• Cell migration nature review

    Cell migration nature review

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    T cells migrate diverse microenvironments of the body to mount antigen-specific immune responses. T cell activation, a key initial process for antigen-specific immune responses, occur in secondary lymphoid organs such as spleens and lymph nodes where high density of T cells migrates rapidly through the reticular networks formed by stromal cells.

    In vitro model system recapitulating key characteristics of secondary lymphoid organs, confined spaces densely packed with rapidly migrating cells, would be useful to investigate mechanisms of T cell migration.

    In this study, we devised a method to fabricate microchannels densely packed with T cells. Microchannel surface chemistry and filling time were optimized to achieve high packing density 0. Particle image velocimetry PIV analysis method was employed to extract velocity field of microchannels densely packed with T cells.

    Using velocity field information, various motility parameters were further evaluated to quantitatively assess the effects of microchannel width and media tonicity on T cell motility within cell dense microenvironments. For immune surveillance, T cells circulate secondary lymphoid organs such as spleens and lymph nodes LNs where information of potentially harmful antigens is collected and presented by antigen presenting cells APCs 34. T cell activation by T cell-APC interactions in secondary lymphoid organs is a key event for the initiation of antigen-specific immune responses.

    Activated T cells undergo clonal expansion, and traffic to effector sites to mount antigen-specific immune responses.

    However, mechanistic study using live animals is technically challenging, thus in vitro model system recapitulating key features of in vivo microenvironments has been developed. For example, parallel flow chambers mimicking blood vessel microenvironments have been widely used to study dynamic T cell-endothelial cell interactions under flow 10 Collagen gels have been used to study 3D interstitial migration of T cells 12 For example, dendritic cell migration in peripheral tissue 16T cell motility in interstitial spaces regulated by myosin proteins 1718and leukocyte chemotactic responses 19 were studied using microchannel devices.

    So far, microchannel experiments have been primarily conducted to observe single leukocyte migration within microchannels using low density of leukocytes, which mimics leukocyte migration in peripheral tissues where leukocytes are sparsely distributed. However, this model may not fully recapitulate cell dense microenvironments in secondary lymphoid organs such as spleens and LNs, where high density of lymphocytes forms segregated compartments and exerts rapid motility through the reticular network generated by stromal cells within the compartments 20 In addition to leukocyte interstitial migration study, microchannels have been widely used to study the migration of various types of cells in confined 3D microenvironments.

    For example, mechanisms of cell migration under confinement 222324cancer cell invasion dynamics 2526and confinement-mediated nuclear envelope rupture and repair were studied 27 However, all the aforementioned studies have primarily focused on single cell migration within microchannel. Particle image velocimetry PIV technique was applied to extract velocity field information of T cells within the microchannels. Using PIV data, other kinematic parameters such as order parameter, which measures directional orientation with respect to microchannel walls, and vorticity, which represents local rotation, were calculated.

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    Pharmachological inhibitors widely used in vitro cell biology study cannot be utilized in this experimental setting because most inhibitors were absorbed by T cells locating near microchannel entries.

    Instead, we adjusted tonicity of media to study the role of cell membrane tension on T cell migration within microchannels densely packed with T cells.

    Each device contained an array of microchannels with one microchannel width, thus different devices were used for microchannels with difference channel widths. The trapezoid shaped reservoir guided sedimentation of T cells toward the entrance of microchannels. T cells sedimented down to the bottoms gradually migrated into the microchannels.

    Schematic illustration of microchannels densely packed with T cells. PDMS microchannel arrays with trapezoid reservoirs located at each microchannel end were fabricated. To assess how microchannel surfaces affects T cell filling, the microchannels were coated with intercellular adhesion molecule 1 ICAM-1which is a ligand of T cell integrin lymphocyte function-associated antigen 1 LFA-1 29or cell-repellent materials such as bovine serum albumin BSA and pluronic T cells labeled with Hoechstwhich stains nuclei of live cells, were seeded in microchannels.Migration and invasion are fundamental features of metastatic cancer cells.

    The Golgi apparatus, an organelle involved in posttranslational modification and sorting of proteins, is widely accepted to regulate directional cell migration. In addition, mounting evidence suggests that the Golgi is a hub for different signaling pathways. In this paper we will give an overview on how polarized secretion and microtubule nucleation at the Golgi regulate directional cell migration.

    We will review different signaling pathways that signal to and from the Golgi. Finally, we will discuss how these signaling pathways regulate the role of the Golgi in cell migration and invasion. We propose that by identifying regulators of the Golgi, we might be able to uncover unappreciated modulators of cell migration.

    Uncovering the regulatory network that orchestrates cell migration is of fundamental importance for the development of new therapeutic strategies against cancer cell metastasis. The development of efficient therapies against cancer represents a continuous challenge for scientist across various disciplines. During metastatic dissemination, a tumor cell acquires a migratory phenotype that enables it to invade the surrounding tissue in order to leave the primary site of the tumor. After entering the blood or the lymph system, the tumor cell colonizes a distant tissue and nucleates a secondary tumor.

    Research in the past three decades has provided valuable insight into the various steps of tumor formation [ 1 ]. This paper does not intend to give a general overview describing the metastatic process. For this, the reader is referred to excellent recent reviews [ 2 ].

    In this paper we will focus on the role of the Golgi apparatus in cell migration and invasion and the implications thereof for cancer cell metastasis. We will first give a brief and general overview about the Golgi and about cell migration. Then, we will discuss in more detail the evidence that links the Golgi to cell migration.

    Finally, we will discuss how signaling pathways regulate the role of the Golgi in cell migration and how this knowledge can be used for designing novel therapeutic strategies against metastatic cancer cell spreading.

    In mammalian cells, the Golgi apparatus is a single-copy organelle, composed of a stack of flattened cisternae that are laterally linked to form the Golgi ribbon.

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    The Golgi localizes to the juxtanuclear region and is intimately associated with the centrosome. The Golgi is polarized in both structure and function, where the cis - and the trans -side exert different roles in terms of posttranslational modification, lipid composition, and sorting events.

    The cis -Golgi receives cargo proteins, lipids, and polysaccharides from the ER and the intermediate compartment. Cargo in the cis -Golgi then progresses to the medial and trans -Golgi where it acquires various post-translational modifications. Finally, cargo reaches the trans- Golgi network TGN for sorting to the various post-Golgi compartments endosomes, lysosomes, and the plasma membrane.

    Besides posttranslational modification and sorting, the Golgi also plays important role in apoptosis, mitosis and cell migration. In this paper we will highlight the evidence for the role of signal transduction in regulating the Golgi during cell migration. A matter of hot and intense debate is how intra-Golgi transport is executed. According to the cisternal maturation model alternatively referred to as cisternal progressioncargo remains in the same cisterna, which matures by acquisition and exclusion of different enzymes that convert the cis -cisterna to a medial and trans -cisterna.

    In an alternative model, the Golgi cisternae are stationary and cargo moves between them either by vesicular carriers or by tubular connections. Finally, a cisternal progenitor model was also recently proposed [ 3 ].

    For detailed reviews about the functional organization of the Golgi and a general overview on signaling events at endomembranes, the reader is referred to other recent reviews [ 3 — 7 ].Thank you for visiting nature.

    T cell migration in microchannels densely packed with T cells

    You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.

    In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. For the more hands-on among you, the first and last sections will probably be most appealing, but the additional information about the Consortium is well worth a read too. Within the Cell Migration Science section, click on 'Migration '— here you'll find a nice overview of cell migration complete with an animated schematic of a migrating cell!

    Another nice feature is the movies, although, at present, the collection's rather sparse. Although the 'News' section is not very current, the rest of the site provides reasonably up-to-date information, such as PubMed links to abstracts of relevant primary papers and reviews within the Cell Migration Science category.

    There are further links and job postings, too. Another useful resource is the links to relevant meetings, which currently extends into Mayand for those of you who are interested in 'migrating' down the slopes, the Cell Migration Consortium will be meeting up at the Keystone Cell Migration and Invasion meeting in Breckenridge next January. Reprints and Permissions. Bussell, K. The A—Z of cell migration. Nat Rev Mol Cell Biol 3, Download citation. Issue Date : 01 December Advanced search. Skip to main content Thank you for visiting nature.

    Download PDF. Authors Katrin Bussell View author publications. Rights and permissions Reprints and Permissions. About this article Cite this article Bussell, K. Search Article Search Search. Quick links Explore articles by subject Find a job Guide to authors Editorial policies. Close banner Close. Email address Sign up. Get the most important science stories of the day, free in your inbox.

    Sign up for Nature Briefing.Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

    cell migration nature review

    Studies of cell migration in three-dimensional 3D cell culture systems and in vivo have revealed several differences when compared with cell migration in two dimensions, including their morphology and mechanical and signalling control. Here, researchers assess the contribution of 3D models to our understanding of cell migration, both in terms of the mechanisms used to drive single cell and collective cell migration and how migrating cells respond to a changing environment in vivo.

    Petrie, R. Nonpolarized signaling reveals two distinct modes of 3D cell migration.

    cell migration nature review

    Cell Biol. Madsen, C. Cancer dissemination — lessons from leukocytes. Cell 1913—26 Friedl, P. Cancer invasion and the microenvironment: plasticity and reciprocity. Cell— Onodera, T. Btbd7 regulates epithelial cell dynamics and branching morphogenesis. Science— Nelson, C. Of extracellular matrix, scaffolds, and signaling: tissue architecture regulates development, homeostasis, and cancer. Cell Dev. Yamada, K. Modeling tissue morphogenesis and cancer in 3D.

    Grinnell, F. Cell motility and mechanics in three-dimensional collagen matrices. DuFort, C. Balancing forces: architectural control of mechanotransduction. Nature Rev. Baker, B. Deconstructing the third dimension — how 3D culture microenvironments alter cellular cues. Cell Sci. Nuclear mechanics during cell migration. Balzer, E.

    New dimensions in cell migration

    Physical confinement alters tumor cell adhesion and migration phenotypes. Rowe, R. Navigating ECM barriers at the invasive front: the cancer cell—stroma interface. Wolf, K. Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion.

    Nature Cell Biol.Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. The conversion of stationary epithelial cells into migratory, invasive cells is important for normal embryonic development and tumour metastasis.

    Border-cell migration in the ovary of Drosophila melanogaster has emerged as a simple, genetically tractable model for studying this process. Three distinct signals, which are also upregulated in cancer, control border-cell migration, so identifying further genes that are involved in border-cell migration could provide new insights into tumour invasion.

    Bai, J. Regulation of invasive cell behavior by Taiman, a Drosophila protein related to AIB1, a steroid receptor coactivator amplified in breast cancer. Cell— This paper reports the surprising finding that Ecdysone, signalling through the Ecdysone receptor and its coactivator Taiman, regulates border-cell migration. Silver, D. This paper reports the identification of the signal and signalling pathway that distinguishes the cells that acquire the ability to migrate from those that cannot.

    Duchek, P. Cell17—26 This paper reports the identification of a growth factor expressed in the germline, which acts through a receptor tyrosine kinase expressed by all of the follicle cells and which is involved in guiding the border cells to the oocyte. King, R. Google Scholar. Spradling, A. Margolis, J. Identification and behavior of epithelial stem cells in the Drosophila ovary. Development— Montell, D. Cell 7151—62 This paper reports the identification of the first mutation showing border-cell migration defects and the cloning of the corresponding gene.

    Savant-Bhonsale, S. Genes Dev.

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    Oda, H. Phenotypic analysis of null mutants for DE-cadherin and Armadillo in Drosophila ovaries reveals distinct aspects of their functions in cell adhesion and cytoskeletal organization. Genes Cells 229—40 Niewiadomska, P.

    DE-cadherin is required for intercellular motility during Drosophila oogenesis. Cell Biol. This work reports the finding that DE-cadherin is required both in border cells and in nurse cells for border-cell migration to occur. Takeichi, M.Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

    Phase transitions from a static to a moving phase are observed in a variety of physical systems and are thought to play a key role in cellular assemblies such as healthy and cancerous tissue.

    Caterina La Porta and Stefano Zapperi discuss how a suitable identification of the control and order parameters can shed light on the nature of phase transitions in cell migration.

    Grosse-Wilde, A. Park, J. Unjamming and cell shape in the asthmatic airway epithelium. La Porta, C. Cell Migrations: Causes and Functions Springer, Liu, A. Jamming is not just cool any more. Nature21—22 Garcia, S. Physics of active jamming during collective cellular motion in a monolayer. Natl Acad. USA— Bi, D. Motility-driven glass and jamming transitions in biological tissues. X 6 Google Scholar. Saw, T.

    cell migration nature review

    Topological defects in epithelia govern cell death and extrusion. Nature— Ilina, O. Cell—cell adhesion and 3D matrix confinement determine jamming transitions in breast cancer invasion. Cell Biol. Font-Clos, F.For these reasons, The Survey System earns our TopTenREVIEWS Gold Award. A recent book by two of our faculty honors a third. Bernie spent almost all of his career here at the University of Minnesota.

    He joined the Department of Statistics, a precursor of the School, in 1963 and was the chair of the department for several years during the 1960's. One of the first Statistics books that I read was one of his and it was a pleasure to have him as a colleague after I moved here.

    He was a gentleman, a scholar and a sweet man. He was 88 and was still ice skating a week before he died. The Department of Psychology and the School of Statistics in the College of Liberal Arts at the University of Minnesota invite applications for a full-time, tenure-track position specializing in quantitative psychology and statistics to begin fall semester 2014 (August 25, 2014).

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    DEADLINE: October 28, 2013 Requisition Number: 185788 Please apply at the University of Minnesota's Employment site. The School of Statistics in the College of Liberal Arts at the University of Minnesota invite applications for a full-time, Teaching Specialist or Lecturer in statistics to begin spring semester 2014. DEADLINE: Open Until Filled Requisition Number: 186942 Please apply at the University of Minnesota's Employment site. The School of Statistics, College of Liberal Arts, University of Minnesota, invites applications for a full-time, tenure-track position beginning fall semester 2013.

    DEADLINE: December 7, 2012 Requisition Number: 179858 Please apply at the University of Minnesota's Employment site. View Reunion SlideshowThe School of Statistics recently celebrated its 40th anniversary at the University of Minnesota on May 13 and 14, 2011, with a reunion for all bachelor, master, and doctoral alumni. View the invitation (PDF), the list of attendees (PDF), Sandy Weisberg's presentation (PDF), or a slideshow from the reunion. Statisticians collect, organize, analyze, interpret, and present data.

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