keyword(s):

Cell Migration ◽

Schwann Cell ◽

Peripheral Nerve Regeneration ◽

Adherens Junction ◽

Cell Interaction ◽

Collective Cell Migration ◽

Cancer Migration ◽

Cell Collective ◽

Migratory Cell ◽

Cell Cell

AbstractCollective cell migration is fundamental for the development of organisms and in the adult, for tissue regeneration and in pathological conditions such as cancer. Migration as a coherent group requires the maintenance of cell-cell interactions, while contact-inhibition-of-locomotion (CIL), a local repulsive force, propels the group forward. Here we show that the cell-cell interaction molecule, N-cadherin, regulates both adhesion and repulsion processes during Schwann cell collective migration, which is required for peripheral nerve regeneration. However, distinct from its role in cell-cell adhesion, the repulsion process is independent of N-cadherin trans-homodimerisation and the associated adherens junction complex. Rather, the extracellular domain of N-cadherin acts to traffic a repulsive Slit2/Slit3 signal to the cell-surface. Inhibiting Slit2/Slit3 signalling inhibits CIL and subsequently collective SC migration, resulting in adherent, non-migratory cell clusters. These findings provide insight into how opposing signals can mediate collective cell migration and how CIL pathways are promising targets for inhibiting pathological cell migration.

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WAVE2 Protein Complex Coupled to Membrane and Microtubules

Journal of Oncology ◽

10.1155/2012/590531 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 3

Author(s):

Kazuhide Takahashi

Keyword(s):

Cell Migration ◽

Cell Adhesion ◽

Cancer Cell ◽

Migration And Invasion ◽

Cancer Cell Migration ◽

Actin Assembly ◽

Cell Migration And Invasion ◽

Directional Cell Migration ◽

E Cadherin ◽

Cell Cell

E-cadherin is one of the key molecules in the formation of cell-cell adhesion and interacts intracellularly with a group of proteins collectively named catenins, through which the E-cadherin-catenin complex is anchored to actin-based cytoskeletal components. Although cell-cell adhesion is often disrupted in cancer cells by either genetic or epigenetic alterations in cell adhesion molecules, disruption of cell-cell adhesion alone seems to be insufficient for the induction of cancer cell migration and invasion. A small GTP-binding protein, Rac1, induces the specific cellular protrusions lamellipodia via WAVE2, a member of WASP/WAVE family of the actin cytoskeletal regulatory proteins. Biochemical and pharmacological investigations have revealed that WAVE2 interacts with many proteins that regulate microtubule growth, actin assembly, and membrane targeting of proteins, all of which are necessary for directional cell migration through lamellipodia formation. These findings might have important implications for the development of effective therapeutic agents against cancer cell migration and invasion.

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Identification of IGPR-1 as a novel adhesion molecule involved in angiogenesis

Molecular Biology of the Cell ◽

10.1091/mbc.e11-11-0934 ◽

2012 ◽

Vol 23 (9) ◽

pp. 1646-1656 ◽

Cited By ~ 34

Author(s):

Nader Rahimi ◽

Kobra Rezazadeh ◽

John E. Mahoney ◽

Edward Hartsough ◽

Rosana D. Meyer

Keyword(s):

Endothelial Cells ◽

Cell Migration ◽

Capillary Tube ◽

Cell Aggregation ◽

Cell Interaction ◽

Tube Formation ◽

Fiber Formation ◽

Actin Stress Fiber ◽

Cell Cell

Angiogenesis—the growth of new blood vessels from preexisting vessels—is an important physiological process and is considered to play a key role in tumor growth and metastasis. We identified the immunoglobulin-containing and proline-rich receptor-1 (IGPR-1, also called TMIGD2) gene as a novel cell adhesion receptor that is expressed in various human organs and tissues, mainly in cells with epithelium and endothelium origins. IGPR-1 regulates cellular morphology, homophilic cell aggregation, and cell–cell interaction. IGPR-1 activity also modulates actin stress fiber formation and focal adhesion and reduces cell migration. Silencing of expression of IGPR-1 by small interfering RNA (siRNA) and by ectopic overexpression in endothelial cells showed that IGPR-1 regulates capillary tube formation in vitro, and B16F melanoma cells engineered to express IGPR-1 displayed extensive angiogenesis in the mouse Matrigel angiogenesis model. Moreover, IGPR-1, through its proline-rich cytoplasmic domain, associates with multiple Src homology 3 (SH3)–containing signaling proteins, including SH3 protein interacting with Nck (SPIN90/WISH), bullous pemphigoid antigen-1, and calcium channel β2. Silencing of expression of SPIN90/WISH by siRNA in endothelial cells showed that SPIN90/WISH is required for capillary tube formation. These features of IGPR-1 suggest that IGPR-1 is a novel receptor that plays an important role in cell–cell interaction, cell migration, and angiogenesis.

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Polar pattern formation induced by contact following locomotion in a multicellular system

10.1101/2019.12.29.890566 ◽

2019 ◽

Author(s):

Masayuki Hayakawa ◽

Tetsuya Hiraiwa ◽

Yuko Wada ◽

Hidekazu Kuwayama ◽

Tatsuo Shibata

Keyword(s):

Cell Migration ◽

Mutant Cell ◽

Cell Interaction ◽

Collective Cell Migration ◽

Contact Site ◽

Band Formation ◽

Polar Order ◽

Agent Based ◽

Cell Cell

AbstractBiophysical mechanisms underlying collective cell migration of eukaryotic cells have been studied extensively in recent years. One paradigm that induces cells to correlate their motions is contact inhibition of locomotion, by which cells migrating away from the contact site. Here, we report that tail-following behavior at the contact site, termed contact following locomotion (CFL), can induce a non-trivial collective behavior in migrating cells. We show the emergence of a traveling band showing polar order in a mutant Dictyostelium cell that lacks chemotactic activity. The traveling band is dynamic in the sense that it continuously assembled at the front of the band and disassembled at the back. A mutant cell lacking cell adhesion molecule TgrB1 did not show both the traveling band formation and CFL. We thus conclude that CFL is the cell-cell interaction underlying the traveling band formation. We then develop an agent-based simulation with CFL, which shows the role of CFL in the formation of traveling band. We further show that the polar order phase consists of subpopulations that exhibit characteristic transversal motions with respect to the direction of band propagation. These findings describe a novel mechanism of collective cell migration involving cell–cell interactions capable of inducing traveling band with polar order.

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Vein Patterning by Tissue-Specific Auxin Transport

10.1101/866632 ◽

2019 ◽

Author(s):

Priyanka Govindaraju ◽

Carla Verna ◽

Tongbo Zhu ◽

Enrico Scarpella

Keyword(s):

Cell Migration ◽

Auxin Transport ◽

Cell Interaction ◽

Auxin Level ◽

Tissue Specific ◽

Direct Cell ◽

Vein Patterning ◽

Auxin Transporter ◽

Cell Cell

AbstractUnlike in animals, in plants vein patterning does not rely on direct cell-cell interaction and cell migration; instead, it depends on the transport of the plant signal auxin, which in turn depends on the activity of the PIN-FORMED1 (PIN1) auxin transporter. The current hypotheses of vein patterning by auxin transport propose that in the epidermis of the developing leaf PIN1-mediated auxin transport converges to peaks of auxin level. From those convergence points of epidermal PIN1 polarity, auxin would be transported in the inner tissues where it would give rise to major veins. Here we tested predictions of this hypothesis and found them unsupported: epidermal PIN1 expression is neither required nor sufficient for auxin-transport-dependent vein patterning, whereas inner-tissue PIN1 expression turns out to be both required and sufficient for auxin-transport-dependent vein patterning. Our results refute all vein patterning hypotheses based on auxin transport from the epidermis and suggest alternatives for future tests.

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