Relevant bibliographies by topics / Cag Type IV Secretion System

Academic literature on the topic 'Cag Type IV Secretion System'

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Published: 7 July 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Journal articles on the topic "Cag Type IV Secretion System":

1

Busler, Valerie J., Victor J. Torres, Mark S. McClain, Oscar Tirado, David B. Friedman, and Timothy L. Cover. "Protein-Protein Interactions among Helicobacter pylori Cag Proteins." Journal of Bacteriology 188, no. 13 (July 1, 2006): 4787–800. http://dx.doi.org/10.1128/jb.00066-06.

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ABSTRACT Many Helicobacter pylori isolates contain a 40-kb region of chromosomal DNA known as the cag pathogenicity island (PAI). The risk for development of gastric cancer or peptic ulcer disease is higher among humans infected with cag PAI-positive H. pylori strains than among those infected with cag PAI-negative strains. The cag PAI encodes a type IV secretion system that translocates CagA into gastric epithelial cells. To identify Cag proteins that are expressed by H. pylori during growth in vitro, we compared the proteomes of a wild-type H. pylori strain and an isogenic cag PAI deletion mutant using two-dimensional difference gel electrophoresis (2D-DIGE) in multiple pH ranges. Seven Cag proteins were identified by this approach. We then used a yeast two-hybrid system to detect potential protein-protein interactions among 14 Cag proteins. One heterotypic interaction (CagY/7 with CagX/8) and two homotypic interactions (involving H. pylori VirB11/ATPase and Cag5) were similar to interactions previously reported to occur among homologous components of the Agrobacterium tumefaciens type IV secretion system. Other interactions involved Cag proteins that do not have known homologues in other bacterial species. Biochemical analysis confirmed selected interactions involving five of the proteins that were identified by 2D-DIGE. Protein-protein interactions among Cag proteins are likely to have an important role in the assembly of the H. pylori type IV secretion apparatus.
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Pinto-Santini, Delia M., and Nina R. Salama. "Cag3 Is a Novel Essential Component of the Helicobacter pylori Cag Type IV Secretion System Outer Membrane Subcomplex." Journal of Bacteriology 191, no. 23 (October 2, 2009): 7343–52. http://dx.doi.org/10.1128/jb.00946-09.

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ABSTRACT Helicobacter pylori strains harboring the cag pathogenicity island (PAI) have been associated with more severe gastric disease in infected humans. The cag PAI encodes a type IV secretion (T4S) system required for CagA translocation into host cells as well as induction of proinflammatory cytokines, such as interleukin-8 (IL-8). cag PAI genes sharing sequence similarity with T4S components from other bacteria are essential for Cag T4S function. Other cag PAI-encoded genes are also essential for Cag T4S, but lack of sequence-based or structural similarity with genes in existing databases has precluded a functional assignment for the encoded proteins. We have studied the role of one such protein, Cag3 (HP0522), in Cag T4S and determined Cag3 subcellular localization and protein interactions. Cag3 is membrane associated and copurifies with predicted inner and outer membrane Cag T4S components that are essential for Cag T4S as well as putative accessory factors. Coimmunoprecipitation and cross-linking experiments revealed specific interactions with HpVirB7 and CagM, suggesting Cag3 is a new component of the Cag T4S outer membrane subcomplex. Finally, lack of Cag3 lowers HpVirB7 steady-state levels, further indicating Cag3 makes a subcomplex with this protein.
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Kumar, Navin, Mohd Shariq, Rajesh Kumari, Rakesh K. Tyagi, and Gauranga Mukhopadhyay. "Cag Type IV Secretion System: CagI Independent Bacterial Surface Localization of CagA." PLoS ONE 8, no. 9 (September 10, 2013): e74620. http://dx.doi.org/10.1371/journal.pone.0074620.

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Cover, Timothy L., D. Borden Lacy, and Melanie D. Ohi. "The Helicobacter pylori Cag Type IV Secretion System." Trends in Microbiology 28, no. 8 (August 2020): 682–95. http://dx.doi.org/10.1016/j.tim.2020.02.004.

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Couturier, Marc Roger, Elizabetta Tasca, Cesare Montecucco, and Markus Stein. "Interaction with CagF Is Required for Translocation of CagA into the Host via the Helicobacter pylori Type IV Secretion System." Infection and Immunity 74, no. 1 (January 2006): 273–81. http://dx.doi.org/10.1128/iai.74.1.273-281.2006.

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ABSTRACT Development of severe gastric diseases is strongly associated with those strains of Helicobacter pylori that contain the cag pathogenicity island (PAI) inserted into the chromosome. The cag PAI encodes a type IV secretion system that translocates the major disease-associated virulence protein, CagA, into the host epithelial cell. CagA then affects host signaling pathways, leading to cell elongations and inflammation. Since the precise mechanism by which the CagA toxin is translocated by the type IV secretion system remained elusive, we used fusion proteins and immunoprecipitation studies to identify CagA-interacting secretion components. Here we demonstrate that CagA, in addition to other yet-unidentified proteins, interacts with CagF, presumably at the inner bacterial membrane. This interaction is required for CagA translocation, since an isogenic nonpolar cagF mutant was translocation deficient. Our results suggest that CagF may be a protein with unique chaperone-like function that is involved in the early steps of CagA recognition and delivery into the type IV secretion channel.
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Kutter, Stefan, Renate Buhrdorf, Jürgen Haas, Wulf Schneider-Brachert, Rainer Haas, and Wolfgang Fischer. "Protein Subassemblies of the Helicobacter pylori Cag Type IV Secretion System Revealed by Localization and Interaction Studies." Journal of Bacteriology 190, no. 6 (January 4, 2008): 2161–71. http://dx.doi.org/10.1128/jb.01341-07.

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ABSTRACT Type IV secretion systems are possibly the most versatile protein transport systems in gram-negative bacteria, with substrates ranging from small proteins to large nucleoprotein complexes. In many cases, such as the cag pathogenicity island of Helicobacter pylori, genes encoding components of a type IV secretion system have been identified due to their sequence similarities to prototypical systems such as the VirB system of Agrobacterium tumefaciens. The Cag type IV secretion system contains at least 14 essential apparatus components and several substrate translocation and auxiliary factors, but the functions of most components cannot be inferred from their sequences due to the lack of similarities. In this study, we have performed a comprehensive sequence analysis of all essential or auxiliary Cag components, and we have used antisera raised against a subset of components to determine their subcellular localization. The results suggest that the Cag system contains functional analogues to all VirB components except VirB5. Moreover, we have characterized mutual stabilization effects and performed a comprehensive yeast two-hybrid screening for potential protein-protein interactions. Immunoprecipitation studies resulted in identification of a secretion apparatus subassembly at the outer membrane. Combining these data, we provide a first low-resolution model of the Cag type IV secretion apparatus.
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Terradot, Laurent, and Gabriel Waksman. "Architecture of the Helicobacter pylori Cag-type IV secretion system." FEBS Journal 278, no. 8 (February 25, 2011): 1213–22. http://dx.doi.org/10.1111/j.1742-4658.2011.08037.x.

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Chung, Jeong Min, Michael J. Sheedlo, Anne M. Campbell, Neha Sawhney, Arwen E. Frick-Cheng, D. Borden Lacy, Timothy L. Cover, and Melanie D. Ohi. "Structure of the Helicobacter pylori Cag Type IV Secretion System." Biophysical Journal 118, no. 3 (February 2020): 295a. http://dx.doi.org/10.1016/j.bpj.2019.11.1671.

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Jurik, Angela, Elisabeth Haußer, Stefan Kutter, Isabelle Pattis, Sandra Praßl, Evelyn Weiss, and Wolfgang Fischer. "The Coupling Protein Cagβ and Its Interaction Partner CagZ Are Required for Type IV Secretion of the Helicobacter pylori CagA Protein." Infection and Immunity 78, no. 12 (September 27, 2010): 5244–51. http://dx.doi.org/10.1128/iai.00796-10.

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ABSTRACT Bacterial type IV secretion systems are macromolecule transporters with essential functions for horizontal gene transfer and for symbiotic and pathogenic interactions with eukaryotic host cells. Helicobacter pylori, the causative agent of type B gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma, uses the Cag type IV secretion system to inject its effector protein CagA into gastric cells. This protein translocation results in altered host cell gene expression profiles and cytoskeletal rearrangements, and it has been linked to cancer development. Interactions of CagA with host cell proteins have been studied in great detail, but little is known about the molecular details of CagA recognition as a type IV secretion substrate or of the translocation process. Apart from components of the secretion apparatus, we previously identified several CagA translocation factors that are either required for or support CagA translocation. To identify protein-protein interactions between these translocation factors, we used a yeast two-hybrid approach comprising all cag pathogenicity island genes. Among several other interactions involving translocation factors, we found a strong interaction between the coupling protein homologue Cagβ (HP0524) and the Cag-specific translocation factor CagZ (HP0526). We show that CagZ has a stabilizing effect on Cagβ, and we demonstrate protein-protein interactions between the cytoplasmic part of Cagβ and CagA and between CagZ and Cagβ, using immunoprecipitation and pull-down assays. Together, our data suggest that these interactions represent a substrate-translocation factor complex at the bacterial cytoplasmic membrane.
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Chang, Yi-Wei, Carrie L. Shaffer, Lee A. Rettberg, Debnath Ghosal, and Grant J. Jensen. "In Vivo Structures of the Helicobacter pylori cag Type IV Secretion System." Cell Reports 23, no. 3 (April 2018): 673–81. http://dx.doi.org/10.1016/j.celrep.2018.03.085.

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You might also be interested in the extended bibliographies on the topic 'Cag Type IV Secretion System' for particular source types:
Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Cag Type IV Secretion System":

1

Pham, Kieu Thuy [Verfasser], and Wolfgang [Akademischer Betreuer] Fischer. "Functional characterization of the Helicobacter pylori Cag Type IV secretion system components CagH, CagI and CagL / Kieu Thuy Pham ; Betreuer: Wolfgang Fischer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1124780033/34.

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Jiménez, Soto Luisa Fernanda. "Studies on the function of the Cag Type IV Secretion System of Helicobacter pylori with integrin Beta1." kostenfrei, 2009. http://edoc.ub.uni-muenchen.de/10659/.

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Jimenez, Soto Luisa Fernanda. "Studies on the function of the Cag Type IV Secretion System of Helicobacter pylori with integrin Beta1." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-106597.

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Zeitler, Anna Friederike [Verfasser], and Rainer [Akademischer Betreuer] Haas. "Identification of cellular mechanisms interfering with the Helicobacter pylori cag type IV secretion system / Anna Friederike Zeitler ; Betreuer: Rainer Haas." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1230754679/34.

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Lopez-Lozano, Nina. "Caractérisation structurale de nanomachines bactériennes impliquées dans l'adaptabilité et la virulence." Electronic Thesis or Diss., Bordeaux, 2023. http://www.theses.fr/2023BORD0482.

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Cette thèse est divisée en deux thématiques.La première porte sur le système de Sécrétion de TypeIV cag (cag-SST4) d’Helicobacter pylori. Il s’agit d’une machinerie de sécrétion complexe enchâssée dans l’enveloppe cellulaire de la bactérie, lui permettant d’injecter l’oncoprotéine CagA dans les cellules épithéliales gastriques humaines. Cette toxine est considérée comme un facteur de virulence majeur d’H. pylori. Elle interagit avec des protéines de l’hôte, perturbant la signalisation cellulaire et entraînant des modifications pouvant favoriser le développement de maladies gastrointestinales, y compris des ulcères et des cancers gastriques. Le cag-SST4 est subdivisé en trois parties : (i) un complexe de membrane interne, composé essentiellement d’ATPases fournissant l’énergie nécessaire à son assemblage et/ ou son fonctionnement ; (ii) un complexe de membrane externe, ou complexe core, formant un canal qui relie les membranes interne et externe et (iii) un pilus extracellulaire, dont l’existence est toujours controversée, et qui permettrait d’établir un contact entre la bactérie et sa cible, et éventuellement de transférer les substrats à travers la membrane de l’hôte.Un premier projet porte sur le pilus extracellulaire. L’objectif est d’obtenir des données concernant une interaction supposée entre les protéines CagI et CagL, essentielles à la sécrétion et pressenties pour entrer dans la composition du pilus. Nous avons surexprimé des versions recombinantes de ces protéines chez Escherichia coli et nous les avons co-purifiées par chromatographie d’affinité, démontrant ainsi une interaction directe entre elles. La capacité de DARPins et Nanobodies de lier ce complexe a été testée. L’analyse de ces complexes a également été entreprise par cryo-microscopie électronique (cryoME).Le second projet porte sur le complexe core avec pour objectif d’obtenir sa structure à haute résolution afin d’éclaircir les zones d’ombre qui persistent concernant cet imposant assemblage. Différentes techniques ont été mises en œuvre afin de pouvoir solubiliser ce complexe. Sa purification reste à optimiser afin de pouvoir envisager une analyse en cryoME. L’obtention de telles structures pourrait permettre de mieux comprendre le fonctionnement du cag-SST4 et d’envisager des stratégies permettant d’inhiber son assemblage et/ ou son fonctionnement, privant ainsi H. pylori d’un facteur de virulence majeur.La seconde thématique porte sur les spirosomes bactériens. L’enzyme AdhE est très conservée dans le règne bactérien et chez certains organismes eucaryotes. Il s’agit d’une enzyme bifonctionnelle alcool/ aldéhyde déshydrogénase, responsable de la conversion de l’acétyl-CoA en acétaldéhyde puis en éthanol au cours de la fermentation alcoolique en anaérobie. Cette enzyme est communément retrouvée sous sa forme oligomérique, appelée spirosome. En fonction des ligands présents dans le milieu, les spirosomes d’E. coli peuvent se présenter dans une conformation compacte ou étendue, cette dernière constituant la forme active de l’enzyme. Contrairement aux spirosomes d’E. coli, ceux de Streptococcus pneumoniae sont naturellement stabilisés dans leur conformation étendue.L’objectif de ce projet est de comprendre quels sont les mécanismes à l’origine de cette différence de conformation. La cryoME nous a permis d’obtenir une structure à haute résolution du spirosome de S. pneumoniae et ainsi de pouvoir la comparer à celle du spirosome étendu d’E. coli. Des expériences de mutagenèse fonctionnelle avec complémentation nous ont permis de déterminer quels sont les résidus impliqués dans l’extension de ces spirosomes. Etant impliqués dans la pathogénicité et révélés indispensables à la physiologie bactérienne en l’absence d’oxygène, l’étude approfondie de leur conformation pourrait donc mener à la découverte de molécules capables de réguler leur activité, ce qui pourrait présenter un intérêt majeur dans les domaines des biotechnologies et de la santé
This thesis is divided into two themes.The first theme focuses on the cag Type IV secretion system (cag-T4SS) of the bacterium Helicobacter pylori. This is a complex secretion machinery embedded in the bacterium's cellular envelope, enabling it to inject the CagA oncoprotein into human gastric epithelial cells. This toxin is considered a major virulence factor of H. pylori. It interacts with host proteins, disrupting cell signaling and leading to changes that can promote the development of gastrointestinal diseases, including gastric ulcers and cancers. The cag-T4SS is subdivided into three parts: (i) an inner membrane complex, composed essentially of ATPases providing the energy required for its assembly and/or its function; (ii) an outer membrane complex, or core complex, forming a channel that connects the inner and outer membranes; and (iii) an extracellular pilus, the existence of which is still controversial, and which would establish contact between the bacterium and its target, and possibly transfer substrates across the host membrane.The first project focuses on the extracellular pilus. The aim is to obtain data concerning a putative interaction between the CagI and CagL proteins, which are essential for secretion and are thought to be involved in the composition of the cag-T4SS pilus. We overexpressed recombinant versions of these proteins in Escherichia coli and co-purified them by affinity chromatography, demonstrating a direct interaction between them. The ability of DARPins and Nanobodies to bind this complex was tested. Analysis of these complexes was also undertaken by cryo-electron microscopy (cryoEM).The second project focuses on the core complex, with the aim of obtaining its structure at high resolution in order to shed light on the remaining grey areas concerning this imposing assembly. Various techniques have been used to solubilize this complex. Its purification remains to be optimized before it can be analyzed by cryoEM. Obtaining such structures could lead to a better understanding of how cag-T4SS functions, and to consider strategies to inhibit its assembly and/or function, thus depriving H. pylori of a major virulence factor.The second theme concerns bacterial spirosomes. The AdhE enzyme is highly conserved in the bacterial kingdom and in certain eukaryotic organisms. It is a bifunctional alcohol/aldehyde dehydrogenase enzyme, responsible for the conversion of acetyl-CoA to acetaldehyde and then to ethanol during anaerobic alcoholic fermentation. This enzyme is commonly found in its oligomeric form, known as spirosome. Depending on the ligands present in the medium, E. coli spirosomes can have a compact or extended conformation, the latter constituting the active form of the enzyme. Unlike E. coli spirosomes, Streptococcus pneumoniae ones are naturally stabilized in their extended conformation.The aim of this project is to understand the mechanisms behind this conformational difference. CryoEM enabled us to obtain a high-resolution structure of the S. pneumoniae spirosome and thus comparing it with the extended E. coli spirosome. Functional mutagenesis experiments with complementation enabled us to determine which residues are involved in the extension of these spirosomes. As they are involved in pathogenicity and have been shown to be essential to bacterial physiology in the absence of oxygen, in-depth study of their conformation could lead to the discovery of molecules capable of regulating their activity, which could be of major interest in the fields of biotechnology and healthcare
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Bauer, Bianca. "Molekulare Charakterisierung von Typ IV Sekretionssytem-spezifischen Wirtszellantworten und bakteriellen Virulenzfaktoren des humanen Magenpathogens Helicobacter pylori." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16045.

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Das humane Magenpathogen Helicobacter pylori (H. pylori) besiedelt den menschlichen Magen und kann zu der Entstehung schwerwiegender Krankheiten wie Magenkrebs und Magengeschwüren führen. Die Pathogenese ist eng mit dem bakteriellen Typ IV Sekretionssystems (T4SS) assoziiert, das die Translokation des Effektorproteins CagA in die Wirtszelle vermittelt. Bisher ist noch unbekannt, in welchem Ausmaß wirtszellspezifische Faktoren die T4SS induzierte Pathogenese beeinflussen. Dieser Aspekt wurde in dieser Arbeit durch die Analyse verschiedenster Zelllinien das erste Mal systematisch untersucht. Interessanterweise unterschied sich die zelluläre Antwort auf die T4SS spezifische Infektion erheblich in Abhängigkeit der verwendeten Zelllinie. Die Ergebnisse beweisen, dass Wirtszellfaktoren eine ebenso große Rolle in der H. pylori induzierten Pathogenese spielen wie bakterielle Effektoren. Zusätzlich wurde in dieser Arbeit eine genomweite Screening-Methode etabliert, die es ermöglicht, neue Komponenten des T4SSs, translozierte NF-B Effektoren und bakterielle Adhäsine zu identifizieren. Auch der Einfluss von CagA auf den EGF-Rezeptor wurde hier näher untersucht. Der Rezeptor steht ebenfalls eng mit der Entstehung von Krebs in Verbindung. Hierbei stellte sich heraus, dass CagA die Endozytose des EGF-Rezeptors durch die Aktivierung der Nicht-Rezeptor Tyrosinkinase c-Abl hemmt und dadurch die Rezeptorpopulation auf der Wirtszelloberfläche erhöht. Interessanterweise führt dieser Effekt jedoch nicht zu einer Verstärkung der EGF-Rezeptor Signaltransduktion. Vielmehr kommt es zu einer Hemmung der EGF-Rezeptor Transaktivierung und zu einer Blockade der EGF vermittelten Wundheilung. Die Daten weisen auf eine Rolle des EGF-Rezeptors in der H. pylori induzierten Geschwürbildung hin. Auch der zu Grunde liegende molekulare Mechanismus der Rezeptor-Inhibierung konnte hier entschlüsselt werden, der sowohl von CagA als auch von der Phosphatase SHP-2 gesteuert wird.
The human gastric pathogen Helicobacter pylori (H. pylori) elicits a tremendous medical burden because of its causative association with peptic ulcer disease and gastric cancer. The pathogenic potential of H. pylori is intricately linked to the expression of a pathogenicity island encoded type IV secretion system (T4SS), which translocates the bacterial effector protein CagA into the eukaryotic host cell. The role of host cell determinants in T4SS mediated pathogenesis has not yet been systematically examined. To elucidate the role of host cell factors within T4SS induced host cell responses, different eukaryotic cell lines were analyzed systematically for respective phenotypes. Remarkably, T4SS mediated host responses among these cell lines varied considerably, thereby demonstrating the importance of host cell components in H. pylori induced pathogenesis. In addition, a H. pylori genome wide bacterial screen for factors important in pathogenesis, such as unknown T4SS components or novel NF-kappaB effector molecules, was developed and optimized. The precise function of the prominent effector protein CagA remains unclear. To functionally characterize the role of CagA, its impact on the epidermal growth factor (EGF)-receptor pathway was analyzed. The results suggest a mechanism where EGF-receptor endocytosis is completely blocked by a CagA induced activation of c-Abl, leading to an elevated receptor surface exposition. Surprisingly, EGF-receptor transactivation and EGF-dependent wound healing are selectively blocked during prolonged infections as well, indicating that an increased receptor-population on the cell surface does not necessarily promote signaling. This data suggests a role for the EGF-receptor in H. pylori- induced ulcer disease. The underlying molecular mechanism was identified as being SHP-2 and CagA dependent.
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Connery, Sarah. "Reconstitution and localisation studies of a type IV secretion system." Thesis, Birkbeck (University of London), 2014. http://bbktheses.da.ulcc.ac.uk/75/.

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Bacterial conjugation is the transport of a DNA molecule from a donor cell to a recipient. Since bacteria do not reproduce sexually, conjugation is a major contributor to prokaryotic genome plasticity and the spread of antibiotic resistance genes. A Type IV Secretion System (T4SS) mediates the DNA transport during conjugation. T4SSs are large macromolecular assemblies embedded in the membrane of bacteria, and are associated with pathogenesis, bacterial conjugation and natural transformation. They are a versatile family of secretion systems, who transport a wide variety of substrates, such as virulence proteins, DNA––protein complexes as well as only DNA. Here, we investigate the minimal requirements for conjugation, and the T4SS’s localisation within the cell. We show that the conjugative T4SS of the plasmid pR388 requires a total of 14 genes to efficiently mobilise DNA from a donor cell to a recipient cell and is arranged around the cell circumfence in a helical array. Our study of two reconstituted and fully functional conjugative T4SSs opens doors for further structural and functional analysis.
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Sutten, Eric Lynn. "The immunogenicity of the type IV secretion system in Anaplasma marginale." Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Thesis/Summer2009/e_sutten_072409.pdf.

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Thesis (M.S. in veterinary science)--Washington State University, August 2009.
Title from PDF title page (viewed on Aug. 7, 2009). "Department of Veterinary Microbiology and Pathology." Includes bibliographical references.
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Schindele, Franziska Maria [Verfasser], and Rainer [Akademischer Betreuer] Haas. "Development and application of a novel Cag type IV secretion reporter assay in Helicobacter pylori / Franziska Maria Schindele ; Betreuer: Rainer Haas." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1156173116/34.

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Engledow, Amanda Suzanne. "Role of type IV secretion systems in trafficking of virulence determinants of Burkholderia cenocepacia." Thesis, [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1841.

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Book chapters on the topic "Cag Type IV Secretion System":

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Backert, Steffen, Rainer Haas, Markus Gerhard, and Michael Naumann. "The Helicobacter pylori Type IV Secretion System Encoded by the cag Pathogenicity Island: Architecture, Function, and Signaling." In Current Topics in Microbiology and Immunology, 187–220. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-75241-9_8.

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Callaghan, Melanie M., Jan-Hendrik Heilers, Chris van der Does, and Joseph P. Dillard. "Secretion of Chromosomal DNA by the Neisseria gonorrhoeae Type IV Secretion System." In Current Topics in Microbiology and Immunology, 323–45. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-75241-9_13.

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Vincent, Carr D., Kwang Cheol Jeong, Jessica Sexton, Emily Buford, and Joseph P. Vogel. "The Legionella pneumophila Dot/Icm Type IV Secretion System." In Legionella, 184–91. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815660.ch47.

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Qiu, Jiazhang, and Zhao-Qing Luo. "Effector Translocation by the Legionella Dot/Icm Type IV Secretion System." In Current Topics in Microbiology and Immunology, 103–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/82_2013_345.

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Vincent, Carr D., Jonathan R. Friedman, and Joseph P. Vogel. "Defining the Translocation Pathway of the Legionella pneumophila Type IV Secretion System." In Legionella, 195–98. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815660.ch49.

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Kubori, Tomoko, and Hiroki Nagai. "Isolation of the Dot/Icm Type IV Secretion System Core Complex from Legionella pneumophila." In Methods in Molecular Biology, 241–47. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9048-1_15.

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Rikihisa, Yasuko. "Role and Function of the Type IV Secretion System in Anaplasma and Ehrlichia Species." In Current Topics in Microbiology and Immunology, 297–321. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-75241-9_12.

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Hilbi, Hubert, Hiroki Nagai, Tomoko Kubori, and Craig R. Roy. "Subversion of Host Membrane Dynamics by the Legionella Dot/Icm Type IV Secretion System." In Current Topics in Microbiology and Immunology, 221–42. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-75241-9_9.

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Zhu, Wenhan, and Zhao-Qing Luo. "Methods for Determining Protein Translocation by the Legionella pneumophila Dot/Icm Type IV Secretion System." In Methods in Molecular Biology, 323–32. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-161-5_19.

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So, Ernest C., Aurélie Mousnier, Gad Frankel, and Gunnar N. Schroeder. "Determination of In Vivo Interactomes of Dot/Icm Type IV Secretion System Effectors by Tandem Affinity Purification." In Methods in Molecular Biology, 289–303. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9048-1_19.

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Conference papers on the topic "Cag Type IV Secretion System":

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Esna Ashari, Zhila, Kelly A. Brayton, and Shira L. Broschat. "Determining Optimal Features for Predicting Type IV Secretion System Effector Proteins for Coxiella burnetii." In BCB '17: 8th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3107411.3107416.

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Saito, Atsushi, Shigeru Ariki, Hiroki Takahashi, and Yoshio Kuroki. "Pulmonary collectins provide a first line of defense against L. Pneumophila through inhibiting their type IV secretion system." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4121.

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Tandon, N. N., and G. A. Jamieson. "ROLE OF PLATELET MEMBRANE GLYCOPROTEIN IV IN PLATELET-COLLAGEN INTERACTION: A MICROTITER ASSAY TO STUDY PLATELET ADHERENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643906.

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Abstract:
The role of platelet glycoprotein IV (GPIV) in platelet function has not been elucidated. We have now isolated GPIV (Mr 88,000) from platelet membranes in homogeneous form by a series of steps involving (i) phase partitioning in Triton X-114, (ii) ion exchange chromatography on DEAE-cellulose, (iii) lectin affinity chromatography on WGA-Sepharose, and (iv) size exclusion chromatography on Ultrogel AcA44. Purified GPIV inhibited platelet shape change and aggregation induced by collagen (2 ug/ml; 7 nM as tropocollagen) in a dose-dependent fashion (ID50 ∼ 1 ug/ml; 10 nM) but did not affect aggregation induced by thrombin, ADP, epinephrine, arachidonate or ionophore A23187. To study the role of GPIV in platelet interaction with collagen we have developed a microtiter assay involving (i) coating acid soluble or fibrillar Type I collagen onto microtiter plates, (ii) incubation of coated collagen with 51Cr-labeled platelets and (iii) quantitation of platelet adherence by analysing the radioactivity of the SDS lysate of the adhered platelets. In this assay system, Fab fragments of anti-GPIV antibody inhibited platelet adherence by 75% to both acid soluble and fibrillar Type I collagen while nonimmune serum was without effect. Fab fragments also inhibited collagen-induced aggregation and secretion (ID∼ 10 ug/ml; 200 nM) and, slightly less effectively, aggregation by ADP and epinephrine (ID∼ 300 NM), but did not affect platelet activation by thrombin, arachidonate or ionophore. Fab fragments also inhibited platelet attachment to collagen-Sepharose columns by 80%. These results suggest a role for GPIV in the interaction of platelets with collagen, probably at the level of primary platelet adherence.

Reports on the topic "Cag Type IV Secretion System":

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Elbaum, Michael, and Peter J. Christie. Type IV Secretion System of Agrobacterium tumefaciens: Components and Structures. United States Department of Agriculture, March 2013. http://dx.doi.org/10.32747/2013.7699848.bard.

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Objectives: The overall goal of the project was to build an ultrastructural model of the Agrobacterium tumefaciens type IV secretion system (T4SS) based on electron microscopy, genetics, and immunolocalization of its components. There were four original aims: Aim 1: Define the contributions of contact-dependent and -independent plant signals to formation of novel morphological changes at the A. tumefaciens polar membrane. Aim 2: Genetic basis for morphological changes at the A. tumefaciens polar membrane. Aim 3: Immuno-localization of VirB proteins Aim 4: Structural definition of the substrate translocation route. There were no major revisions to the aims, and the work focused on the above questions. Background: Agrobacterium presents a unique example of inter-kingdom gene transfer. The process involves cell to cell transfer of both protein and DNA substrates via a contact-dependent mechanism akin to bacterial conjugation. Transfer is mediated by a T4SS. Intensive study of the Agrobacterium T4SS has made it an archetypal model for the genetics and biochemistry. The channel is assembled from eleven protein components encoded on the B operon in the virulence region of the tumor-inducing plasmid, plus an additional coupling protein, VirD4. During the course of our project two structural studies were published presenting X-ray crystallography and three-dimensional reconstruction from electron microscopy of a core complex of the channel assembled in vitro from homologous proteins of E. coli, representing VirB7, VirB9, and VirB10. Another study was published claiming that the secretion channels in Agrobacterium appear on helical arrays around the membrane perimeter and along the entire length of the bacterium. Helical arrangements in bacterial membranes have since fallen from favor however, and that finding was partially retracted in a second publication. Overall, the localization of the T4SS within the bacterial membranes remains enigmatic in the literature, and we believe that our results from this project make a significant advance. Summary of achievements : We found that polar inflations and other membrane disturbances relate to the activation conditions rather than to virulence protein expression. Activation requires low pH and nutrient-poor medium. These stress conditions are also reflected in DNA condensation to varying degrees. Nonetheless, they must be considered in modeling the T4SS as they represent the relevant conditions for its expression and activity. We identified the T4SS core component VirB7 at native expression levels using state of the art super-resolution light microscopy. This marker of the secretion system was found almost exclusively at the cell poles, and typically one pole. Immuno-electron microscopy identified the protein at the inner membrane, rather than at bridges across the inner and outer membranes. This suggests a rare or transient assembly of the secretion-competent channel, or alternatively a two-step secretion involving an intermediate step in the periplasmic space. We followed the expression of the major secreted effector, VirE2. This is a single-stranded DNA binding protein that forms a capsid around the transferred oligonucleotide, adapting the bacterial conjugation to the eukaryotic host. We found that over-expressed VirE2 forms filamentous complexes in the bacterial cytoplasm that could be observed both by conventional fluorescence microscopy and by correlative electron cryo-tomography. Using a non-retentive mutant we observed secretion of VirE2 from bacterial poles. We labeled the secreted substrates in vivo in order detect their secretion and appearance in the plant cells. However the low transfer efficiency and significant background signal have so far hampered this approach.
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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.

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