In Migrating Cells, the Golgi Complex and the Position of the Centrosome Depend on Geometrical Constraints of the Substratum
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CD2 Molecules Redistribute to the Uropod During T Cell Scanning: Implications for Cellular Activation and Immune Surveillance
CD2 molecules redistribute to the uropod during T cell scanning: Implications for cellular activation and immune surveillance Elena V. Tibaldi*†, Ravi Salgia†‡, and Ellis L. Reinherz*†§ *Laboratory of Immunobiology and ‡Division of Adult Oncology, Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, and †Department of Medicine, Harvard Medical School, Boston, MA 02115 Communicated by Stuart F. Schlossman, Dana-Farber Cancer Institute, Boston, MA, April 9, 2002 (received for review February 14, 2002) Dynamic binding between CD2 and CD58 counter-receptors on op- cells, whereas its counter-receptor CD58 is expressed on a posing cells optimizes immune recognition through stabilization of diverse array of nucleated and non-nucleated cells including cell–cell contact and juxtaposition of surface membranes at a distance APCs and stromal cells (reviewed in refs. 11 and 12). CD2 suitable for T cell receptor–ligand interaction. Digitized time-lapse functions in both T cell adhesion and activation processes (13). Ϸ differential interference contrast and immunofluorescence micros- Of note, the weak affinity of the CD2-CD58 interaction (Kd copy on living cells now show that this binding also induces T cell 1 M) is associated with remarkably fast on and off rates that polarization. Moreover, CD2 can facilitate motility of T cells along foster rapid and extensive exchange between CD2 and CD58 antigen-presenting cells via a movement referred to as scanning. Both partners on opposing cell surfaces (14–16). These biophysical activated CD4 and CD8 T cells are able to scan antigen-presenting cells characteristics are reminiscent of the selectin–ligand interactions surfaces in the absence of cognate antigen. -
Wnt/PCP Signaling Contribution to Carcinoma Collective Cell Migration and Metastasis Kacey Vandervorst1, Courtney A
Published OnlineFirst April 5, 2019; DOI: 10.1158/0008-5472.CAN-18-2757 Cancer Review Research Wnt/PCP Signaling Contribution to Carcinoma Collective Cell Migration and Metastasis Kacey VanderVorst1, Courtney A. Dreyer1, Sara E. Konopelski2, Hyun Lee1, Hsin-Yi Henry Ho2, and Kermit L. Carraway III1 Abstract Our understanding of the cellular mechanisms governing discerned. Wnt/PCP (planar cell polarity) signaling, one of carcinoma invasiveness and metastasis has evolved dramati- the noncanonical Wnt signaling pathways, mediates collective cally over the last several years. The previous emphasis on the migratory events such as convergent extension during devel- epithelial–mesenchymal transition as a driver of the migratory opmental processes. Wnt/PCP signaling components are fre- properties of single cells has expanded with the observation quently dysregulated in solid tumors, and aberrant pathway that carcinoma cells often invade and migrate collectively as activation contributes to tumor cell migratory properties. Here adherent groups. Moreover, recent analyses suggest that cir- we summarize key studies that address the mechanisms by culating tumor cells within the vasculature often exist as which Wnt/PCP signaling mediate collective cell migration in multicellular clusters and that clusters more efficiently seed developmental and tumor contexts. We emphasize Wnt/PCP metastatic lesions than single circulating tumor cells. While component localization within migrating cells and discuss these observations point to a key role for collective cell how component asymmetry may govern the spatiotemporal migration in carcinoma metastasis, the molecular mechan- control of downstream cytoskeletal effectors to promote isms driving collective tumor cell migration remain to be collective cell motility. Introduction properties of the surrounding environment (haptotaxis or dur- otaxis; refs. -
A Single Class II Myosin Modulates T Cell Motility and Stopping, but Not Synapse Formation
ARTICLES A single class II myosin modulates T cell motility and stopping, but not synapse formation Jordan Jacobelli1, Stephen A Chmura1, Denis B Buxton2, Mark M Davis3 & Matthew F Krummel1 Upon encountering an antigen, motile T cells stop crawling, change morphology and ultimately form an ‘immunological synapse’. Although myosin motors are thought to mediate various aspects of this process, the molecules involved and their exact roles are not defined. Here we show that nonmuscle myosin heavy chain IIA, or MyH9, is the only class II myosin expressed in T cells and is associated with the uropod during crawling. MyH9 function is required for maintenance of the uropod and for T cell motility but is dispensable for synapse formation. Phosphorylation of MyH9 in its multimerization domain by T cell receptor–generated signals indicates that inactivation of this motor may be a key step in the ‘stop’ response during http://www.nature.com/natureimmunology antigen recognition. T lymphocytes circulate through vasculature into peripheral lym- signaling10. Over time, these microclusters coalesce into a charac- phoid tissues, scanning antigen-presenting cells (APCs) for pep- teristic mature synapse, defined by a central core of TCR-CD3 com- tide–major histocompatibility complex (MHC) ligands for their T plexes surrounded by a ring of adhesion molecules11,12. The cell receptors (TCRs). After leaving the vasculature, T cells acquire a MTOC, formerly in the uropod, translocates to the contact site13. polarized morphology and initiate crawling, probably as a result of In this process, the nucleus is displaced away from the nascent chemotactic stimuli, earlier activating stimuli or both1–3. -
Cell Polarity Ing
news and views ment of the RAFOS float speeds to results of N a e e the MODAS — Modular Ocean Data Assimi- o t r r S B th ia e ra d d t zi e e a l C R w lation System — model, which assimilates 0° . rm te Benguela in satellite altimetric measurement of sea-level undercurrent variability. m ic o f fr i Benguela C. r c There is still a great deal to learn about the a te a P e Agulhas valve, and its variation under differ- ° il W h 30 S z nt Cape t a e r r Agulhas Current ent climatic conditions. Ensuring that it is r Cauldron B u C properly represented in global ocean and cli- mate models remains a daunting challenge. South Atlantic Agulhas return current ke rrent 2 ra e Cu Agulhas retroflection But this collection of papers shows how the ° D ag 60 S ss Pa brotherhood of observers armed with new tools, aided by satellite-based remote sens- 60°W0° 60°E 120°E ing, and modellers with their increasingly realistic simulations, can take us forward. ■ Figure 1 The Agulhas system and associated flow patterns. The Agulhas Current draws water from the Arnold L. Gordon is at the Lamont–Doherty Earth Pacific Ocean through the Indonesian throughflow and Drake Passage, and from the Tasman Sea. It Observatory, Columbia University, Palisades, New abruptly turns back towards the Indian Ocean near 20° E. Here, at the Agulhas retroflection, ‘leakage’ York 10964, USA. of water occurs within an array of cyclonic (clockwise) and anticyclonic (anticlockwise) eddies that e-mail: [email protected] are injected into the vigorous stirring and mixing environment of the Cape Basin (the ‘Cape 1. -
Of Polarity Ups and Downs of Guided Vessel Sprouting
Ups and Downs of Guided Vessel Sprouting: The Role of Polarity Christina Y. Lee and Victoria L. Bautch Physiology 26:326-333, 2011. doi:10.1152/physiol.00018.2011 You might find this additional info useful... This article cites 82 articles, 38 of which can be accessed free at: /content/26/5/326.full.html#ref-list-1 This article has been cited by 2 other HighWire hosted articles Rasip1 regulates vertebrate vascular endothelial junction stability through Epac1-Rap1 signaling Christopher W. Wilson, Leon H. Parker, Christopher J. Hall, Tanya Smyczek, Judy Mak, Ailey Crow, George Posthuma, Ann De Mazière, Meredith Sagolla, Cecile Chalouni, Philip Vitorino, Merone Roose-Girma, Søren Warming, Judith Klumperman, Philip S. Crosier and Weilan Ye Blood, November 21, 2013; 122 (22): 3678-3690. [Abstract] [Full Text] [PDF] Cas and NEDD9 Contribute to Tumor Progression through Dynamic Regulation of the Cytoskeleton Michael S. Guerrero, J. Thomas Parsons and Amy H. Bouton Genes & Cancer, May , 2012; 3 (5-6): 371-381. [Abstract] [Full Text] [PDF] Downloaded from Updated information and services including high resolution figures, can be found at: /content/26/5/326.full.html Additional material and information about Physiology can be found at: http://www.the-aps.org/publications/physiol on August 25, 2014 This information is current as of August 25, 2014. Physiology (formerly published as News in Physiological Science) publishes brief review articles on major physiological developments. It is published bimonthly in February, April, June, August, October, and December by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2011 by the American Physiological Society. -
Non-Muscle Myosin 2A (NM2A): Structure, Regulation and Function
cells Review Non-Muscle Myosin 2A (NM2A): Structure, Regulation and Function Cláudia Brito 1,2 and Sandra Sousa 1,* 1 Group of Cell Biology of Bacterial Infections, i3S-Instituto de Investigação e Inovação em Saúde, IBMC, Universidade do Porto, 4200-135 Porto, Portugal; [email protected] 2 Programa Doutoral em Biologia Molecular e Celular (MCBiology), Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4099-002 Porto, Portugal * Correspondence: [email protected] Received: 19 May 2020; Accepted: 29 June 2020; Published: 1 July 2020 Abstract: Non-muscle myosin 2A (NM2A) is a motor cytoskeletal enzyme with crucial importance from the early stages of development until adulthood. Due to its capacity to convert chemical energy into force, NM2A powers the contraction of the actomyosin cytoskeleton, required for proper cell division, adhesion and migration, among other cellular functions. Although NM2A has been extensively studied, new findings revealed that a lot remains to be discovered concerning its spatiotemporal regulation in the intracellular environment. In recent years, new functions were attributed to NM2A and its activity was associated to a plethora of illnesses, including neurological disorders and infectious diseases. Here, we provide a concise overview on the current knowledge regarding the structure, the function and the regulation of NM2A. In addition, we recapitulate NM2A-associated diseases and discuss its potential as a therapeutic target. Keywords: non-muscle myosin 2A (NM2A); NM2A activity regulation; NM2A filament assembly; actomyosin cytoskeleton; cell migration; cell adhesion; plasma membrane blebbing 1. Superfamily of Myosins The cell cytoskeleton is an interconnected and dynamic network of filaments essential for intracellular organization and cell shape maintenance. -
Segregation of Leading-Edge and Uropod Components Into Specific Lipid Rafts During T Cell Polarization
Segregation of leading-edge and uropod components into specific lipid rafts during T cell polarization Concepcio´ nGo´ mez-Mouto´ n*, Jose Luis Abad*, Emilia Mira*, Rosa Ana Lacalle*, Eduard Gallardo†, Sonia Jime´ nez-Baranda*, Isabel Illa†, Antonio Bernad*, Santos Man˜ es*‡, and Carlos Marti´nez-A.* *Department of Immunology and Oncology, Centro Nacional de Biotecnologı´a,Consejo Superior de Investigaciones Cientı´ficas,Universidad Auto´noma de Madrid, Cantoblanco, E-28049 Madrid, Spain; and †Laboratorio de Neurologı´aExperimental, Santa Creu i Sant Pau Hospital, 08025 Barcelona, Spain Edited by Kai Simons, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany, and approved June 11, 2001 (received for review April 2, 2001) Redistribution of specialized molecules in migrating cells develops CCR5, and other raft-associated proteins accumulate preferentially asymmetry between two opposite cell poles, the leading edge and at the leading lamella of migrating cells (4). Modification of the uropod. We show that acquisition of a motile phenotype in T raft-located proteins such that they no longer associate with rafts lymphocytes results in the asymmetric redistribution of ganglioside inhibits their asymmetric redistribution. The functional role of GM3- and GM1-enriched raft domains to the leading edge and to the asymmetric raft redistribution is shown in this article, as membrane uropod, respectively. This segregation to each cell pole parallels the cholesterol depletion impairs cell polarization and chemotaxis. specific redistribution of membrane proteins associated to each raft Cholesterol-depleted cells showed isotropic pseudopodial protru- subfraction. Our data suggest that raft partitioning is a major deter- sion, suggesting that raft redistribution is needed for location- minant for protein redistribution in polarized T cells, as ectopic specific induction of pseudopod protrusion during cell polarization. -
Cross-Talk Between Shigella and Cells of the Adaptive Immunity: the TTS Effector Ipgd Inhibits T Cell Migration
Cross-talk between Shigella and cells of the adaptive immunity: The TTS effector IpgD inhibits T cell migration Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Julius-Maximilians-Universität Würzburg vorgelegt von Christoph Konradt aus Schäßburg Würzburg, 2010 Eingereicht am: ........................................................................... Mitglieder der Promotionskommission: Vorsitzender: ............................................................................... 1. Gutachter: Prof. Dr. Dr. h.c. mult. Jörg Hacker 2. Gutachter: Prof. Dr. Ulrich Dobrindt Tag des Promotionskolloquiums: ................................................... Doktorurkunde ausgehändigt am: .................................................. Erklärung Die vorliegende Arbeit wurde von mir selbständig und nur unter Verwendung der angegebenen Quellen und Hilfsmittel angefertigt. Weiterhin erkläre ich, dass die Dissertation bisher nicht in gleicher oder ähnlicher Form in einem anderen Prüfungsverfahren vorgelegen hat, und ich bisher keine akademischen Grade erworben oder zu erwerben versucht habe. Würzburg, August 2010 Christoph Konradt Acknowledgements First of all I want to thank Prof. Dr. Dr. h. c. mult. Jörg Hacker for accepting the responsibility of supervising my PhD in the distance while the experiments where carried out in France and I also want to thank him for his support through all this time. I want to thank Prof. Dr. Ulrich Dobrindt for his kindness of being my second examiner. A special thanks goes to Prof. Philippe Sansonetti for giving me the opportunity of joining the Unité de Pathogénie Microbienne Moléculaire at the Institut Pasteur, for offering me an exciting PhD topic and for his scientific expertise and support during my thesis. I especially want to thank my supervisor Dr. Armelle Phalipon for her strong guidance during this work. I am grateful for the excellent supervision I received. She was a great support in so many situations in and beside the lab. -
From Cells to Organs: Building Polarized Tissue
FOCUS ON CELL POLAREVIEWSRITY From cells to organs: building polarized tissue David M. Bryant* and Keith E. Mostov*‡ Abstract | How do animal cells assemble into tissues and organs? A diverse array of tissue structures and shapes can be formed by organizing groups of cells into different polarized arrangements and by coordinating their polarity in space and time. Conserved design principles underlying this diversity are emerging from studies of model organisms and tissues. We discuss how conserved polarity complexes, signalling networks, transcription factors, membrane-trafficking pathways, mechanisms for forming lumens in tubes and other hollow structures, and transitions between different types of polarity, such as between epithelial and mesenchymal cells, are used in similar and iterative manners to build all tissues. Basement membrane The defining feature of metazoa is that their cells ultimately, underlying blood vessels. The basal and A thin extracellular matrix layer are organized into multicellular tissues and organs. lateral surfaces are fairly similar in composition and that specifically lines the basal Although almost every eukaryotic cell is spatially organization and are often referred to together as side of epithelial sheets, and asymmetric or polarized, polarity must be coordi- the basolateral surface. The apical and basolateral certain other tissues, to which cells are attached. Also nated in space and time for individual cells to form surfaces, however, have very different compositions. 1 referred to as the basal lamina. a tissue . Cell polarity involves the asymmetric In vertebrates, tight junctions (TJs) are found at the organization of most of the physical aspects of the apical-most portion of the lateral surfaces, where Extracellular matrix cell, including the cell surface, intracellular organelles the TJs form barriers both between the apical and baso- An extracellular scaffolding gel and the cytoskeleton2,3. -
Planar Cell Polarity Axon Guidance
Planar Cell Polarity Axon Guidance Is Basil added when Kendall overspecializing alarmedly? Full-faced and double-breasted Ware still stumming his prier broadside. Aborning Danny stupefy some nomarch and muddies his cyclographs so rigidly! Molecular mechanism by axons through the polarity establishment and mesenchymal tissue polarity, we summarize the response of the neurite and planar cell movement The different quantities of my different species drawn are must to toll an expanse of character relative concentration at sea state. Wnt signalling in the development of axon dendrites and. Between cells during vertebrate epithelial cells establish cell migration, it is widely promoted regrowth axons by which networks use drosophila, axons sort into functional. Proneural genes and the specification of neural cell types. Request PDF Wnt-Signaling and Planar Cell Polarity Genes Regulate Axon Guidance Along the Anteroposterior Axis in C elegans During. Recent advances on rodent hippocampal cells during neuritic growth cone collapse induced by regulating cell cycle activity during ce movements remains unclear whether or ryk. Derailed receptor demonstrates chemical affinity to demonstrate an article. The guidance and ds gradients and dachsous cadherins and axon guidance cues are interested in organizing center, they modify responsiveness. Dvl complexes are. In vertebrates, the PCP pathway recruits the same downstream actin regulators during cell migration, as we made below. Mutual inhibition among postmitotic neurons regulates robustness of brain wiring in Drosophila. These various functions for electrophysiological recording and thus having negative impact on axon guidance during neuritic growth cones integrate simultaneous guidance is important. Proper axon guidance is essential for both the developing nervous system gain the. -
The Prion Protein Inhibits Monocytic Cell Migration by Stimulating Β1 Integrin Adhesion and Uropod Formation Dion D
© 2015. Published by The Company of Biologists Ltd | Journal of Cell Science (2015) 128, 3018-3029 doi:10.1242/jcs.165365 RESEARCH ARTICLE The prion protein inhibits monocytic cell migration by stimulating β1 integrin adhesion and uropod formation Dion D. Richardson1,*, Simon Tol1,*, Eider Valle-Encinas1, Cayetano Pleguezuelos1, Ruben Bierings2, Dirk Geerts3 and Mar Fernandez-Borja1,‡ ABSTRACT PrP is highly expressed in the hematopoietic system, particularly The broad tissue distribution and evolutionary conservation of the in hematopoietic stem cells and in mature mononuclear leukocytes glycosylphosphatidylinositol (GPI)-anchored prion protein (PrP, also (Isaacs et al., 2006). Accordingly, PrP has been reported to have a in vivo known as PRNP) suggests that it plays a role in cellular homeostasis. role in several hematopoietic and immune cell functions , Given that integrin adhesion determines cell behavior, the proposed such as the self-renewal of long-term repopulating hematopoietic role of PrP in cell adhesion might underlie the various in vitro and stem cells (Kent et al., 2009; Zhang et al., 2006), macrophage in vivo effects associated with PrP loss-of-function, including the phagocytosis (de Almeida et al., 2005) and T cell activation immune phenotypes described in PrP−/− mice. Here, we investigated (Ballerini et al., 2006). However, the role of PrP in the innate the role of PrP in the adhesion and (transendothelial) migration of immune response has hardly been explored with the exception of −/− human (pro)monocytes. We found that PrP regulates β1-integrin- one study in which peritonitis was induced in PrP mice with −/− mediated adhesion of monocytes. Additionally, PrP controls the cell zymosan (de Almeida et al., 2005). -
Cell and Tissue Polarity As a Non-Canonical Tumor Suppressor
Commentary 1141 Cell polarity and cancer – cell and tissue polarity as a non-canonical tumor suppressor Minhui Lee1,2 and Valeri Vasioukhin1,3,* 1Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N., C3-168, Seattle, WA 98109, USA 2Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98109, USA 3Department of Pathology and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98195, USA *Author for correspondence (e-mail: [email protected]) Accepted 19 February 2008 Journal of Cell Science 121, 1141-1150 Published by The Company of Biologists 2008 doi:10.1242/jcs.016634 Summary Correct establishment and maintenance of cell polarity is and differentiation of cancer stem cells. Data from in vivo and required for the development and homeostasis of all three-dimensional (3D) cell-culture models demonstrate that metazoans. Cell-polarity mechanisms are responsible not only tissue organization attenuates the phenotypic outcome of for the diversification of cell shapes but also for regulation of oncogenic signaling. We suggest that polarized 3D tissue the asymmetric cell divisions of stem cells that are crucial for organization uses cell-cell and cell-substratum adhesion their correct self-renewal and differentiation. Disruption of cell structures to reinforce and maintain the cell polarity of pre- polarity is a hallmark of cancer. Furthermore, recent evidence cancerous cells. In this model, polarized 3D tissue organization indicates that loss of cell polarity is intimately involved in functions as a non-canonical tumor suppressor that prevents cancer: several crucial cell-polarity proteins are known proto- the manifestation of neoplastic features in mutant cells and, oncogenes or tumor suppressors, basic mechanisms of cell ultimately, suppresses tumor development and progression.