Статті в журналах: "Cell migration"

1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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

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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16

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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17

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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18

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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19

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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20

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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21

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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22

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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23

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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24

Ramos, Tiago, Maqsood Ahmed, Paul Wieringa, and Lorenzo Moroni. "Schwann cells promote endothelial cell migration." Cell Adhesion & Migration 9, no. 6 (October 22, 2015): 441–51. http://dx.doi.org/10.1080/19336918.2015.1103422.

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25

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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26

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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27

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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28

Ou, Yen-Chuan, Jian-Ri Li, Jiaan-Der Wang, Cheng-Yi Chang, Chih-Cheng Wu, Wen-Ying Chen, Yu-Hsiang Kuan, Su-Lan Liao, Hsi-Chi Lu, and Chun-Jung Chen. "Fibronectin Promotes Cell Growth and Migration in Human Renal Cell Carcinoma Cells." International Journal of Molecular Sciences 20, no. 11 (June 7, 2019): 2792. http://dx.doi.org/10.3390/ijms20112792.

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The prognostic and therapeutic values of fibronectin have been reported in patients with renal cell carcinoma (RCC). However, the underlying mechanisms of malignancy in RCC are not completely understood. We found that silencing of fibronectin expression attenuated human RCC 786-O and Caki-1 cell growth and migration. Silencing of potential fibronectin receptor integrin α5 and integrin β1 decreased 786-O cell ability in movement and chemotactic migration. Biochemical examination revealed a reduction of cyclin D1 and vimentin expression, transforming growth factor-β1 (TGF-β1) production, as well as Src and Smad phosphorylation in fibronectin-silenced 786-O and Caki-1 cells. Pharmacological inhibition of Src decreased 786-O cell growth and migration accompanied by a reduction of cyclin D1, fibronectin, vimentin, and TGF-β1 expression, as well as Src and Smad phosphorylation. In 786-O cells, higher activities in cell growth and migration than in Caki-1 cells were noted, along with elevated fibronectin and TGF-β1 expression. The additions of exogenous fibronectin and TGF-β1 promoted Caki-1 cell growth and migration, and increased cyclin D1, fibronectin, vimentin, and TGF-β1 expression, as well as Src and Smad phosphorylation. These findings highlight the role of fibronectin in RCC cell growth and migration involving Src and TGF-β1 signaling.

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29

Voura, Evelyn B., Martin Sandig, and Chi-Hung Siu. "Cell-cell interactions during transendothelial migration of tumor cells." Microscopy Research and Technique 43, no. 3 (November 1, 1998): 265–75. http://dx.doi.org/10.1002/(sici)1097-0029(19981101)43:3<265::aid-jemt9>3.0.co;2-z.

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30

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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31

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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32

Maijenburg, Marijke W., Christian Gilissen, Joris A. Veltman, Marion Kleijer, Cris Mudde Jadra, Kees Weijer, Claudia M. van Tiel, Carlie J. M. de Vries, C. Ellen Van der Schoot, and Carlijn Voermans. "Molecular Signature of Migratory Human Mesenchymal Stromal Cells; Influence of the Cell Cycle." Blood 114, no. 22 (November 20, 2009): 1450. http://dx.doi.org/10.1182/blood.v114.22.1450.1450.

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Abstract Abstract 1450 Poster Board I-473 Mesenchymal stromal cells (MSC) are a potential cell source for cellular therapies, in which recruitment and migration of MSC towards injured tissue is crucial. However, in vitro and in vivo experiments reveal that the capacity to migrate and home to sites of injury is limited and huge cell numbers have to be transplanted. Therefore, better understanding of the mechanisms of MSC migration will improve the design and efficacy of future cellular therapies. With respect to these therapies, we are studying the process of migration in MSC. In Transwell migration experiments it was observed that MSC derived from various tissues all contain only a small percentage (10-25%) of migratory MSC, which was determined to be the same cell fraction migrating towards various chemokines. This migratory fraction could not be defined as a specific subpopulation by surface marker expression. Interestingly, actin rearrangement and increased paxillin phosphorylation were observed in the majority of the MSC upon stimulation with chemokines. This indicates that functionality of the machinery involved in the initial response to migratory cues is not restricted to the migratory MSC subset. However, the migratory MSC fraction contained significantly less cells in S- and G2/M-phase (ratio S:0.81±0.13, p<0.028; G2/M: 0.75±0.13, p<0.031) as compared to non-migrating MSC. Ki67 antigen expression, which discriminates between G0- and G1-phase, revealed a trend of more cells in G1-phase in migratory MSC. A similar role for the cell cycle in homing and mobilization of hematopoietic stem cells has been described previously (1). Here we report for the first time that the cell cycle also affects MSC migration. To further study the molecular signature of the migratory MSC, a micro array was performed on migrating and non-migrating fetal bone marrow MSC, SDF-1 was used as chemokine. MSC that were only exposed to a SDF-1 gradient and cultured fetal bone marrow MSC were included as controls. SDF-1 exposure induced differential expression of 674 genes (383 up, 291 down) compared to cultured MSC. This list is enriched for genes involved in the (regulation of) cell cycle, response to wound healing and regulation of cell differentiation. These results indicate that besides promoting MSC migration, SDF-1 also induces other (paracrine) functions that MSC may have in the injured niche. A remarkable small number of genes was differentially expressed between migrating and non-migrating MSC. Nurr1, Nur77, CYR61, SMAD7, AXIN1 and ID3 were upregulated (range 1,5 to 2.3-fold), HIST1H2AK and HIST1H4B were downregulated (-1.5 fold). These results were confirmed by RQ-PCR. Only for the two genes of the nuclear orphan receptor family (Nurr1 and Nur77) the upregulation was >2-fold. Therefore these genes were studied in more detail. After 4 hrs exposure to SDF-1, expression levels of Nurr1 and Nur77 were increased 14 and 5 fold respectively in fetal bone marrow-derived MSC as compared to MSC that were not exposed to SDF-1. Another chemoattractant for MSC (PDGF-BB) also induced their expression, but less pronounced. Nurr1 and Nur77 are members of the nuclear orphan receptor family and were first described as early response transcription factors upon growth factor stimulation (2). More recently, roles in the inflammatory response (downregulation of cytokines) have been described (3). The functional requirement of Nurr1 and Nur77 in MSC was studied by lentiviral knock down of Nur77 or Nurr1. This resulted in a 3-4 fold increase of MSC in S- and G2/M phase of the cell cycle compared to the scrambled control and is in agreement with the observation that overexpression of Nur77 inhibits the cell cycle by inducing P27kip (3). From these knock down studies, micro array results and our observation that S and G2/M phase negatively influence MSC migration, it could be hypothesized that overexpression of Nur77 and Nurr1 will lead to increased MSC migration. In conclusion, our results have identified a role for cell cycle in MSC migration. Similar to HSC, S- and G2/M-phase negatively influence MSC migration. Considering the possible functions in MSC homing and in modulating the immune response, unraveling the role of Nur77 and Nurr1 in MSC may have dual implications for future regenerative medicine. Disclosures No relevant conflicts of interest to declare.

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33

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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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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35

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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36

Qin, Lei, Dazhi Yang, Weihong Yi, Huiling Cao, and Guozhi Xiao. "Roles of leader and follower cells in collective cell migration." Molecular Biology of the Cell 32, no. 14 (July 1, 2021): 1267–72. http://dx.doi.org/10.1091/mbc.e20-10-0681.

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Collective cell migration is a widely observed phenomenon during animal development, tissue repair, and cancer metastasis. Considering its broad involvement in biological processes, it is essential to understand the basics behind the collective movement. Based on the topology of migrating populations, tissue-scale kinetics, called the “leader–follower” model, has been proposed for persistent directional collective movement. Extensive in vivo and in vitro studies reveal the characteristics of leader cells, as well as the special mechanisms leader cells employ for maintaining their positions in collective migration. However, follower cells have attracted increasing attention recently due to their important contributions to collective movement. In this Perspective, the current understanding of the molecular mechanisms behind the “leader–follower” model is reviewed with a special focus on the force transmission and diverse roles of leaders and followers during collective cell movement.

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37

Tee, Jing Yang, and Alan Mackay-Sim. "Directional Persistence of Cell Migration in Schizophrenia Patient-Derived Olfactory Cells." International Journal of Molecular Sciences 22, no. 17 (August 25, 2021): 9177. http://dx.doi.org/10.3390/ijms22179177.

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Cell migration is critical for brain development and linked to several neurodevelopmental disorders, including schizophrenia. We have shown previously that cell migration is dysregulated in olfactory neural stem cells from people with schizophrenia. Although they moved faster than control cells on plastic substrates, patient cells were insensitive to regulation by extracellular matrix proteins, which increase the speeds of control cells. As well as speed, cell migration is also described by directional persistence, the straightness of movement. The aim of this study was to determine whether directional persistence is dysregulated in schizophrenia patient cells and whether it is modified on extracellular matrix proteins. Directional persistence in patient-derived and control-derived olfactory cells was quantified from automated live-cell imaging of migrating cells. On plastic substrates, patient cells were more persistent than control cells, with straighter trajectories and smaller turn angles. On most extracellular matrix proteins, persistence increased in patient and control cells in a concentration-dependent manner, but patient cells remained more persistent. Patient cells therefore have a subtle but complex phenotype in migration speed and persistence on most extracellular matrix protein substrates compared to control cells. If present in the developing brain, this could lead to altered brain development in schizophrenia.

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38

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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39

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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40

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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41

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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42

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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43

Gao, Zhuo, Ruiqi Liu, Na Ye, Chao Liu, Xiuli Li, Xiaodong Guo, Zhuoran Zhang, Xiaoxi Li, Yuanfei Yao, and Xiaofeng Jiang. "FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells." Cellular Physiology and Biochemistry 48, no. 1 (2018): 138–48. http://dx.doi.org/10.1159/000491670.

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Background/Aims: Cell surface morphology plays pivotal roles in malignant progression and epithelial-mesenchymal transition (EMT). Previous research demonstrated that microvilli play a key role in cell migration of non-small cell lung cancer (NSCLC). In this study, we report that Forkhead box class O1 (FOXO1) is downregulated in human NSCLC and that silencing of FOXO1 is associated with the invasive stage of tumor progression. Methods: The cell proliferation, migration, and invasion were characterized in vitro, and we tested the expression of the Epithelial-mesenchymal transition (EMT) marker by immunofluorescence staining and also identified the effect of FOXO1 on the microvilli by scanning electron microscopy (SEM). Results: Functional analyses revealed that silencing of FOXO1 resulted in an increase in NSCLC cell proliferation, migration, and invasion; whereas overexpression of FOXO1 significantly inhibited the migration and invasive capability of NSCLC cells in vitro. Furthermore, cell morphology imaging showed that FOXO1 maintained the characteristics of epithelial cells. Immunofluorescence staining and western blotting showed that the E-cadherin level was elevated and Vimentin was reduced by FOXO1 overexpression. Conversely, the E-cadherin level was reduced and Vimentin was elevated in cells silenced for FOXO1. Furthermore, scanning electron microscopy (SEM) showed that FOXO1 overexpression increased the length of the microvilli on the cell surface, whereas FOXO1 silencing significantly reduced their length. Conclusions: FOXO1 is involved in human lung carcinogenesis and may serve as a potential therapeutic target in the migration of human lung cancer.

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44

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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45

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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46

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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47

Sun, Wei, Nicholas Agung Kurniawan, Alan Prem Kumar, Raj Rajagopalan, and Chwee Teck Lim. "Effects of Migrating Cell-Induced Matrix Reorganization on 3D Cancer Cell Migration." Cellular and Molecular Bioengineering 7, no. 2 (February 19, 2014): 205–17. http://dx.doi.org/10.1007/s12195-014-0324-0.

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48

Yoon, Sungjun, and Rudolf E. Leube. "Keratin intermediate filaments: intermediaries of epithelial cell migration." Essays in Biochemistry 63, no. 5 (October 2019): 521–33. http://dx.doi.org/10.1042/ebc20190017.

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Abstract Migration of epithelial cells is fundamental to multiple developmental processes, epithelial tissue morphogenesis and maintenance, wound healing and metastasis. While migrating epithelial cells utilize the basic acto-myosin based machinery as do other non-epithelial cells, they are distinguished by their copious keratin intermediate filament (KF) cytoskeleton, which comprises differentially expressed members of two large multigene families and presents highly complex patterns of post-translational modification. We will discuss how the unique mechanophysical and biochemical properties conferred by the different keratin isotypes and their modifications serve as finely tunable modulators of epithelial cell migration. We will furthermore argue that KFs together with their associated desmosomal cell–cell junctions and hemidesmosomal cell–extracellular matrix (ECM) adhesions serve as important counterbalances to the contractile acto-myosin apparatus either allowing and optimizing directed cell migration or preventing it. The differential keratin expression in leaders and followers of collectively migrating epithelial cell sheets provides a compelling example of isotype-specific keratin functions. Taken together, we conclude that the expression levels and specific combination of keratins impinge on cell migration by conferring biomechanical properties on any given epithelial cell affecting cytoplasmic viscoelasticity and adhesion to neighboring cells and the ECM.

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49

COFFMAN, CLARK R. "Cell Migration and Programmed Cell Death of Drosophila Germ Cells." Annals of the New York Academy of Sciences 995, no. 1 (May 2003): 117–26. http://dx.doi.org/10.1111/j.1749-6632.2003.tb03215.x.

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50

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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