Vibrio cholerae

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Theoretical assessment of the impact of climatic factors in a vibrio cholerae model

Theoretical assessment of the impact of climatic factors in a vibrio cholerae model

Keywords Mathematical model · V. Cholerae · Climatic factors · Cooperative systems · Stability 1 Introduction Vibrio Cholerae (V. Cholerae) is a Gram-negative, comma-shaped bacterium that causes cholera in humans. Cholera is an acute intestinal infection caused by the inges- tion of contaminated foods and water with V. Cholerae bacterium. There are 200 sero- groups of V. Cholerae but only the V. Cholerae O1 and O139 are responsible of epi- demics (WHO 2017 ). The etiological agent passes through and survives the gastric acid barrier of the stomach and then penetrates the mucus lining that coats the intesti- nal epithelial (Reidl and Karl Klose 2002 ). Once they colonise the intestinal gut, they produce enterotoxin (which stimulates water and electrolyte secretion by the endothe- lial cells of the small intestine) that leads to watery diarrhea. Vibrio Cholerae has been reported to be associated with a variety of living organisms, including animals with an exoskeleton of chitin, aquatic plants, protozoa, bivalves, waterbirds, as well as abiotic substrates (e.g. sediments). Most of these are well-known or putative environmental reservoirs for the bacterium, defined as places where the pathogen lives over time, with the potential to be released and to cause human infection. These bacteria are then associated with these environmental reservoirs forming commensal relationships (Huq et  al. 1984 ). In many mathematical model of cholera (Copasso and Paveri-Fontana
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Constitutive Type VI Secretion System Expression Gives Vibrio cholerae Intra- and Interspecific Competitive Advantages

Constitutive Type VI Secretion System Expression Gives Vibrio cholerae Intra- and Interspecific Competitive Advantages

1 Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada, 2 Department of Biomedical Sciences, University of Texas Brownsville, Brownsville, Texas, United States of America Abstract The type VI secretion system (T6SS) mediates protein translocation across the cell membrane of Gram-negative bacteria, including Vibrio cholerae – the causative agent of cholera. All V. cholerae strains examined to date harbor gene clusters encoding a T6SS. Structural similarity and sequence homology between components of the T6SS and the T4 bacteriophage cell-puncturing device suggest that the T6SS functions as a contractile molecular syringe to inject effector molecules into prokaryotic and eukaryotic target cells. Regulation of the T6SS is critical. A subset of V. cholerae strains, including the clinical O37 serogroup strain V52, express T6SS constitutively. In contrast, pandemic strains impose tight control that can be genetically disrupted: mutations in the quorum sensing gene luxO and the newly described regulator gene tsrA lead to constitutive T6SS expression in the El Tor strain C6706. In this report, we examined environmental V. cholerae isolates from the Rio Grande with regard to T6SS regulation. Rough V. cholerae lacking O-antigen carried a nonsense mutation in the gene encoding the global T6SS regulator VasH and did not display virulent behavior towards Escherichia coli and other environmental bacteria. In contrast, smooth V. cholerae strains engaged constitutively in type VI-mediated secretion and displayed virulence towards prokaryotes (E. coli and other environmental bacteria) and a eukaryote (the social amoeba Dictyostelium discoideum). Furthermore, smooth V. cholerae strains were able to outcompete each other in a T6SS- dependent manner. The work presented here suggests that constitutive T6SS expression provides V. cholerae with an advantage in intraspecific and interspecific competition.
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La bactérie Vibrio cholerae lyse les bactéries environnantes et assimile leur ADN qu’elle intègre dans son propre génome

La bactérie Vibrio cholerae lyse les bactéries environnantes et assimile leur ADN qu’elle intègre dans son propre génome

compétence SST6 Protéines de compétence ADN Figure 1. Le transfert horizontal de gènes est favorisé par le SST6 chez Vibrio cholerae. Le transfert horizontal de gènes est favorisé par la co- régulation du régulon com des gènes de compétence et du SST6, contrôlée par le facteur de transcription QstR. Ce dernier est lui-même régulé conjointement par tfox, gène régulateur de la transformation, activé par le milieu chitineux, et hapR, gène maître du quorum sensing, activé à haute densité cellulaire.

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Detection of Vibrio cholerae, V. parahaemolyticus and V. vulnificus in seafood using real time PCR.

Detection of Vibrio cholerae, V. parahaemolyticus and V. vulnificus in seafood using real time PCR.

Detection of Vibrio cholerae, V. Parahaemolyticus and V. Vulnificus in seafood using real time PCR C. Lemaire 1 , A. Darcis 1 , B. China 2 , G. Daube 1 1 Food Microbiology, Faculty of Veterinary Medicine, University of Liege, Liege, Belgium 2 Public Health Institute - Louis Pasteur, Brussels, Belgium

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FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae

FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae

1 CNRS, Centre de Ge´ne´tique Mole´culaire, UPR 2167, Gif-sur-Yvette, France, 2 Universite´ Paris-Sud, Orsay, France, 3 Universite´ Pierre et Marie Curie, Paris 6, Paris, France, 4 INRA, Unite´ des Bacte´ries Lactiques et Pathoge`nes Opportunistes, UR888, Jouy en Josas, France Abstract Unlike most bacteria, Vibrio cholerae harbors two distinct, nonhomologous circular chromosomes (chromosome I and II). Many features of chromosome II are plasmid-like, which raised questions concerning its chromosomal nature. Plasmid replication and segregation are generally not coordinated with the bacterial cell cycle, further calling into question the mechanisms ensuring the synchronous management of chromosome I and II. Maintenance of circular replicons requires the resolution of dimers created by homologous recombination events. In Escherichia coli, chromosome dimers are resolved by the addition of a crossover at a specific site, dif, by two tyrosine recombinases, XerC and XerD. The process is coordinated with cell division through the activity of a DNA translocase, FtsK. Many E. coli plasmids also use XerCD for dimer resolution. However, the process is FtsK-independent. The two chromosomes of the V. cholerae N16961 strain carry divergent dimer resolution sites, dif1 and dif2. Here, we show that V. cholerae FtsK controls the addition of a crossover at dif1 and dif2 by a common pair of Xer recombinases. In addition, we show that specific DNA motifs dictate its orientation of translocation, the distribution of these motifs on chromosome I and chromosome II supporting the idea that FtsK translocation serves to bring together the resolution sites carried by a dimer at the time of cell division. Taken together, these results suggest that the same FtsK-dependent mechanism coordinates dimer resolution with cell division for each of the two V. cholerae chromosomes. Chromosome II dimer resolution thus stands as a bona fide chromosomal process.
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Architectural transitions in Vibrio cholerae biofilms at single-cell resolution

Architectural transitions in Vibrio cholerae biofilms at single-cell resolution

confocal microscope that enables 3D imaging at high axial reso- lution with low-light doses and by combining this instrument with bespoke image analysis software, we were able to visualize and segment all individual cells in thousands of Vibrio cholerae biofilms grown on submerged glass surfaces under flow containing nutri- ents. From these data, we could construct ensemble averages of biofilm structure during every phase of growth. We discovered that the internal community architecture and global biofilm morphology undergo several distinct transitions, which manifest as changes in the relative arrangements of individual cells over the course of biofilm development. From these data, we identified four fundamental phases of biofilm growth, each characterized by its own unique architecture: 1D growth of 1–6 cells, 2D growth of 20–100 cells, 3D growth of 200–1,000 cells with low local order, and highly ordered growth of communities with more than 2,000 cells. These phases can be explained by transitions in the physical dimensionality of the particular biofilm combined with changes in local cell density. Of the three known V. cholerae matrix proteins RbmA, Bap1, and RbmC, only deletion of RbmA substantially perturbs cellular orientations and the overarching biofilm archi- tecture. We thus provide, to our knowledge, the first steps toward resolving how the 3D biofilm architecture results from the inter- actions of the constituent cells.
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Whole genome sequence of Vibrio cholerae directly from dried spotted filter paper

Whole genome sequence of Vibrio cholerae directly from dried spotted filter paper

* adebes1@jhu.edu Abstract Background Global estimates for cholera annually approximate 4 million cases worldwide with 95,000 deaths. Recent outbreaks, including Haiti and Yemen, are reminders that cholera is still a global health concern. Cholera outbreaks can rapidly induce high death tolls by overwhelm- ing the capacity of health facilities, especially in remote areas or areas of civil unrest. Recent studies demonstrated that stool specimens preserved on filter paper facilitate molecular analysis of Vibrio cholerae in resource limited settings. Specimens preserved in a rapid, low-cost, safe and sustainable manner for sequencing provides previously unavailable data about circulating cholera strains. This may ultimately contribute new information to shape public policy response on cholera control and elimination.
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L'étude des antimicrobiens comme modulateurs du système de sécrétion de type VI de vibrio cholerae

L'étude des antimicrobiens comme modulateurs du système de sécrétion de type VI de vibrio cholerae

Discussion Vibrio cholerae est une bactérie environnementale aquatique ayant la capacité de coloniser le tractus digestif de l’Homme et induire des symptômes diarrhéiques grâce à ces facteurs de virulence, aussi exprimés lorsque la bactérie est dans l’eau (Colwell et al., 1996). Le choléra est une maladie encore à ce jour classée par l’OMS comme un problème majeur de santé publique et dont le traitement le plus efficace reste la réhydratation et l’administration de sels permettant la compensation des pertes d’électrolytes et d’eau (Ali et al., 2015). Les cas sévères de choléra peuvent être traités par antibiotiques où la durée et l’intensité des symptômes seront raccourcies, ce qui permet alors une diminution de la probabilité de propagation de la maladie (Towner et al., 1980). Cependant les traitements antibiotiques induisent chez Vibrio cholerae la mise en place de mécanismes de résistance alors que la bactérie est déjà fréquemment en contact avec des molécules antimicrobiennes dans son environnement aquatique et chez son hôte (Garg et al., 2001). En effet, les eaux des rivières et les environnements aquatiques de manière générale sont aujourd’hui pollués par de petites doses en antibiotiques rejetés par les déchets médicaux et de l’agriculture (Larsson, 2014). De plus, lorsque Vibrio cholerae colonise le tractus digestif de l’Homme elle se retrouve confrontée à des doses variables en peptides antimicrobiens de système immunitaire inné et du microbiote intestinal (Destoumieux-Garzón et al., 2014). Les molécules antimicrobiennes sont, de plus; connues pour leurs capacités de modulation d’expression des gènes de virulence des pathogènes à des doses sous-létales (Romero et al., 2011). De ce fait les objectifs de ce projet ont été d’analyser la modulation que pourraient avoir certains peptides antimicrobiens d’origine bactérienne et certains antibiotiques sur un facteur de virulence particulier de Vibrio
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Case Report: Vibrio cholerae Biliary Tract Infections in Two North Africans in France

Case Report: Vibrio cholerae Biliary Tract Infections in Two North Africans in France

Abstract. The origin of a cholera outbreak may be unclear, as recently in Algeria. In two patients from North Africa, Vibrio cholerae was isolated in the context of hepatobiliary tract infections without any known outbreak. Gallbladder and asymptomatic long-term carriers might play a role in the emergence of cholera. Cholera is an acute, watery diarrheal illness caused by the bacterium Vibrio cholerae. It remains a public health issue in many parts of the world, with millions of cases and around 100,000 deaths annually. 1 The environmental niches of V. cholerae include saline coastal waters, rivers, and estuaries, often in association with crustacean zooplankton. Thus far, 210 serogroups of V. cholerae have been described, among which those secreting the cholera toxin can cause outbreaks. Vibrio cholerae serogroup O1 biotype El Tor is the cause of the current pandemic that has been ongoing since the 1960s. 1 Major out- breaks are currently ongoing, mainly in sub-Saharan Africa and in Hispaniola. 1 Serotype O139, which emerged in the 1990s and spanned most of Asia, is now rarely isolated. 1
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Theoretical assessment of the impact of climatic factors in a vibrio cholerae model

Theoretical assessment of the impact of climatic factors in a vibrio cholerae model

Keywords Mathematical model · V. Cholerae · Climatic factors · Cooperative systems · Stability 1 Introduction Vibrio Cholerae (V. Cholerae) is a Gram-negative, comma-shaped bacterium that causes cholera in humans. Cholera is an acute intestinal infection caused by the inges- tion of contaminated foods and water with V. Cholerae bacterium. There are 200 sero- groups of V. Cholerae but only the V. Cholerae O1 and O139 are responsible of epi- demics (WHO 2017 ). The etiological agent passes through and survives the gastric acid barrier of the stomach and then penetrates the mucus lining that coats the intesti- nal epithelial (Reidl and Karl Klose 2002 ). Once they colonise the intestinal gut, they produce enterotoxin (which stimulates water and electrolyte secretion by the endothe- lial cells of the small intestine) that leads to watery diarrhea. Vibrio Cholerae has been reported to be associated with a variety of living organisms, including animals with an exoskeleton of chitin, aquatic plants, protozoa, bivalves, waterbirds, as well as abiotic substrates (e.g. sediments). Most of these are well-known or putative environmental reservoirs for the bacterium, defined as places where the pathogen lives over time, with the potential to be released and to cause human infection. These bacteria are then associated with these environmental reservoirs forming commensal relationships (Huq et  al. 1984 ). In many mathematical model of cholera (Copasso and Paveri-Fontana
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Highly diverse recombining populations of Vibrio cholerae and Vibrio parahaemolyticus in French Mediterranean coastal lagoons

Highly diverse recombining populations of Vibrio cholerae and Vibrio parahaemolyticus in French Mediterranean coastal lagoons

Microbiologie, Plouzané, France, 3 Département d’Hygiène Hospitalière, Centre Hospitalier Universitaire, Montpellier, France Vibrio parahaemolyticus and Vibrio cholerae are ubiquitous to estuarine and marine environments. These two species found in Mediterranean coastal systems can induce infections in humans. Environmental isolates of V. cholerae (n = 109) and V. parahaemolyticus (n = 89) sampled at different dates, stations and water salinities were investigated for virulence genes and by a multilocus sequence-based analysis (MLSA). V. cholerae isolates were all ctxA negative and only one isolate of V. parahaemolyticus displayed trh2 gene. Most Sequence Types (ST) corresponded to unique ST isolated at one date or one station. Frequent recombination events were detected among different pathogenic species, V. parahaemolyticus, V. cholerae, Vibrio mimicus, and Vibrio metoecus. Recombination had a major impact on the diversification of lineages. The genetic diversity assessed by the number of ST/strain was higher in low salinity condition for V. parahaemolyticus and V. cholerae whereas the frequency of recombination events in V. cholerae was lower in low salinity condition. Mediterranean coastal lagoon systems housed V. cholerae and V. parahaemolyticus with genetic diversities equivalent to the worldwide diversity described so far. The presence of STs found in human infections as well as the frequency of recombination events in environmental vibrios populations could predict a potential epidemiological risk.
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Chorégraphie de ségrégation des deux chromosomes de Vibrio cholerae

Chorégraphie de ségrégation des deux chromosomes de Vibrio cholerae

dans un macrodomaine par rapport à une région non-structurée. Ce travail est en cours et grâce à un nouveau logiciel d’analyse des timelapses, sera plus aisé par rapport à une analyse avec MicrobeTracker. La chorégraphie du chromosome I semble être en partie orientée par la répli- cation. Son système de partition, qui semblait être le candidat idéal pour expliquer le positionnement de l’origine au pôle, semble n’avoir qu’un rôle d’ancrage, car une souche ∆parS ou ∆parAB se positionne et se ségrège toujours de la même façon qu’une souche sauvage, à la différence que l’origine semble moins polaire. D’ailleurs, chez E. coli, le nucléoide n’occupe qu’une partie de la cellule, et une délétion de son système MinCDE provoque la formation de mini-cellules, à cause de division aberrantes près des pôles. Chez Vibrio cholerae, une délétion du système MinCDE ne provoque aucun changement phénotypique, car le nucléoide occupe tout l’espace cellulaire et le système SlmA d’Occlusion du Nucléoide empêche la formation de l’anneau de septation sur l’ADN. Mais si la mutation ∆minCDE est couplée avec une mutation ∆parABS, des mini-cellules vont apparaitre, car le désancrage de l’origine au pôle laisse un espace libre pour que l’anneau de septation se forme près d’un pôle (données du laboratoire encore non-publiées). L’utilité du système de partition pour le chromosome I devient ainsi évidente : malgré des systèmes redondants pour éviter des divisions aberrantes, il semble indispensable pour les chromosomes de Vibrio cholerae d’occuper tout l’espace cellulaire, et l’ancrage de l’origine au pôle aide à cela. On pourrait probablement dire la même chose du système MatP/matS pour le terminus du chromosome I : chez E. coli, ce système ancre le terminus au septum jusqu’à la division. Et même si une délétion de ce système n’entraine pas de phénotype particulier (données du laboratoire non publiées), il est possible que couplée à une délétion du système MinCDE ou SlmA, il nous soit possible d’observer des mini-cellules. Ceci étant dit, il est tout à fait probable que le positionnement au pôle du terminus ne soit pas seulement dû au système MatP/matS, puisque ce positionnement est également observé chez des espèces ne possédant pas ce système. Il existe donc peut être un système redondant. Ainsi en occupant tout l’espace cellulaire, le chromosome I de Vibrio cholerae prévient des divisions aberrantes, ce qui est une façon de plus de contrôler que la ségrégation et la division soient bien coordonnées.
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Mécanisme d'intégration du phage TLC dans le génome de Vibrio cholerae

Mécanisme d'intégration du phage TLC dans le génome de Vibrio cholerae

Edited by David J. Sherratt, University of Oxford, Oxford, United Kingdom, and accepted by the Editorial Board October 7, 2014 (received for review March 5, 2014) As in most bacteria, topological problems arising from the circularity of the two Vibrio cholerae chromosomes, chrI and chrII, are resolved by the addition of a crossover at a specific site of each chromosome, dif, by two tyrosine recombinases, XerC and XerD. The reaction is under the control of a cell division protein, FtsK, which activates the formation of a Holliday Junction (HJ) intermediate by XerD catalysis that is resolved into product by XerC catalysis. Many plasmids and phages exploit Xer recombination for dimer resolution and for inte- gration, respectively. In all cases so far described, they rely on an alternative recombination pathway in which XerC catalyzes the for- mation of a HJ independently of FtsK. This is notably the case for CTX ϕ, the cholera toxin phage. Here, we show that in contrast, in- tegration of TLCϕ, a toxin-linked cryptic satellite phage that is almost always found integrated at the chrI dif site before CTXϕ, depends on the formation of a HJ by XerD catalysis, which is then resolved by XerC catalysis. The reaction nevertheless escapes the normal cellular control exerted by FtsK on XerD. In addition, we show that the same reaction promotes the excision of TLC ϕ, along with any CTXϕ copy present between dif and its left attachment site, providing a plau- sible mechanism for how chrI CTX ϕ copies can be eliminated, as occurred in the second wave of the current cholera pandemic.
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Controle de qualité externe - souche de Vibrio cholerae non toxinogène

Controle de qualité externe - souche de Vibrio cholerae non toxinogène

• Pratiquement, on recommande d’ensemencer en parallèle des milieux d’enrichissement et d’isolement. Les selles sont ensemencées sur TCBS, milieu sélectif inhibant la flore fécale et permettant la croissance des vibrions, incubé 16-18h, à 35°C, en aérobiose.
Pour l’enrichissement sélectif, l’échantillon est inoculé dans un tube d’eau peptonée alcaline (EPA), ensuite incubée 6 à 8 heures à 35°C puis repiquée sur gélose de type TCBS (prélèvement à l’öse juste sous la surface de l’EPA non agitée préalablement). Après 16-18h d’incubation sur TCBS, les colonies suspectes de Vibrio cholerae mais aussi d’autres vibrions fermentant le saccharose sont arrondies, bombées, de taille moyenne (2-4 mm), lisses et colorées en jaune. De très rares souches de Vibrio cholerae ainsi que la plupart des autres vibrions importants au plan clinique, notamment V. parahaemolyticus, ne fermentent pas le saccharose et se présentent sous forme de colonies vertes.
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Vibrio cholerae (Cholera)

Vibrio cholerae (Cholera)

dans un second temps ont été analysées les données d’hospitalisations pour lesquelles la mention d’un pathogène, sur base d’un code icd-9 spécifique, complétait le[r]

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Crystal Structure of an Integron Gene Cassette-Associated Protein from Vibrio cholerae Identifies a Cationic Drug-Binding Module

Crystal Structure of an Integron Gene Cassette-Associated Protein from Vibrio cholerae Identifies a Cationic Drug-Binding Module

We have, however, noted surface features in the Cass2 structure consistent with a protein interaction site adjacent to the active-site cavity. We propose this to comprise a potential site for interaction of the effector-binding module with a specific DNA- binding domain, so as to mimic the organisation of the multi- domain transcription regulators. This is congruent with the more general observation that two interacting prokaryotic proteins, not necessarily encoded by neighbouring genes, may be found fused as a single chain homolog in another organism [35,36,37]. Such component proteins might be engaged in either direct physical interaction or an indirect functional association [35]. Sequence searches were conducted to locate any likely companion module(s) for Cass2 in V. cholerae; no sequence homolog of the single- domain protein MarA (from E. coli) [38] was found amongst gene cassettes from the same environmental isolate as Cass2. However, wider sequence searches across published Vibrio genomes do reveal the existence of single-domain homologs (ZP_01062623.1; ZP_01976746.1) containing the helix-turn-helix motifs present in both MarA and Rob relatives.
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en
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en fr Study of the system of chromosome dimers resolution in Vibrio cholerae - Implication in the control of the lysogeny of the phage CTXφ coding for choleric toxin Etude du système de résolution des dimères de chromosome chez Vibrio cholerae - Implication dans le contrôle de la lysogénie du phage CTXφ codant pour la toxine cholérique

Figure 34. Modèle représentant les étapes clefs du cycle de vie du phage CTXφ (infection, integration, réplication, assemblage du virion et sécrétion). Schéma adapté de (Davis & Waldor, 2003). L’infection par CTXφ de V. cholerae requiert les pilis et récepteurs TCP et TolQ,R,A. Le génome simple brin (+) ssDNA de CTXφ perd ses protéines de capsides et est transféré dans le cytoplasme bactérien (a). L’ADN complémentaire du brin (+) est synthétisé pour générer pCTX, la forme réplicative double brin de CTXφ (b). La forme réplicative sert à la synthèse de nouveaux génomes simple brin (c) et permet la production des protéines phagiques (d). Les nouveaux génomes simple brin et les protéines phagiques peuvent servir à l’assemblage de nouveaux virions qui sont simultanément sécrétés à l’extérieur de la cellule par le système EpsD (e, f). La forme simple brin (+) peut également être intégrée directement au site dif du chromosome grâce aux recombinases XerC et XerD de l’hôte et à la protéine phagique RstB (g, g’). CTXφ peut être intégré seul ou en tandem avec d’autres prophages RS1 (h). Cet arrangement en tandem sert de matrice pour la production d’ADN extra-chromosomique (i). Ce processus est initié par la protéine phagique RstA. Il en résulte la formation de nouveaux génomes phagiques simple brin (+) ssDNA (j).
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Régulation de l'expression et localisation de deux diguanylate cyclases chez Vibrio Cholerae

Régulation de l'expression et localisation de deux diguanylate cyclases chez Vibrio Cholerae

Ces bandes peuvent etre le resultat d'une degradation de Mex07 ou bien de son clivage, car elles ne sont pas detectees dans le controle negatif (Figure 3 5 A). Les differentes fraction[r]

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The Dynamics of Genetic Interactions Between Vibrio metoecus and Vibrio cholerae, Two Close Relatives Co-Occurring in the Environment

The Dynamics of Genetic Interactions Between Vibrio metoecus and Vibrio cholerae, Two Close Relatives Co-Occurring in the Environment

cholerae core genome to contain 2,432 gene families based on 23 strains, a higher core genome size than we obtained at UPMC on January 29, 2016 http://gbe.oxfordjournals.org/ Download[r]

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Copper homeostasis at the host vibrio interface: lessons from intracellular vibrio transcriptomics

Copper homeostasis at the host vibrio interface: lessons from intracellular vibrio transcriptomics

Introduction Vibrios have long been considered extracellular organisms. However, an increasing number of studies show that some vibrio strains have evolved cell invasive properties. The capacity to survive in host cells was reported for vibrio strains pathogenic for humans. Examples include Vibrio cholerae, which survives in mouse cell lines (Duperthuy et al., 2010), and V. parahaemolyticus, which disrupts the intestinal epithelium (Ritchie et al., 2012) and can also invade and replicate in human HeLa cell line (Zhang et al., 2012; de Souza Santos and Orth, 2014). Interestingly, in a few animal species, such vibrio intracellular stages have been associated with diseases. For example, the coral pathogens V. shiloi (Rosenberg and Falkovitz, 2004) and V. coralliilyticus (Vidal-Dupiol et al., 2011) enter coral epithelial cells as part of their pathogenic process. Similarly, the oyster pathogen V. tasmaniensis LGP32 enters oyster immune cells, the hemocytes, and this is required for virulence in oysters (Duperthuy et al., 2011).
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