Artículos de revistas: "Cell migration"

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Trepat, Xavier, Zaozao Chen, and Ken Jacobson. "Cell Migration." Comprehensive Physiology 2, no. 4 (October 2012): 2369–92. https://doi.org/10.1002/j.2040-4603.2012.tb00467.x.

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AbstractCell migration is fundamental to establishing and maintaining the proper organization of multicellular organisms. Morphogenesis can be viewed as a consequence, in part, of cell locomotion, from large‐scale migrations of epithelial sheets during gastrulation, to the movement of individual cells during development of the nervous system. In an adult organism, cell migration is essential for proper immune response, wound repair, and tissue homeostasis, while aberrant cell migration is found in various pathologies. Indeed, as our knowledge of migration increases, we can look forward to, for example, abating the spread of highly malignant cancer cells, retarding the invasion of white cells in the inflammatory process, or enhancing the healing of wounds. This article is organized in two main sections. The first section is devoted to the single‐cell migrating in isolation such as occurs when leukocytes migrate during the immune response or when fibroblasts squeeze through connective tissue. The second section is devoted to cells collectively migrating as part of multicellular clusters or sheets. This second type of migration is prevalent in development, wound healing, and in some forms of cancer metastasis. © 2012 American Physiological Society. Compr Physiol 2:2369‐2392, 2012.

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Thomas, L. A., and K. M. Yamada. "Contact stimulation of cell migration." Journal of Cell Science 103, no. 4 (December 1, 1992): 1211–14. http://dx.doi.org/10.1242/jcs.103.4.1211.

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Mass migrations of dense cell populations occur periodically during embryonic development. It is known that extracellular matrices, through which the cells migrate, facilitate locomotion. However, this does not explain how cells, such as neural crest, can migrate as a dense cohort of cells in essentially continuous contact with one another. We report here that unique behavioral characteristics of the migrating cells may contribute to cohesive migration. We used time-lapse video microscopy to analyze the migration of quail neural crest cells and of two crest derivatives, human melanoma cells and melanocytes. These cells migrated poorly, if at all, when isolated, but could be stimulated up to 200-fold to travel following contact with migrating cells. This phenomenon, which we have termed “contact-stimulated migration,” appeared to activate and sustain migration of the mass of cells. Cells that became dissociated from the others ceased directional migration, thereby limiting aberrant cell dispersion. Fibroblasts were minimally responsive to this novel phenomenon, which may be crucial for major, mass cell migrations.

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.

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Ffrench-Constant, C., and R. O. Hynes. "Patterns of fibronectin gene expression and splicing during cell migration in chicken embryos." Development 104, no. 3 (November 1, 1988): 369–82. http://dx.doi.org/10.1242/dev.104.3.369.

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A variety of evidence suggests that fibronectin (FN) promotes cell migration during embryogenesis, and it has been suggested that the deposition of FN along migratory pathways may also play a role in cell guidance. In order to investigate such a role for FN, it is important to determine the relative contribution of migrating and pathway-forming cells to the FN in the migratory track, as any synthesis of FN by the migrating cells might be expected to mask guidance cues provided by the exogenous FN from pathway-forming cells. We have therefore used in situ hybridization to determine in developing chicken embryos the distribution and alternative splicing of FN mRNA during three different cell migrations known to occur through FN-rich environments; neural crest cell migration, mesenchymal cell migration in the area vasculosa and endocardial cushion cell migration in the heart. Our results show that trunk neural crest cells do not contain significant FN mRNA during their initial migration. In contrast, migrating mesenchymal cells of the area vasculosa and endocardial cushion cells both contain abundant FN mRNA. Furthermore, the FN mRNA in these migrating mesenchymal and endocardial cells appears to be spliced in a manner identical with that present in the cells adjacent to their pathways. This in vivo evidence for FN synthesis by migrating and pathway cells argues against a generalized role for exogenously produced FN as a guidance mechanism for cell migration.

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Deryugina, E. I., and M. A. Bourdon. "Tenascin mediates human glioma cell migration and modulates cell migration on fibronectin." Journal of Cell Science 109, no. 3 (March 1, 1996): 643–52. http://dx.doi.org/10.1242/jcs.109.3.643.

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The role of tenascin in mediating tumor cell migration was studied using two cell migration models. In migration/invasion Transwell assays U251.3 glioma cells rapidly migrated through the 8 mu m pore size membranes onto tenascin- and fibronectin-coated surfaces. In this assay the number of cells migrating onto tenascin was 52.2 +/- 9.6% greater than on fibronectin within 4 hours. To assess cell migration rates and cell morphology, U251.3 migration was examined in a two-dimension spheroid outgrowth assay. The radial distance migrated by U251.3 cells from tumor spheroids was found to be 53.8 +/- 4.9% greater on tenascin than on fibronectin. Cells migrating on tenascin display a very motile appearance, while cells migrating on fibronectin spread and maintain close intercellular contacts. Cell migration in the presence of integrin blocking antibodies demonstrated that migration on tenascin and fibronectin is mediated by distinct integrins, alpha2beta1 and alphavbeta5/alphavbeta3, respectively. Since tenascin is coexpressed in malignant tumor matrices with fibronectin, we assessed the effects of tenascin on U251.3 cell migration mediated by fibronectin. Tenascin was found to provide a positive effect on fibronectin-mediated migration by altering cell morphology and enhancing cell motility. These effects of tenascin on fibronectin-mediated cell migration were inhibited by blocking beta1 and alpha2beta1 integrins. The results suggest that tenascin may play a significant role in promoting tumor cell migration and invasiveness by modulating cell responses to normal matrix components.

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6

Torrence, S. A. "Positional cues governing cell migration in leech neurogenesis." Development 111, no. 4 (April 1, 1991): 993–1005. http://dx.doi.org/10.1242/dev.111.4.993.

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The stereotyped distribution of identified neurons and glial cells in the leech nervous system is the product of stereotyped cell migrations and rearrangements during embryogenesis. To examine the dependence of long-distance cell migrations on positional cues provided by other tissues, embryos of Theromyzon rude were examined for the effects of selective ablation of various embryonic cell lines on the migration and final distribution of neural and glial precursor cells descended from the bilaterally paired ectodermal cell lines designated q bandlets. The results suggest that neither the commitment of q-bandlet cells to migrate nor the general lateral-to-medial direction of their migration depend on interactions with any other cell line. However, the ability of the migrating cells to follow their normal pathways and to find their normal destinations does depend on interactions with cells of the mesodermal cell line, which appears to provide positional cues that specify the migration pathways.

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7

Li, David, and Yu-li Wang. "Coordination of cell migration mediated by site-dependent cell–cell contact." Proceedings of the National Academy of Sciences 115, no. 42 (October 1, 2018): 10678–83. http://dx.doi.org/10.1073/pnas.1807543115.

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Contact inhibition of locomotion (CIL), the repulsive response of cells upon cell–cell contact, has been the predominant paradigm for contact-mediated responses. However, it is difficult for CIL alone to account for the complex behavior of cells within a multicellular environment, where cells often migrate in cohorts such as sheets, clusters, and streams. Although cell–cell adhesion and mechanical interactions play a role, how individual cells coordinate their migration within a multicellular environment remains unclear. Using micropatterned substrates to guide cell migration and manipulate cell–cell contact, we show that contacts between different regions of cells elicit different responses. Repulsive responses were limited to interaction with the head of a migrating cell, while contact with the tail of a neighboring cell promoted migration toward the tail. The latter behavior, termed contact following of locomotion (CFL), required the Wnt signaling pathway. Inhibition of the Wnt pathway disrupted not only CFL but also collective migration of epithelial cells, without affecting the migration of individual cells. In contrast, inhibition of myosin II with blebbistatin disrupted the migration of both individual epithelial cells and collectives. We propose that CFL, in conjunction with CIL, plays a major role in guiding and coordinating cell migration within a multicellular environment.

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8

Bradley, David. "Cell migration." Materials Today 14, no. 1-2 (January 2011): 10. http://dx.doi.org/10.1016/s1369-7021(11)70010-4.

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9

Horwitz, Rick, and Donna Webb. "Cell migration." Current Biology 13, no. 19 (September 2003): R756—R759. http://dx.doi.org/10.1016/j.cub.2003.09.014.

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10

Wang, Heng, and Jiong Chen. "Cell migration: Collective cell migration is intrinsically stressful." Current Biology 34, no. 7 (April 2024): R275—R278. http://dx.doi.org/10.1016/j.cub.2024.02.061.

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Harris, J., L. Honigberg, N. Robinson, and C. Kenyon. "Neuronal cell migration in C. elegans: regulation of Hox gene expression and cell position." Development 122, no. 10 (October 1, 1996): 3117–31. http://dx.doi.org/10.1242/dev.122.10.3117.

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In C. elegans, the Hox gene mab-5, which specifies the fates of cells in the posterior body region, has been shown to direct the migrations of certain cells within its domain of function. mab-5 expression switches on in the neuroblast QL as it migrates into the posterior body region. mab-5 activity is then required for the descendants of QL to migrate to posterior rather than anterior positions. What information activates Hox gene expression during this cell migration? How are these cells subsequently guided to their final positions? We address these questions by describing four genes, egl-20, mig-14, mig-1 and lin-17, that are required to activate expression of mab-5 during migration of the QL neuroblast. We find that two of these genes, egl-20 and mig-14, also act in a mab-5-independent way to determine the final stopping points of the migrating Q descendants. The Q descendants do not migrate toward any obvious physical targets in wild-type or mutant animals. Therefore, these genes appear to be part of a system that positions the migrating Q descendants along the anteroposterior axis.

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12

Ridley, Anne J. "Rho GTPases and cell migration." Journal of Cell Science 114, no. 15 (August 1, 2001): 2713–22. http://dx.doi.org/10.1242/jcs.114.15.2713.

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Cell migration involves dynamic and spatially regulated changes to the cytoskeleton and cell adhesion. The Rho GTPases play key roles in coordinating the cellular responses required for cell migration. Recent research has revealed new molecular links between Rho family proteins and the actin cytoskeleton, showing that they act to regulate actin polymerization, depolymerization and the activity of actin-associated myosins. In addition, studies on integrin signalling suggest that the substratum continuously feeds signals to Rho proteins in migrating cells to influence migration rate. There is also increasing evidence that Rho proteins affect the organization of the microtubule and intermediate filament networks and that this is important for cell migration.

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13

Garcin, Clare, and Anne Straube. "Microtubules in cell migration." Essays in Biochemistry 63, no. 5 (July 29, 2019): 509–20. http://dx.doi.org/10.1042/ebc20190016.

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Abstract Directed cell migration is critical for embryogenesis and organ development, wound healing and the immune response. Microtubules are dynamic polymers that control directional migration through a number of coordinated processes: microtubules are the tracks for long-distance intracellular transport, crucial for delivery of new membrane components and signalling molecules to the leading edge of a migrating cell and the recycling of adhesion receptors. Microtubules act as force generators and compressive elements to support sustained cell protrusions. The assembly and disassembly of microtubules is coupled to Rho GTPase signalling, thereby controlling actin polymerisation, myosin-driven contractility and the turnover of cellular adhesions locally. Cross-talk of actin and microtubule dynamics is mediated through a number of common binding proteins and regulators. Furthermore, cortical microtubule capture sites are physically linked to focal adhesions, facilitating the delivery of secretory vesicles and efficient cross-talk. Here we summarise the diverse functions of microtubules during cell migration, aiming to show how they contribute to the spatially and temporally coordinated sequence of events that permit efficient, directional and persistent migration.

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14

Legrand, Claire, Christine Gilles, Jean-Marie Zahm, Myriam Polette, Anne-Cécile Buisson, Hervé Kaplan, Philippe Birembaut, and Jean-Marie Tournier. "Airway Epithelial Cell Migration Dynamics: MMP-9 Role in Cell–Extracellular Matrix Remodeling." Journal of Cell Biology 146, no. 2 (July 26, 1999): 517–29. http://dx.doi.org/10.1083/jcb.146.2.517.

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Cell spreading and migration associated with the expression of the 92-kD gelatinase (matrix metalloproteinase 9 or MMP-9) are important mechanisms involved in the repair of the respiratory epithelium. We investigated the location of MMP-9 and its potential role in migrating human bronchial epithelial cells (HBEC). In vivo and in vitro, MMP-9 accumulated in migrating HBEC located at the leading edge of a wound and MMP-9 expression paralleled cell migration speed. MMP-9 accumulated through an actin-dependent pathway in the advancing lamellipodia of migrating cells and was subsequently found active in the extracellular matrix (ECM). Lamellipodia became anchored through primordial contacts established with type IV collagen. MMP-9 became amassed behind collagen IV where there were fewer cell–ECM contacts. Both collagen IV and MMP-9 were involved in cell migration because when cell–collagen IV interaction was blocked, cells spread slightly but did not migrate; and when MMP-9 activation was prevented, cells remained fixed on primordial contacts and did not advance at all. These observations suggest that MMP-9 controls the migration of repairing HBEC by remodeling the provisional ECM implicated in primordial contacts.

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15

Zhao, Jieling, Youfang Cao, Luisa A. DiPietro, and Jie Liang. "Dynamic cellular finite-element method for modelling large-scale cell migration and proliferation under the control of mechanical and biochemical cues: a study of re-epithelialization." Journal of The Royal Society Interface 14, no. 129 (April 2017): 20160959. http://dx.doi.org/10.1098/rsif.2016.0959.

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Computational modelling of cells can reveal insight into the mechanisms of the important processes of tissue development. However, current cell models have limitations and are challenged to model detailed changes in cellular shapes and physical mechanics when thousands of migrating and interacting cells need to be modelled. Here we describe a novel dynamic cellular finite-element model (DyCelFEM), which accounts for changes in cellular shapes and mechanics. It also models the full range of cell motion, from movements of individual cells to collective cell migrations. The transmission of mechanical forces regulated by intercellular adhesions and their ruptures are also accounted for. Intra-cellular protein signalling networks controlling cell behaviours are embedded in individual cells. We employ DyCelFEM to examine specific effects of biochemical and mechanical cues in regulating cell migration and proliferation, and in controlling tissue patterning using a simplified re-epithelialization model of wound tissue. Our results suggest that biochemical cues are better at guiding cell migration with improved directionality and persistence, while mechanical cues are better at coordinating collective cell migration. Overall, DyCelFEM can be used to study developmental processes when a large population of migrating cells under mechanical and biochemical controls experience complex changes in cell shapes and mechanics.

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16

Shellard, Adam, and Roberto Mayor. "Supracellular migration – beyond collective cell migration." Journal of Cell Science 132, no. 8 (April 15, 2019): jcs226142. http://dx.doi.org/10.1242/jcs.226142.

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17

Murakami, Shinya, Yo Otsuka, Manabu Sugimoto, and Toshiyuki Mitsui. "3H1010 Controlled cell migration with ultrasound(Cell Biology III:Cytoskeleton & Motility,Oral Presentation)." Seibutsu Butsuri 52, supplement (2012): S70. http://dx.doi.org/10.2142/biophys.52.s70_4.

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18

Boehm, Manfred, and Elizabeth G. Nabel. "Cell Cycle and Cell Migration." Circulation 103, no. 24 (June 19, 2001): 2879–81. http://dx.doi.org/10.1161/01.cir.103.24.2879.

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McLane, Louis T., Anthony Kramer, Carrie Harris, Edward Park, Hang Lu, and Jennifer E. Curtis. "Cell Coat Mediated Cell Migration." Biophysical Journal 96, no. 3 (February 2009): 629a. http://dx.doi.org/10.1016/j.bpj.2008.12.3325.

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Chen, Zaozao, Qiwei Li, Shihui Xu, Jun Ouyang, and Hongmei Wei. "Nanotopography-Modulated Epithelial Cell Collective Migration." Journal of Biomedical Nanotechnology 17, no. 6 (June 1, 2021): 1079–87. http://dx.doi.org/10.1166/jbn.2021.3086.

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Matrix nanotopography plays an essential role in regulating cell behaviors including cell proliferation, differentiation, and migration. While studies on isolated single cell migration along the nanostructural orientation have been reported for various cell types, there remains a lack of understanding of how nanotopography regulates the behavior of collectively migrating cells during processes such as epithelial wound healing. We demonstrated that collective migration of epithelial cells was promoted on nanogratings perpendicular to, but not on those parallel to, the wound-healing axis. We further discovered that nanograting-modulated epithelial migration was dominated by the adhesion turnover process, which was Rho-associated protein kinase activity-dependent, and the lamellipodia protrusion at the cell leading edge, which was Rac1-GTPase activity-dependent. This work provides explanations to the distinct migration behavior of epithelial cells on nanogratings, and indicates that the effect of nanotopographic modulations on cell migration is cell-type dependent and involves complex mechanisms

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Rørth, Pernille. "Collective Cell Migration." Annual Review of Cell and Developmental Biology 25, no. 1 (November 2009): 407–29. http://dx.doi.org/10.1146/annurev.cellbio.042308.113231.

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Cumberbatch, M., R. J. Dearman, C. E. M. Griffiths, and I. Kimber. "Langerhans cell migration." Clinical and Experimental Dermatology 25, no. 5 (September 2000): 413–18. http://dx.doi.org/10.1046/j.1365-2230.2000.00678.x.

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23

Spector, Mario, Leandro Peretti, Favio Vincitorio, and Luciano Iglesias. "Bacterial Migration Cell." Procedia Materials Science 8 (2015): 346–50. http://dx.doi.org/10.1016/j.mspro.2015.04.083.

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24

Sutherland, Stephani. "Targeting cell migration." Drug Discovery Today 8, no. 1 (January 2003): 6–7. http://dx.doi.org/10.1016/s1359-6446(02)02549-7.

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Augustin-Voss, H. G., and B. U. Pauli. "Migrating endothelial cells are distinctly hyperglycosylated and express specific migration-associated cell surface glycoproteins." Journal of Cell Biology 119, no. 2 (October 15, 1992): 483–91. http://dx.doi.org/10.1083/jcb.119.2.483.

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Migration of endothelial cells is one of the first cellular responses in the cascade of events that leads to re-endothelialization of an injured vessel and neovascularization of growing tissues and tumors. To examine the hypothesis that endothelial cells express a specific migration-associated phenotype, we analyzed the cell surface glycoprotein expression of migrating bovine aortic endothelial cell (BAECs). Light microscopic analysis revealed an upregulation of binding sites for the lectins Concanavalin A (Con A), wheat germ agglutinin (WGA), and peanut agglutinin after neuraminidase treatment (N-PNA) on migrating endothelial cells relative to contact-inhibited cells. These findings were confirmed and quantitated with an enzyme-linked lectin assay (ELLA) of circularly scraped BAEC monolayers. The expression of migration-associated cell surface glycoproteins was also analyzed by SDS-PAGE. The overall expression of cell surface glycoproteins was upregulated on migrating BAECs. Migrating BAECs expressed Con A- and WGA-binding glycoproteins with apparent molecular masses of 25 and 48 kD that were not expressed by contact-inhibited BAEC monolayers and, accordingly, disappeared as circularly scraped monolayers reached confluence. Subconfluent BAEC monolayers expressed the same cell surface glycoconjugate pattern as migrating endothelial cells. FACS analysis of circularly scraped BAEC monolayers showed that the phenotypic changes of cell surface glycoprotein expression after release from growth arrest occurred before the recruitment of the cells into the cell cycle (3 vs. 12 h). Suramin, which inhibits endothelial cell migration, abrogated the expression of the migration-associated phenotype and induced the expression of a prominent 28-kD Con A- and WGA-binding cell surface glycoprotein. These results indicate that endothelial cells express a specific migration-associated phenotype, which is characterized by the upregulation of distinct cellular glycoconjugates and the expression of specific migration-associated cell surface glycoproteins.

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Golden, J. A., J. C. Zitz, K. McFadden, and C. L. Cepko. "Cell migration in the developing chick diencephalon." Development 124, no. 18 (September 15, 1997): 3525–33. http://dx.doi.org/10.1242/dev.124.18.3525.

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We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryonic day 4, all clones were organized in radial columns spanning the neuroepithelium, which was composed primarily of a ventricular zone at this age. No tangential migration was seen in the ventricular zone. On embryonic day 5, most clones remained radial with many cells located in the ventricular zone; however, a few clones had cells migrating perpendicular to the radial column, in either a rostrocaudal or dorsoventral direction. The tangential migration began just beyond the basal limit of the ventricular zone. On embryonic days 6 and 7, many clones had cells migrating perpendicular to the radial column, which spanned from the ventricular to the pial surface. The migrating cells appeared to be aligned along axes that were perpendicular to the radial column. Using a combination of DiI tracing, immunohistochemistry and electron microscopy, we have determined that axonal tracts are present and are aligned with the migrating cells, suggesting that they support the non-radial cell migration. These data indicate that migration along pathways independent of radial glia occur outside of the ventricular zone in more than 50% of the clones in the chick diencephalon.

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Kim, Jin Man, Minji Lee, Nury Kim, and Won Do Heo. "Optogenetic toolkit reveals the role of Ca2+sparklets in coordinated cell migration." Proceedings of the National Academy of Sciences 113, no. 21 (May 17, 2016): 5952–57. http://dx.doi.org/10.1073/pnas.1518412113.

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Cell migration is controlled by various Ca2+signals. Local Ca2+signals, in particular, have been identified as versatile modulators of cell migration because of their spatiotemporal diversity. However, little is known about how local Ca2+signals coordinate between the front and rear regions in directionally migrating cells. Here, we elucidate the spatial role of local Ca2+signals in directed cell migration through combinatorial application of an optogenetic toolkit. An optically guided cell migration approach revealed the existence of Ca2+sparklets mediated by L-type voltage-dependent Ca2+channels in the rear part of migrating cells. Notably, we found that this locally concentrated Ca2+influx acts as an essential transducer in establishing a global front-to-rear increasing Ca2+gradient. This asymmetrical Ca2+gradient is crucial for maintaining front–rear morphological polarity by restricting spontaneous lamellipodia formation in the rear part of migrating cells. Collectively, our findings demonstrate a clear link between local Ca2+sparklets and front–rear coordination during directed cell migration.

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Nishita, Michiru, Chinatsu Tomizawa, Masahiro Yamamoto, Yuji Horita, Kazumasa Ohashi, and Kensaku Mizuno. "Spatial and temporal regulation of cofilin activity by LIM kinase and Slingshot is critical for directional cell migration." Journal of Cell Biology 171, no. 2 (October 17, 2005): 349–59. http://dx.doi.org/10.1083/jcb.200504029.

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Cofilin mediates lamellipodium extension and polarized cell migration by accelerating actin filament dynamics at the leading edge of migrating cells. Cofilin is inactivated by LIM kinase (LIMK)–1-mediated phosphorylation and is reactivated by cofilin phosphatase Slingshot (SSH)-1L. In this study, we show that cofilin activity is temporally and spatially regulated by LIMK1 and SSH1L in chemokine-stimulated Jurkat T cells. The knockdown of LIMK1 suppressed chemokine-induced lamellipodium formation and cell migration, whereas SSH1L knockdown produced and retained multiple lamellipodial protrusions around the cell after cell stimulation and impaired directional cell migration. Our results indicate that LIMK1 is required for cell migration by stimulating lamellipodium formation in the initial stages of cell response and that SSH1L is crucially involved in directional cell migration by restricting the membrane protrusion to one direction and locally stimulating cofilin activity in the lamellipodium in the front of the migrating cell. We propose that LIMK1- and SSH1L-mediated spatiotemporal regulation of cofilin activity is critical for chemokine-induced polarized lamellipodium formation and directional cell movement.

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Petrie, Ryan J., Núria Gavara, Richard S. Chadwick, and Kenneth M. Yamada. "Nonpolarized signaling reveals two distinct modes of 3D cell migration." Journal of Cell Biology 197, no. 3 (April 30, 2012): 439–55. http://dx.doi.org/10.1083/jcb.201201124.

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We search in this paper for context-specific modes of three-dimensional (3D) cell migration using imaging for phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and active Rac1 and Cdc42 in primary fibroblasts migrating within different 3D environments. In 3D collagen, PIP3 and active Rac1 and Cdc42 were targeted to the leading edge, consistent with lamellipodia-based migration. In contrast, elongated cells migrating inside dermal explants and the cell-derived matrix (CDM) formed blunt, cylindrical protrusions, termed lobopodia, and Rac1, Cdc42, and PIP3 signaling was nonpolarized. Reducing RhoA, Rho-associated protein kinase (ROCK), or myosin II activity switched the cells to lamellipodia-based 3D migration. These modes of 3D migration were regulated by matrix physical properties. Specifically, experimentally modifying the elasticity of the CDM or collagen gels established that nonlinear elasticity supported lamellipodia-based migration, whereas linear elasticity switched cells to lobopodia-based migration. Thus, the relative polarization of intracellular signaling identifies two distinct modes of 3D cell migration governed intrinsically by RhoA, ROCK, and myosin II and extrinsically by the elastic behavior of the 3D extracellular matrix.

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Bachmann, Alice, and Anne Straube. "Kinesins in cell migration." Biochemical Society Transactions 43, no. 1 (January 26, 2015): 79–83. http://dx.doi.org/10.1042/bst20140280.

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Human cells express 45 kinesins, microtubule motors that transport a variety of molecules and organelles within the cell. Many kinesins also modulate the tracks they move on by either bundling or sliding or regulating the dynamic assembly and disassembly of the microtubule polymer. In migrating cells, microtubules control the asymmetry between the front and rear of the cell by differentially regulating force generation processes and substrate adhesion. Many of these functions are mediated by kinesins, transporters as well as track modulators. In this review, we summarize the current knowledge on kinesin functions in cell migration.

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Hammad, Ayat S., and Khaled Machaca. "Store Operated Calcium Entry in Cell Migration and Cancer Metastasis." Cells 10, no. 5 (May 19, 2021): 1246. http://dx.doi.org/10.3390/cells10051246.

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Ca2+ signaling is ubiquitous in eukaryotic cells and modulates many cellular events including cell migration. Directional cell migration requires the polarization of both signaling and structural elements. This polarization is reflected in various Ca2+ signaling pathways that impinge on cell movement. In particular, store-operated Ca2+ entry (SOCE) plays important roles in regulating cell movement at both the front and rear of migrating cells. SOCE represents a predominant Ca2+ influx pathway in non-excitable cells, which are the primary migrating cells in multicellular organisms. In this review, we summarize the role of Ca2+ signaling in cell migration with a focus on SOCE and its diverse functions in migrating cells and cancer metastasis. SOCE has been implicated in regulating focal adhesion turnover in a polarized fashion and the mechanisms involved are beginning to be elucidated. However, SOCE is also involved is other aspects of cell migration with a less well-defined mechanistic understanding. Therefore, much remains to be learned regarding the role and regulation of SOCE in migrating cells.

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Schwab, Albrecht. "Function and spatial distribution of ion channels and transporters in cell migration." American Journal of Physiology-Renal Physiology 280, no. 5 (May 1, 2001): F739—F747. http://dx.doi.org/10.1152/ajprenal.2001.280.5.f739.

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Cell migration plays a central role in many physiological and pathophysiological processes, such as embryogenesis, immune defense, wound healing, or the formation of tumor metastases. Detailed models have been developed that describe cytoskeletal mechanisms of cell migration. However, evidence is emerging that ion channels and transporters also play an important role in cell migration. The purpose of this review is to examine the function and subcellular distribution of ion channels and transporters in cell migration. Topics covered will be a brief overview of cytoskeletal mechanisms of migration, the role of ion channels and transporters involved in cell migration, and ways by which a polarized distribution of ion channels and transporters can be achieved in migrating cells. Moreover, a model is proposed that combines ion transport with cytoskeletal mechanisms of migration.

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33

Maeda, Nobuaki, та Masaharu Noda. "Involvement of Receptor-like Protein Tyrosine Phosphatase ζ/RPTPβ and Its Ligand Pleiotrophin/Heparin-binding Growth-associated Molecule (HB-GAM) in Neuronal Migration". Journal of Cell Biology 142, № 1 (13 липня 1998): 203–16. http://dx.doi.org/10.1083/jcb.142.1.203.

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Pleiotrophin/heparin-binding growth-associated molecule (HB-GAM) is a specific ligand of protein tyrosine phosphatase ζ (PTPζ)/receptor-like protein tyrosine phosphatase β (RPTPβ) expressed in the brain as a chondroitin sulfate proteoglycan. Pleiotrophin and PTPζ isoforms are localized along the radial glial fibers, a scaffold for neuronal migration, suggesting that these molecules are involved in migratory processes of neurons during brain development. In this study, we examined the roles of pleiotrophin-PTPζ interaction in the neuronal migration using cell migration assay systems with glass fibers and Boyden chambers. Pleiotrophin and poly-l-lysine coated on the substratums stimulated cell migration of cortical neurons, while laminin, fibronectin, and tenascin exerted almost no effect. Pleiotrophin-induced and poly-l-lysine–induced neuronal migrations showed significant differences in sensitivity to various molecules and reagents. Polyclonal antibodies against the extracellular domain of PTPζ, PTPζ-S, an extracellular secreted form of PTPζ, and sodium vanadate, a protein tyrosine phosphatase inhibitor, added into the culture medium strongly suppressed specifically the pleiotrophin-induced neuronal migration. Furthermore, chondroitin sulfate C but not chondroitin sulfate A inhibited pleiotrophin-induced neuronal migration, in good accordance with our previous findings that chondroitin sulfate constitutes a part of the pleiotrophin-binding site of PTPζ, and PTPζ-pleiotrophin binding is inhibited by chondroitin sulfate C but not by chondroitin sulfate A. Immunocytochemical analysis indicated that the transmembrane forms of PTPζ are expressed on the migrating neurons especially at the lamellipodia along the leading processes. These results suggest that PTPζ is involved in the neuronal migration as a neuronal receptor of pleiotrophin distributed along radial glial fibers.

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34

Canver, Adam C., and Alisa Morss Clyne. "Quantification of Multicellular Organization, Junction Integrity, and Substrate Features in Collective Cell Migration." Microscopy and Microanalysis 23, no. 1 (February 2017): 22–33. http://dx.doi.org/10.1017/s1431927617000071.

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AbstractQuantitative analysis of multicellular organization, cell–cell junction integrity, and substrate properties is essential to understand the mechanisms underlying collective cell migration. However, spatially and temporally defining these properties is difficult within collectively migrating cell groups due to challenges in accurate cell segmentation within the monolayer. In this paper, we present Matlab®-based algorithms to spatially quantify multicellular organization (migration distance, interface roughness, and cell alignment, area, and morphology), cell–cell junction integrity, and substrate features in confocal microscopy images of two-dimensional collectively migrating endothelial monolayers. We used novel techniques, including measuring the migrating front roughness using a parametric curve formulation, automatically binning cells to obtain data as a function of distance from the migrating front, using iterative morphological closings to fully define cell boundaries, quantifying β-catenin localization as a measure of cell–cell junction integrity, and skeletonizing fibronectin to determine fiber length and orientation. These algorithms are widely accessible, as they use common fluorescent markers and Matlab® functions, and provide high-throughput critical feature quantification within collectively migrating cell groups. These image analysis algorithms can help standardize feature quantification among different experimental techniques, cell types, and research groups studying collective cell migration.

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35

Zhu, Zhiwen, Yongping Chai, Huifang Hu, Wei Li, Wen-Jun Li, Meng-Qiu Dong, Jia-Wei Wu, Zhi-Xin Wang, and Guangshuo Ou. "Spatial confinement of receptor activity by tyrosine phosphatase during directional cell migration." Proceedings of the National Academy of Sciences 117, no. 25 (June 8, 2020): 14270–79. http://dx.doi.org/10.1073/pnas.2003019117.

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Directional cell migration involves signaling cascades that stimulate actin assembly at the leading edge, and additional pathways must inhibit actin polymerization at the rear. During neuroblast migration inCaenorhabditis elegans, the transmembrane protein MIG-13/Lrp12 acts through the Arp2/3 nucleation-promoting factors WAVE and WASP to guide the anterior migration. Here we show that a tyrosine kinase, SRC-1, directly phosphorylates MIG-13 and promotes its activity on actin assembly at the leading edge. In GFP knockin animals, SRC-1 and MIG-13 distribute along the entire plasma membrane of migrating cells. We reveal that a receptor-like tyrosine phosphatase, PTP-3, maintains the F-actin polarity during neuroblast migration. Recombinant PTP-3 dephosphorylates SRC-1–dependent MIG-13 phosphorylation in vitro. Importantly, the endogenous PTP-3 accumulates at the rear of the migrating neuroblast, and its extracellular domain is essential for directional cell migration. We provide evidence that the asymmetrically localized tyrosine phosphatase PTP-3 spatially restricts MIG-13/Lrp12 receptor activity in migrating cells.

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Bradley, Pamela L., and Deborah J. Andrew. "ribbon encodes a novel BTB/POZ protein required for directed cell migration in Drosophila melanogaster." Development 128, no. 15 (August 1, 2001): 3001–15. http://dx.doi.org/10.1242/dev.128.15.3001.

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During development, directed cell migration is crucial for achieving proper shape and function of organs. One well-studied example is the embryonic development of the larval tracheal system of Drosophila, in which at least four signaling pathways coordinate cell migration to form an elaborate branched network essential for oxygen delivery throughout the larva. FGF signaling is required for guided migration of all tracheal branches, whereas the DPP, EGF receptor, and Wingless/WNT signaling pathways each mediate the formation of specific subsets of branches. Here, we characterize ribbon, which encodes a BTB/POZ-containing protein required for specific tracheal branch migration. In ribbon mutant tracheae, the dorsal trunk fails to form, and ventral branches are stunted; however, directed migrations of the dorsal and visceral branches are largely unaffected. The dorsal trunk also fails to form when FGF or Wingless/WNT signaling is lost, and we show that ribbon functions downstream of, or parallel to, these pathways to promote anterior-posterior migration. Directed cell migration of the salivary gland and dorsal epidermis are also affected in ribbon mutants, suggesting that conserved mechanisms may be employed to orient cell migrations in multiple tissues during development.

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Ozcelikkale, Altug, J. Craig Dutton, Frederick Grinnell, and Bumsoo Han. "Effects of dynamic matrix remodelling on en masse migration of fibroblasts on collagen matrices." Journal of The Royal Society Interface 14, no. 135 (October 2017): 20170287. http://dx.doi.org/10.1098/rsif.2017.0287.

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Fibroblast migration plays a key role during various physiological and pathological processes. Although migration of individual fibroblasts has been well studied, migration in vivo often involves simultaneous locomotion of fibroblasts sited in close proximity, so-called ‘ en masse migration’, during which intensive cell–cell interactions occur. This study aims to understand the effects of matrix mechanical environments on the cell–matrix and cell–cell interactions during en masse migration of fibroblasts on collagen matrices. Specifically, we hypothesized that a group of migrating cells can significantly deform the matrix, whose mechanical microenvironment dramatically changes compared with the undeformed state, and the alteration of the matrix microenvironment reciprocally affects cell migration. This hypothesis was tested by time-resolved measurements of cell and extracellular matrix movement during en masse migration on collagen hydrogels with varying concentrations. The results illustrated that a group of cells generates significant spatio-temporal deformation of the matrix before and during the migration. Cells on soft collagen hydrogels migrate along tortuous paths, but, as the matrix stiffness increases, cell migration patterns become aligned with each other and show coordinated migration paths. As cells migrate, the matrix is locally compressed, resulting in a locally stiffened and dense matrix across the collagen concentration range studied.

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38

Brückner, David B., Alexandra Fink, Joachim O. Rädler, and Chase P. Broedersz. "Disentangling the behavioural variability of confined cell migration." Journal of The Royal Society Interface 17, no. 163 (February 2020): 20190689. http://dx.doi.org/10.1098/rsif.2019.0689.

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Cell-to-cell variability is inherent to numerous biological processes, including cell migration. Quantifying and characterizing the variability of migrating cells is challenging, as it requires monitoring many cells for long time windows under identical conditions. Here, we observe the migration of single human breast cancer cells (MDA-MB-231) in confining two-state micropatterns. To describe the stochastic dynamics of this confined migration, we employ a dynamical systems approach. We identify statistics to measure the behavioural variance of the migration, which significantly exceeds that predicted by a population-averaged stochastic model. This additional variance can be explained by the combination of an ‘ageing’ process and population heterogeneity. To quantify population heterogeneity, we decompose the cells into subpopulations of slow and fast cells, revealing the presence of distinct classes of dynamical systems describing the migration, ranging from bistable to limit cycle behaviour. Our findings highlight the breadth of migration behaviours present in cell populations.

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39

Andalur Nandagopal, Saravanan, Deepak Upreti, Susy Santos, Ruey Chyi Su, Blake Ball, Francis Lin, and Sam Kung. "Dual roles of GM-CSF in modulating NK-cell migratory properties (CAM4P.147)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 185.5. http://dx.doi.org/10.4049/jimmunol.194.supp.185.5.

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Abstract Background: Natural Killer (NK) cells play a key role in innate immunity against viral, microbial infections and transformed cells and their migration for effector function to peripheral tissues or inflamed lymph nodes are tightly regulated. Of interest, production of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) by cancer cells is correlated to host immune suppression and tumor metastasis, suggesting an immune evasion property of GM-CSF. Here we examined role(s) of recombinant GM-CSF in the regulation of NK-cell migratory properties in vitro. Methods: Previously published “Y” shape microfluidic platform was used to study the roles of GM-CSF gradient on NK-cell migrations. IL-2 activated human primary NK cells were used in the migration studies. Results: Our microfluidic-based migration study demonstrated a novel role of GM-CSF in regulating repulsive NK-cell migration under the stable GM-CSF gradient (at 20 ng/ml), followed by subsequent arrest in cell migration. Blocking of GM-CSF-Rα abolished the repulsive migratory behavior but not the arrest. In contrast, lower concentrations of GM-CSF induced hyper-polarization, immediate arrest of NK cells, and little/or no NK-cell migrations. Circularity measurement in controls and above experiments confirmed statistically the correlation between hyperpolarization and migration arrest. Future analyses will elucidate the mechanisms underlying the dual roles of GM-CSF in the regulation of NK-cell migratory properties.

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40

Hathaway, HJ, and BD Shur. "Cell surface beta 1,4-galactosyltransferase functions during neural crest cell migration and neurulation in vivo." Journal of Cell Biology 117, no. 2 (April 15, 1992): 369–82. http://dx.doi.org/10.1083/jcb.117.2.369.

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Mesenchymal cell migration and neurite outgrowth are mediated in part by binding of cell surface beta 1,4-galactosyltransferase (GalTase) to N-linked oligosaccharides within the E8 domain of laminin. In this study, we determined whether cell surface GalTase functions during neural crest cell migration and neural development in vivo using antibodies raised against affinity-purified chicken serum GalTase. The antibodies specifically recognized two embryonic proteins of 77 and 67 kD, both of which express GalTase activity. The antibodies also immunoprecipitated and inhibited chick embryo GalTase activity, and inhibited neural crest cell migration on laminin matrices in vitro. Anti-GalTase antibodies were microinjected into the head mesenchyme of stage 7-9 chick embryos or cranial to Henson's node of stage 6 embryos. Anti-avian GalTase IgG decreased cranial neural crest cell migration on the injected side but did not cross the embryonic midline and did not affect neural crest cell migration on the uninjected side. Anti-avian GalTase Fab crossed the embryonic midline and perturbed cranial neural crest cell migration throughout the head. Neural fold elevation and neural tube closure were also disrupted by Fab fragments. Cell surface GalTase was localized to migrating neural crest cells and to the basal surfaces of neural epithelia by indirect immunofluorescence, whereas GalTase was undetectable on neural crest cells prior to migration. These results suggest that, during early embryogenesis, cell surface GalTase participates during neural crest cell migration, perhaps by interacting with laminin, a major component of the basal lamina. Cell surface GalTase also appears to play a role in neural tube formation, possibly by mediating neural epithelial adhesion to the underlying basal lamina.

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41

Venkatachalam, Thejasvi, Sushma Mannimala, Yeshaswi Pulijala, and Martha C. Soto. "CED-5/CED-12 (DOCK/ELMO) can promote and inhibit F-actin formation via distinct motifs that may target different GTPases." PLOS Genetics 20, no. 7 (July 31, 2024): e1011330. http://dx.doi.org/10.1371/journal.pgen.1011330.

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Coordinated activation and inhibition of F-actin supports the movements of morphogenesis. Understanding the proteins that regulate F-actin is important, since these proteins are mis-regulated in diseases like cancer. Our studies of C. elegans embryonic epidermal morphogenesis identified the GTPase CED-10/Rac1 as an essential activator of F-actin. However, we need to identify the GEF, or Guanine-nucleotide Exchange Factor, that activates CED-10/Rac1 during embryonic cell migrations. The two-component GEF, CED-5/CED-12, is known to activate CED-10/Rac1 to promote cell movements that result in the engulfment of dying cells during embryogenesis, and a later cell migration of the larval Distal Tip Cell. It is believed that CED-5/CED-12 powers cellular movements of corpse engulfment and DTC migration by promoting F-actin formation. Therefore, we tested if CED-5/CED-12 was involved in embryonic migrations, and got a contradictory result. CED-5/CED-12 definitely support embryonic migrations, since their loss led to embryos that died due to failed epidermal cell migrations. However, CED-5/CED-12 inhibited F-actin in the migrating epidermis, the opposite of what was expected for a CED-10 GEF. To address how CED-12/CED-5 could have two opposing effects on F-actin, during corpse engulfment and cell migration, we investigated if CED-12 harbors GAP (GTPase Activating Protein) functions. A candidate GAP region in CED-12 faces away from the CED-5 GEF catalytic region. Mutating a candidate catalytic Arginine in the CED-12 GAP region (R537A) altered the epidermal cell migration function, and not the corpse engulfment function. We interfered with GEF function by interfering with CED-5’s ability to bind Rac1/CED-10. Mutating Serine-Arginine in CED-5/DOCK predicted to bind and stabilize Rac1 for catalysis, resulted in loss of both ventral enclosure and corpse engulfment. Genetic and expression studies strongly support that the GAP function likely acts on different GTPases. Thus, we propose CED-5/CED-12 support the cycling of multiple GTPases, by using distinct domains, to both promote and inhibit F-actin nucleation.

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42

Goldfinger, Lawrence E., Jaewon Han, William B. Kiosses, Alan K. Howe та Mark H. Ginsberg. "Spatial restriction of α4 integrin phosphorylation regulates lamellipodial stability and α4β1-dependent cell migration". Journal of Cell Biology 162, № 4 (11 серпня 2003): 731–41. http://dx.doi.org/10.1083/jcb.200304031.

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Întegrins coordinate spatial signaling events essential for cell polarity and directed migration. Such signals from α4 integrins regulate cell migration in development and in leukocyte trafficking. Here, we report that efficient α4-mediated migration requires spatial control of α4 phosphorylation by protein kinase A, and hence localized inhibition of binding of the signaling adaptor, paxillin, to the integrin. In migrating cells, phosphorylated α4 accumulated along the leading edge. Blocking α4 phosphorylation by mutagenesis or by inhibition of protein kinase A drastically reduced α4-dependent migration and lamellipodial stability. α4 phosphorylation blocks paxillin binding in vitro; we now find that paxillin and phospho-α4 were in distinct clusters at the leading edge of migrating cells, whereas unphosphorylated α4 and paxillin colocalized along the lateral edges of those cells. Furthermore, enforced paxillin association with α4 inhibits migration and reduced lamellipodial stability. These results show that topographically specific integrin phosphorylation can control cell migration and polarization by spatial segregation of adaptor protein binding.

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43

Runyan, R. B., G. D. Maxwell, and B. D. Shur. "Evidence for a novel enzymatic mechanism of neural crest cell migration on extracellular glycoconjugate matrices." Journal of Cell Biology 102, no. 2 (February 1, 1986): 432–41. http://dx.doi.org/10.1083/jcb.102.2.432.

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Migrating embryonic cells have high levels of cell surface galactosyltransferase (GalTase) activity. It has been proposed that GalTase participates during migration by recognizing and binding to terminal N-acetylglucosamine (GlcNAc) residues on glycoconjugates within the extracellular matrix (Shur, B. D., 1982, Dev. Biol. 91:149-162). We tested this hypothesis using migrating neural crest cells as an in vitro model system. Cell surface GalTase activity was perturbed using three independent sets of reagents, and the effects on cell migration were analyzed by time-lapse microphotography. The GalTase modifier protein, alpha-lactalbumin (alpha-LA), was used to inhibit surface GalTase binding to terminal GlcNAc residues in the underlying substrate. alpha-LA inhibited neural crest cell migration on basal lamina-like matrices in a dose-dependent manner, while under identical conditions, alpha-LA had no effect on cell migration on fibronectin. Control proteins, such as lysozyme (structurally homologous to alpha-LA) and bovine serum albumin, did not effect migration on either matrix. Second, the addition of competitive GalTase substrates significantly inhibited neural crest cell migration on basal lamina-like matrices, but as above, had no effect on migration on fibronectin. Comparable concentrations of inappropriate sugars also had no effect on cell migration. Third, addition of the GalTase catalytic substrate, UDPgalactose, produced a dose-dependent increase in the rate of cell migration. Under identical conditions, the inappropriate sugar nucleotide, UDPglucose, had no effect. Quantitative enzyme assays confirmed the presence of GalTase substrates in basal lamina matrices, their absence in fibronectin matrices, and the ability of alpha-LA to inhibit GalTase activity towards basal lamina substrates. Laminin was found to be a principle GalTase substrate in the basal lamina, and when tested in vitro, alpha-LA inhibited cell migration on laminin. Together, these experiments show that neural crest cells have at least two distinct mechanisms for interacting with the substrate during migration, one that is fibronectin-dependent and one that uses GalTase recognition of basal lamina glycoconjugates.

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44

Montell, D. J. "The genetics of cell migration in Drosophila melanogaster and Caenorhabditis elegans development." Development 126, no. 14 (July 15, 1999): 3035–46. http://dx.doi.org/10.1242/dev.126.14.3035.

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Cell migrations are found throughout the animal kingdom and are among the most dramatic and complex of cellular behaviors. Historically, the mechanics of cell migration have been studied primarily in vitro, where cells can be readily viewed and manipulated. However, genetic approaches in relatively simple model organisms are yielding additional insights into the molecular mechanisms underlying cell movements and their regulation during development. This review will focus on these simple model systems where we understand some of the signaling and receptor molecules that stimulate and guide cell movements. The chemotactic guidance factor encoded by the Caenorhabditis elegans unc-6 locus, whose mammalian homolog is Netrin, is perhaps the best known of the cell migration guidance factors. In addition, receptor tyrosine kinases (RTKs), and FGF receptors in particular, have emerged as key mediators of cell migration in vivo, confirming the importance of molecules that were initially identified and studied in cell culture. Somewhat surprisingly, screens for mutations that affect primordial germ cell migration in Drosophila have revealed that enzymes involved in lipid metabolism play a role in guiding cell migration in vivo, possibly by producing and/or degrading lipid chemoattractants or chemorepellents. Cell adhesion molecules, such as integrins, have been extensively characterized with respect to their contribution to cell migration in vitro and genetic evidence now supports a role for these receptors in certain instances in vivo as well. The role for non-muscle myosin in cell motility was controversial, but has now been demonstrated genetically, at least in some cell types. Currently the best characterized link between membrane receptor signaling and regulation of the actin cytoskeleton is that provided by the Rho family of small GTPases. Members of this family are clearly essential for the migrations of some cells; however, key questions remain concerning how chemoattractant and chemorepellent signals are integrated within the cell and transduced to the cytoskeleton to produce directed cell migration. New types of genetic screens promise to fill in some of these gaps in the near future.

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45

Rappel, Wouter-Jan. "Cell–cell communication during collective migration." Proceedings of the National Academy of Sciences 113, no. 6 (January 22, 2016): 1471–73. http://dx.doi.org/10.1073/pnas.1524893113.

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46

Mishra, Abhinava K., Joseph P. Campanale, James A. Mondo, and Denise J. Montell. "Cell interactions in collective cell migration." Development 146, no. 23 (December 1, 2019): dev172056. http://dx.doi.org/10.1242/dev.172056.

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47

Conway, James R. W., and Guillaume Jacquemet. "Cell matrix adhesion in cell migration." Essays in Biochemistry 63, no. 5 (August 23, 2019): 535–51. http://dx.doi.org/10.1042/ebc20190012.

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Abstract The ability of cells to migrate is a fundamental physiological process involved in embryonic development, tissue homeostasis, immune surveillance and wound healing. In order for cells to migrate, they must interact with their environment using adhesion receptors, such as integrins, and form specialized adhesion complexes that mediate responses to different extracellular cues. In this review, we discuss the role of integrin adhesion complexes (IACs) in cell migration, highlighting the layers of regulation that are involved, including intracellular signalling cascades, mechanosensing and reciprocal feedback to the extracellular environment. We also discuss the role of IACs in extracellular matrix remodeling and how they impact upon cell migration.

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48

Kino-oka, Masahiro, Yasunori Takezawa, Ngo Xuan Trung, and Masahito Taya. "Cell migration in multilayer cell sheet." Journal of Bioscience and Bioengineering 108 (November 2009): S36. http://dx.doi.org/10.1016/j.jbiosc.2009.08.085.

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Isozaki, Yusuke, Kouki Sakai, Kenta Kohiro, Katsuhiko Kagoshima, Yuma Iwamura, Hironori Sato, Daniel Rindner, et al. "The Rho-guanine nucleotide exchange factor Solo decelerates collective cell migration by modulating the Rho-ROCK pathway and keratin networks." Molecular Biology of the Cell 31, no. 8 (April 1, 2020): 741–52. http://dx.doi.org/10.1091/mbc.e19-07-0357.

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Collective cell migration is crucial for tissue remodeling and cancer invasion. A RhoA-targeting guanine nucleotide exchange factor, Solo, localizes to the cell–cell contact sites in collectively migrating cells and acts as a brake for collective cell migration via promoting the RhoA-ROCK pathway and regulating the keratin-8/keratin-18 networks.

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Law, Ah-Lai, Anne Vehlow, Maria Kotini, Lauren Dodgson, Daniel Soong, Eric Theveneau, Cristian Bodo, et al. "Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo." Journal of Cell Biology 203, no. 4 (November 18, 2013): 673–89. http://dx.doi.org/10.1083/jcb.201304051.

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Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo.

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