Siga este link para ver outros tipos de publicações sobre o tema: Vibrio cholerae.
Teses / dissertações sobre o tema "Vibrio cholerae"
Crie uma referência precisa em APA, MLA, Chicago, Harvard, e outros estilos
Veja os 50 melhores trabalhos (teses / dissertações) para estudos sobre o assunto "Vibrio cholerae".
Ao lado de cada fonte na lista de referências, há um botão "Adicionar à bibliografia". Clique e geraremos automaticamente a citação bibliográfica do trabalho escolhido no estilo de citação de que você precisa: APA, MLA, Harvard, Chicago, Vancouver, etc.
Você também pode baixar o texto completo da publicação científica em formato .pdf e ler o resumo do trabalho online se estiver presente nos metadados.
Veja as teses / dissertações das mais diversas áreas científicas e compile uma bibliografia correta.
1
Nygren, Erik. "A mouse model for direct evaluation of cholera vaccines /". Göteborg : Dept. of Microbiology and immunology, Institute of Biomedicine, The Sahlgrenska Academy at University of Gothenburg, 2009. http://hdl.handle.net/2077/19376.
Texto completo da fonte
2
Falklind, Jerkérus Susanna. "Vibrio cholerae O139 : identification, characterization and vaccine strategies /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-696-0/.
Texto completo da fonte
3
Le, Roux Wouter Jacobus. "Population dynamics of Vibrio cholerae in the Vaal Barrage". Pretoria : [s.n.], 2005. http://upetd.up.ac.za/thesis/available/etd-02162007-175110.
Texto completo da fonte
4
Occhino, Deborah Ann. "Vibrio cholerae iron transport : characterization of two tonB systems and components of a heme transport system /". Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
Texto completo da fonte
5
Chow, Ka-hang. "Molecular characterization of RTX toxin of vibrio cholerae causing epidemics". Click to view the E-thesis via HKUTO, 2001. http://sunzi.lib.hku.hk/hkuto/record/B42575898.
Texto completo da fonte
6
Lee, Jason J. "Neutrophil responses to Vibrio cholerae autoinducer-1 and structural analogues". Thesis, Griffith University, 2021. http://hdl.handle.net/10072/404172.
Texto completo da fonteResumo:
Vibrio cholerae is a pathogen responsible for cholera, an infectious disease that usually manifests as severe diarrhea. V. cholerae cells can regulate population-wide gene expression changes in a density-dependent manner, in a process known as quorum sensing (QS). QS involves communication between bacterial cells using secreted signalling molecules. V. cholerae autoinducer-1 (CAI-1) is the dominant signalling molecule in the V. cholerae QS circuit and has roles in regulating biofilm formation/degradation and expression of virulence genes.
Interactions between bacterial-produced QS molecules and eukaryotic cells have been documented. This is known as interkingdom or cross-kingdom signalling. CAI-1 has been reported to act as a chemoattractant for the nematode, Caenorhabditis elegans which feeds on V. cholerae cells as a food source. Legionella autoinducer-1 (LAI-1), which is structurally similar to CAI-1, is a signalling molecule produced by Legionella pneumophila. LAI-1 has been reported to impede the migration of Dictyostelium discoideum amoebae and macrophage-like RAW 264.7 cells, and has also been shown to destabilise the cytoskeleton of RAW 264.7 cells. Structural analogues of CAI-1 with more potent activity within the V. cholerae QS circuit have been developed as potential novel therapeutics against cholera. These QS agonists would force the bacterial cells to express high cell density behaviours, impairing colonisation and promoting detachment, therefore reducing pathogenesis.
These previous findings led to the hypothesis that CAI-1 and structural analogues may have immunomodulatory effects on host cells during V. cholerae infection, particularly recruited immune cells which may be exposed to CAI-1 during cholera. There are several lines of evidence the neutrophil recruitment is prominent during cholera and that these granular leukocytes play a role in controlling infection.
Thus, the key aims of this study were to characterise interactions between CAI-1, as well as structural analogues of CAI-1, and neutrophils. In vitro HL-60 cell culture revealed an upregulation of CD11b expression when cells were differentiated with DMSO in the presence of CAI-1. This increased differentiation marker expression was at the expense of both cell viability and total cell count. Additionally, two 3-acyl pyrrole analogues of CAI-1 also increased CD11b expression greater than CAI-1, when cells were differentiated with DMSO in the presence of either analogue. Again, this resulted in significantly reduced cell viability and total cell count, although at similar levels to CAI-1. HL-60 cells differentiated in the presence of CAI-1 or either analogue were generally more granular than cells differentiated with DMSO alone.
The effects of CAI-1 and structural analogues on neutrophil effector functions were assessed, namely chemotaxis and oxidative burst. CAI-1 did not act as a chemoattractant for DMSO-differentiated HL-60 cells, nor did it reduce or enhance migration towards fMLP, a known chemoattractant. Pre-treatment of differentiated HL-60 cells with CAI-1 or one of the 3-acyl pyrrole analogues for 3 h resulted in decreased reactive oxygen species production. However, concomitant reduction in cell viability was observed over 3 h.
Preliminary experiments assessed the effect of CAI-1 on primary human neutrophils. Isolated neutrophils appeared larger and less round with CAI-1 treatment. In contrast, CAI-1 treatment of whole blood resulted in apparent reductions in cell size as assessed by flow cytometry. Expression of activation markers (CD11b, CD64, CD66b) on granulocytes in whole blood appeared unaffected by CAI-1.
Overall, the results within this study shed light onto the cross-kingdom interactions that may exist between host cells and bacterial signalling molecules. Identifying these interactions may lead to a deeper understanding of additional mechanisms that may be involved in V. cholerae pathogenesis. Additionally, these interactions may be important in revealing off-target effects that developing novel therapies, which interfere with bacterial QS, may have on host cells.
These data highlight an advance that reveals many opportunities for further investigations surrounding host-microbe interactions.Thesis (Masters)
Master of Medical Research (MMedRes)
School of Medical Science
Griffith Health
Full Text
7
Moore, Sandra. "Dynamics of cholera epidemics in Haiti and Africa". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5505/document.
Texto completo da fonteResumo:
Le cholera est une maladie diarrhéique aiguë due à la consommation d’eau ou d’aliments contaminés par des souches toxigéniques de Vibrio cholerae. Selon le “paradigme du choléra”, la maladie est provoquée par une exposition à un réservoir environnemental de V. cholerae avec des épidémies directement modulées par des facteurs environnementaux. Cependant, comme divers arguments plaident contre ce dogme, nous avons voulu élucider les mécanismes de la dynamique des épidémies de cholera dans trois foyers situés en Haïti, en République Démocratique du Congo (RDC) et en Afrique de l’Ouest. Nous avons associé une analyse temporo-spatiale des épidémies à une étude génétique des isolats de V. cholerae. En Haïti, nous avons cherché à savoir si les épidémies actuelles étaient dues à des souches toxigéniques de V. cholerae O1 durablement implantées dans l’environnement aquatique. En Afrique de l’Ouest, notre étude a révélé qu’Accra, la capitale du Ghana, était le principal foyer de choléra pour l’ensemble des pays d’Afrique de l’Ouest situés à l’Ouest du Nigeria. Le réseau d’eau d’Accra a probablement joué un rôle dans la propagation rapide de V. cholerae vers la majorité des quartiers de la ville. Les épidémies de choléra ont diffusé vers les autres pays sous la forme de vagues épidémiques et plusieurs épidémies ont été liées à la migration de populations à risque comme certains pêcheurs. En conclusion, notre réflexion globale sur les épidémies de choléra dans ces trois foyers distincts nous donne une vision cohérente des mécanismes d’émergence et de diffusion du choléraCholera is an acute diarrheal disease caused by consumption of water or food contaminated with toxigenic Vibrio cholerae. According to the "cholera paradigm", the disease is contracted by exposure to environmental reservoirs of V. cholerae, with outbreaks driven directly by climatic factors. However, as recent findings argue against this dogma, we aimed to elucidate the dynamics of cholera outbreaks in three global foci: Haiti, Democratic Republic of the Congo (DRC) and West Africa. We combined spatiotemporal analysis of epidemics with genetic assessment of V. cholerae isolates. In Haiti, we assessed whether outbreak re-emergence during the rainy season was due to toxigenic V. cholerae O1 strains that have settled into the aquatic environment. Instead, we found that the re-emergence of outbreaks was likely due to persisting outbreaks during the dry season that were insufficiently controlled, rather than an environmental reservoir of V. cholerae O1. In West Africa, our study revealed that Accra, Ghana was the hotspot of cholera in the entire region of West Africa, west of Nigeria. The Accra water network likely played a role in rapid diffusion of V. cholerae throughout the city. Cholera outbreaks spread from Accra into other countries in a wave-like fashion. Distinct outbreaks were linked via migration of at-risk populations, such as certain fishermen. In conclusion, our global reflection of cholera epidemics in these three distinct foci provides a coherent vision of the mechanisms of cholera emergence and diffusion
8
Mann, Maretta Clare, e n/a. "Sialylmimetics as Potential Inhibitors fo Vibrio Cholerae Sialidase". Griffith University. Institute for Glycomics, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061006.083947.
Texto completo da fonteResumo:
Cholera is an epidemic infectious diarrhoeal disease that for centuries has proven its frightening ability to cause rapid and widespread loss of human life. All symptoms associated with cholera are a result of rapid dehydration due to infection by pathogenic strains of the bacterium Vibrio cholerae. The damaging effects associated with cholera are mainly attributed to the toxin, which is secreted by the bacterium and infects cells lining the gastrointestinal tract. A sialidase, also secreted by the bacterium, is believed to facilitate toxin uptake by the gastrointestinal epithelium. V. cholerae sialidase is therefore a potential target for therapeutic intervention. A survey of the literature reveals that sialidases from different species share common features with respect to their structure, substrate specificity and catalytic mechanism. The unsaturated sialic acid, Neu5Ac2en, inhibits most exosialidases with a dissociation constant of inhibitor of -10-4 to-10-6 M and has frequently been used as a template in the design of more potent sialidase inhibitors. In the case of V. cholerae sialidase, there have been no inhibitors reported to date that are significantly more potent than Neu5Ac2en itself The present research aimed to develop a range of mimics of Neu5Ac2en, which contain various substituents to replace the C-6 glycerol side chain, as potential inhibitors of V cholerae sialidase. The x-ray crystal structure of V cholerae sialidase was used to explore potential interactions between active site residues and C-6 modified Neu5Ac2en mimetics of known inhibitory potency. Opportunities for interactions within the glycerol side chain pocket in the active site of V cholerae sialidase are discussed. A novel synthetic strategy was developed for the synthesis of a series of glucuronidebased Neu5Ac2en mimetics starting from readily available GIcNAc. This approach was employed for the preparation of Neu5Ac2en mimetics that contained an ether or thioether substituent as replacement of the glycerol side chain of Neu5Ac2en. Progress was also made towards the synthesis of a series of C-6 acylamino Neu5Ac2en mimetics. Analysis by 1H NMR spectroscopy showed that the acylamino derivatives adopted a half-chair conformation that was similar to the conformation of Neu5Ac2en but different to the conformation adopted by the ether and thioether derivatives prepared. The inhibitory activity of the C-6 ether and thioether Neu5Ac2en mimetics prepared was evaluated in vitro using an enzyme assay. It was found that most of the derivatives inhibited V. cholerae sialidase with a K1 of approximately 1O-4 M. The derivatives containing a hydrophobic side chain were found to be slightly more potent compared to derivatives with more hydrophilic side chains. A more detailed study of binding interactions between the C-6 thioether Neu5Ac2en mimetics and V cholerae sialdiase was carried out using STD 1H NMR spectroscopy and computational molecular modelling.
9
Mann, Maretta Clare. "Sialylmimetics as Potential Inhibitors fo Vibrio Cholerae Sialidase". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/367187.
Texto completo da fonteResumo:
Cholera is an epidemic infectious diarrhoeal disease that for centuries has proven its frightening ability to cause rapid and widespread loss of human life. All symptoms associated with cholera are a result of rapid dehydration due to infection by pathogenic strains of the bacterium Vibrio cholerae. The damaging effects associated with cholera are mainly attributed to the toxin, which is secreted by the bacterium and infects cells lining the gastrointestinal tract. A sialidase, also secreted by the bacterium, is believed to facilitate toxin uptake by the gastrointestinal epithelium. V. cholerae sialidase is therefore a potential target for therapeutic intervention. A survey of the literature reveals that sialidases from different species share common features with respect to their structure, substrate specificity and catalytic mechanism. The unsaturated sialic acid, Neu5Ac2en, inhibits most exosialidases with a dissociation constant of inhibitor of -10-4 to-10-6 M and has frequently been used as a template in the design of more potent sialidase inhibitors. In the case of V. cholerae sialidase, there have been no inhibitors reported to date that are significantly more potent than Neu5Ac2en itself The present research aimed to develop a range of mimics of Neu5Ac2en, which contain various substituents to replace the C-6 glycerol side chain, as potential inhibitors of V cholerae sialidase. The x-ray crystal structure of V cholerae sialidase was used to explore potential interactions between active site residues and C-6 modified Neu5Ac2en mimetics of known inhibitory potency. Opportunities for interactions within the glycerol side chain pocket in the active site of V cholerae sialidase are discussed. A novel synthetic strategy was developed for the synthesis of a series of glucuronidebased Neu5Ac2en mimetics starting from readily available GIcNAc. This approach was employed for the preparation of Neu5Ac2en mimetics that contained an ether or thioether substituent as replacement of the glycerol side chain of Neu5Ac2en. Progress was also made towards the synthesis of a series of C-6 acylamino Neu5Ac2en mimetics. Analysis by 1H NMR spectroscopy showed that the acylamino derivatives adopted a half-chair conformation that was similar to the conformation of Neu5Ac2en but different to the conformation adopted by the ether and thioether derivatives prepared. The inhibitory activity of the C-6 ether and thioether Neu5Ac2en mimetics prepared was evaluated in vitro using an enzyme assay. It was found that most of the derivatives inhibited V. cholerae sialidase with a K1 of approximately 1O-4 M. The derivatives containing a hydrophobic side chain were found to be slightly more potent compared to derivatives with more hydrophilic side chains. A more detailed study of binding interactions between the C-6 thioether Neu5Ac2en mimetics and V cholerae sialdiase was carried out using STD 1H NMR spectroscopy and computational molecular modelling.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Full Text
10
Zo, Young-Gun. "Phylogenomic and structural analyses of Vibrio cholerae populations and endemic cholera". College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/3090.
Texto completo da fonteResumo:
Thesis (Ph. D.) -- University of Maryland, College Park, 2005.Thesis research directed by: Marine-Estuarine-Environmental Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
11
Guidolin, Angelo. "Molecular biology of "Vibrio cholerae" bacteriophage CP-T1 and its host interactions". Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phg948.pdf.
Texto completo da fonte
12
Cofie, Daniel Quarcoopome Guthrie Rufus K. "Effect of chitin on Vibrio cholerae /". See options below, 1988. http://proquest.umi.com/pqdweb?did=746612041&sid=1&Fmt=2&clientId=68716&RQT=309&VName=PQD.
Texto completo da fonte
13
Stroher, Vive Horst. "Serotype conversion in Vibrio cholerae 01 /". Title page, contents and abstract only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phs919.pdf.
Texto completo da fonte
14
Jahan, Nasrin. "Structural studies of Vibrio cholerae quorum sensing proteins". Thesis, University of St Andrews, 2011. http://hdl.handle.net/10023/2565.
Texto completo da fonteResumo:
The spread of cholera is always associated with contaminated food or water and this is the reason this disease has been endemic in developing countries for centuries due to their lack of proper sanitation facilities and poor or no infrastructure for sewage systems. Cholera can spread quickly and sporadically after any natural disaster that destroys the sewage system or safe drinking water supply of both developed and undeveloped countries. In Southeast Asia in December 2004 and in Pakistan and Haiti 2010, cholera outbreaks followed the natural disasters; with most of the cholera victims being children. Although it is known that the best way to prevent cholera outbreak is the development of the infrastructure, provision of a safe drinking water supply and proper sanitation, this is a very long-term process, and most of the developing countries cannot afford such improvements. These situations can be made worse by natural disasters. Therefore there is a pressing need for the development of a cholera vaccine and there have been numerous research projects working towards this end for several decades. A few of them have been successful to date but because of the severe side effects and narrow range of protection, more effective and wider range vaccine development is still ongoing. In this study, crystallographic and enzymatic studies have been carried out on several novel proteins involved in the control of the production of the factors required for quorum sensing. Quorum sensing is a process in which bacterial cells communicate among themselves by the synthesis, release and detection of small chemical compounds called autoinducers. In this work, structural analysis was carried out on proteins involved in the synthesis and detection of the major autoinducer of Vibrio cholerae, named CAI-1. The crystal structure of CqsA involved in CAI-1 synthesis has been successfully solved and its enzymatic properties have been characterized. The structure of one domain of the cytoplasmic region of the CAI-1 receptor CqsS was also elucidated, and other domains were expressed. The crystal structure of another enzyme (VCA0859, an aldo-keto reductase) thought to have been involved in the synthesis of CAI-1 was also determined. Another protein named VCA0939 was also studied, due to its importance in biofilm development, and its ability to control quorum-sensing in an alternative pathway in the mutated version of pathogenic strains of V. cholerae that were responsible for the seventh cholera pandemic. The aim of this project was to understand the three dimensional structure of some proteins that are involved in quorum sensing and control of the expression of virulence genes for the pathogenesis of V. cholerae. Understanding the three dimensional structure of the proteins and the mode of autoinducer binding to its specific receptor could be highly valuable in the development of a chemical compound that could lead to the discovery of a novel drug with the ability to target cross species specification.
15
Chow, Ka-hang, e 周嘉恆. "Molecular characterization of RTX toxin of vibrio cholerae causing epidemics". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B42575898.
Texto completo da fonte
16
Purins, Leanne Roslyn. "Molecular characterisation of the transcriptional activator, HLYU, of Vibrio cholerae O1 /". Title page, abstract and table of contents only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09php9857.pdf.
Texto completo da fonteResumo:
Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Science , Discipline of Microbiology and Immunology, 2005."May, 2004" Includes corrigenda. includes bibliographical references (leaves 118-156).
17
Bougoudogo, Fiabou. "Contribution à l'étude de l'immunité protectrice contre le choléra : rôle des anticorps vibriocides reconnaissant le polysaccharide spécifique du lipopolysaccharide de "Vibrio cholerae" O:1". Paris 11, 1994. http://www.theses.fr/1994PA114831.
Texto completo da fonte
18
Sheikh, Md Arif. "Structural biology of Vibrio cholerae pathogenicity factors". Thesis, St Andrews, 2009. http://hdl.handle.net/10023/696.
Texto completo da fonte
19
Focareta, Tony. "The extracellular DNase(s) of vibrio cholerae /". Title page, abstract and table of contents only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09phf652.pdf.
Texto completo da fonte
20
Sharma, Dharam Pal. "Non-lipopolysaccharide protective antigens of Vibrio cholerae /". Title page, abstract and contents only, 1990. http://web4.library.adelaide.edu.au/theses/09PH/09phs5314.pdf.
Texto completo da fonte
21
Findlay, Gordon. "Biogenesis of virulence factors in Vibrio cholerae". Thesis, University of Kent, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294636.
Texto completo da fonte
22
Berg, Thorsten. "Virulenzregulationskaskade und Chitobiose-Metabolismus in Vibrio cholerae". Doctoral thesis, kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2829/.
Texto completo da fonte
23
Ogierman, Monica A. "Molecular characterisation of the fungus Corynespora cassicola /". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09pho344.pdf.
Texto completo da fonte
24
Mutreja, Ankur. "The origins and evolution of Vibro cholerae O1 E1 Tor". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648490.
Texto completo da fonte
25
Edwin, Aaron. "Structural and functional studies of the secreted metalloprotease PrtV from Vibrio cholerae". Doctoral thesis, Umeå universitet, Kemiska institutionen, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-84553.
Texto completo da fonteResumo:
Cholera, an acute diarrheal diseases caused by the intestinal infection of the pathogenic bacterium Vibrio cholerae, continues to be a global killer in the world today. PrtV, a secreted zinc metalloprotease, is a potent cytotoxic virulence factor of V. cholerae. The 102 kDa full length multi-domain PrtV protein undergoes several N and C terminal modifications before being secreted as a 81 kDa pro-protein. The activation of the pro-protein is calcium dependent. The removal of calcium triggers auto-proteolysis to give a stable active protease with the catalytic zinc binding domain. The aim of the thesis was to study the structure and function of the PrtV protein. The results from paper I, identified the end product of the maturation of PrtV as the stable 37 kDa M6 active domain, and not a 55 kDa complex as reported earlier. Results also showed the this 37 kDa active M6 domain alone was sufficient for catalytic activity. A revised model for the maturation of PrtV was proposed. Individual domains were isolated from the PrtV protein by domain phasing methods. This included the N-terminal domain (residues 23-103), the PKD1 domain (residues 755-839), and a 25 kDa fragment (residues 589-839). The isolated domains were recombinantly over expressed as fusion proteins to increase expression and solubility. The PKD1 domain was purified to homogeneity and crystallized. The structure of the PKD1 domain reported in paper II, was solved by X-ray crystallography at an atomic resolution of 1.1 Å. From the structure, a previously unknown calcium binding site was identified at the N-terminal of the PKD1 domain. The structure also revealed two conformations for the PKD1 domain depending on free or bound calcium. From the structure, a function of the PKD1 domain as a protector of the cleavage site in the linker region between the M6 domain and the PKD1 domain in the presence of calcium was elucidated. A new model for the activation of PrtV was given. In paper III, the structure of the N-terminal domain solved by NMR spectroscopy was reported. The structure revealed two well defined helices but a third predicted helix was found to be unstructured.
26
Wennberg, Aina Charlotte. "PCR-detection of Vibrio cholerae in ballast water". Thesis, Norwegian University of Science and Technology, Department of Biotechnology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-6883.
Texto completo da fonte
27
Lindmark, Barbro. "Modulators of Vibrio cholerae predator interaction and virulence". Doctoral thesis, Umeå universitet, Molekylärbiologi (Medicinska fakulteten), 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-30211.
Texto completo da fonteResumo:
Vibrio cholerae, the causal agent of cholera typically encodes two critical virulence factors: cholera toxin (CT), which is primarily responsible for the diarrhoeal purge, and toxin-co-regulated pilus (TCP), an essential colonisation factor. Nontoxigenic strains expressing TCP can efficiently acquire the CT gene through lysogenic conversion with CTXΦ, a filamentous phage that encodes CT and uses TCP as a receptor. V. cholerae is a Gram-negative bacterium and a natural inhabitant of estuarine and coastal waters throughout both temperate and tropical regions of the world. In the aquatic environment, V. cholerae encounters several environmental stresses, such as change in salinity, UV stress, nutrient limitation, temperature fluctuations, viral infections and protozoan predation. To fully understand the pathogenic and virulence potential of V. cholerae, knowledge is required of its interactions with, not only human, but also environmental factors. By using the nematode Caenorhabditis elegans as host model, we were able to identify a previously uncharacterised protein, the extracellular protease PrtV. PrtV was shown to be required for the killing of. elegans and also necessary for survival from grazing by the ciliate Tetrahymena pyriformis and the flagellate Cafeteria roenbergensis. The PrtV protein, which belongs to a M6 family of metallopeptidases was cloned and purified for further characterisations. The purified PrtV was cytotoxic against the human intestinal cell line HCT8. By using human blood plasma, fibrinogen, fibronectin and plasminogen were identified as candidate substrates for the PrtV protease. Outer membrane vesicles (OMVs) are released to the surroundings by most Gram-negative bacteria through “bulging and pinching” of the outer membrane. OMVs have been shown to contain many virulence factors important in pathogenesis. Therefore, we investigated the association of PrtV with OMVs. PrtV was not associated with OMVs from the wild type O1 strain. In contrast, in an LPS mutant lacking two sugar chains in the core oligosaccharide PrtV was found to be associated with the OMVs. The OMV-associated PrtV was shown to be proteolytically and cytotoxically active. V. cholerae strains are grouped into >200 serogroups. Only the O1 and O139 serogroups have been associated with pandemic cholera, a severe diarrhoeal disease. All other serogroups are collectively referred to as non-O1 non-O139 V. cholerae. Non-O1 non-O139 V. cholerae can cause gastroenteritis and extraintestinal infections, but unlike O1 and O139 strains of V. cholerae, little is known about the virulence gene content and their potential to become human pathogens. We analysed clinical and environmental non-O1 non-O139 isolates for their putative virulence traits. None of them carry the genes encoding CT or the TCP, but other putative virulence factors were present in these isolates. The incidence of serum resistance was found to vary considerably and was independent of encapsulation. Three strains were strongly serum-resistant, and these same strains could also kill C. elegans.
28
Saul-McBeth, Jessica. "Characterization of SipA, A Protein Important for Stress Responses in Vibrio cholerae". University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1544540466901883.
Texto completo da fonte
29
Ha, Thi Quyen, e Duy Khang Dinh. "The changes in antigenic components of Vibrio cholerae strains isolated in Vietnam". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-190840.
Texto completo da fonteResumo:
Whole cells of Vibrio cholerare serotype Inaba and serotype Ogawa (strains I389 and O395) were injected into rabbits to obtain antiserum. The antiserums were used for immune reaction with antigenic components of 25 strains of V.cholerae isolated from five provinces of Vietnam and the two standard strains I389 and O395 by Western-blot technique. Analysis of immune hybrid results showed that there were 11 antigenic components with molecular weights approximately 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa and 20kDa. In which the antigens of 45kDa, 42kDa, 31kDa and 20kDa were similar to OmpT, OmpS, Omp-31kDa and TcpA that have been considered as vaccine-candidate antigens. Among 25 V.cholerae strains, there were 6 antigenic components in common including 79kDa, 62kDa, 45kDa, 35kDa, 31kDa and 20kDa. 23/25 strains contained 42kDa antigen; 5/25 strains contained 38kDa and 23kDa antigens; 11/25 had 26kDa antigen. In addition, 7/25 strains contained antigens identical to V.cholerae I389 serotype Inaba; 6/25 strains contained antigens of I389 and O395; 12/25 strains had changes of antigenic components. These changes were actually the lack of antigens, not appearing new antigens. These results are considered as basis for researches about immune response and prevention of cholera diseaseToàn bộ tế bào của các chủng Vibrio cholerare typ huyết thanh Inaba và typ huyết thanh Ogawa (chủng I389 và O395) được sử dụng để gây miễn dịch trên thỏ để thu kháng huyết thanh. Các kháng huyết thanh được dùng để thực hiện phản ứng miễn dịch với các thành phần kháng nguyên của 25 chủng V.cholerae phân lập từ 5 tỉnh thành của Việt Nam và hai chủng chuẩn I389 và O395 bằng kỹ thuật Western-blot. Phân tích kết quả lai miễn dịch cho thấy, có tổng số 11 thành phần kháng nguyên có kích thước khoảng 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa và 20kDa. Các kháng nguyên này chủ yếu là các protein màng ngoài (Omp) và kháng nguyên lông (TcpA). Trong đó các kháng nguyên 45kDa, 42kDa, 31kDa và 20kDa trùng với các kháng nguyên OmpS, OmpT, Omp-31kDa và TcpA được xem là những kháng nguyên dự tuyển vacxin tả. Có 6 kháng nguyên chung giữa 25 chủng với kích thước 79kDa, 62kDa, 45kDa, 35kDa, 31kDa và 20kDa. 7/25 chủng có các kháng nguyên giống với kháng nguyên của chủng V. cholerae I389 typ huyết thanh Inaba; 6/25 chủng có các kháng nguyên giống với kháng nguyên của cả hai chủng V.cholerae I389 và O395; 12/25 chủng có sự biến đổi thành phần kháng nguyên. Tuy nhiên, sự biến đổi này thực chất là sự thiếu hụt chứ không phải là sự xuất hiện các thành phần kháng nguyên mới. Các kết quả nghiên cứu này có thể được xem là nền tảng ban đầu cho các nghiên cứu về miễn dịch và dự phòng bệnh tả
30
Midonet, Caroline. "Mécanisme d'intégration du phage TLC dans le génome de Vibrio cholerae". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS314/document.
Texto completo da fonteResumo:
La plupart des bactéries ont un unique chromosome circulaire. Lors de la réplication de l’ADN, la circularité lie topologiquement les deux chromatides sœurs résultant de la réplication (caténanes et dimères). Ces liens topologiques doivent être résolus afin de permettre une bonne ségrégation de l’information génétique entre les deux cellules filles au cours de la division cellulaire. Les bactéries possèdent une machinerie très conservée: les recombinases à tyrosines XerC et XerD, capables de résoudre les dimères et une partie des caténanes, en catalysant un crossover au site spécifique dif situé dans la région Ter du chromosome. Lors de ce processus elles réalisent successivement deux échanges de brins. La réaction Xer est spatio-temporellement contrôlée par une protéine du divisome: FtsK. FtsK est une translocase qui pompe l’ADN à travers le septum de division. Lorsqu’elle rencontre une synapse constituée de deux sites dif chargés de XerC et XerD, elle active la catalyse de XerD pour initier le premier échange de brins. Dans un second temps XerC catalyse un second échange de brins indépendamment de FtsK. A ce jour le mécanisme d’activation de XerD n’est pas bien compris. Certains éléments mobiles résolvent leur états multimériques (tels que les plasmides) ou intègrent leur génome dans celui de leur hôte en détournant les recombinases XerCD. On parle d’IMEXs (integrative Mobile Element using Xer). Les éléments mobiles étudiés avant ma thèse utilisaient tous des voies de recombinaison initiées par la catalyse de XerC et ne nécessitant pas l’activation de XerD. Au cours de ma thèse j’ai étudié dans un premier temps le mécanisme d’intégration / excision d’une nouvelle classe d’IMEXs en utilisant comme modèle le phage TLCphi de Vibrio cholerae, la bactérie responsable du choléra. Par des approches de génétique j’ai démontré que TLCphi utilise une voie de recombinaison initiée par la catalyse de XerD et indépendante de FtsK. Mes travaux ont également montré que l’excision du phage participe à l’évolution des souches pandémiques de V.cholerae. Dans une seconde partie, j’ai identifié un facteur phagique qui permet à TLCphi de contourner le contrôle de FtsK sur l’activation de XerD. Ce facteur était une protéine de fonction inconnue présentant un domaine HTH et un domaine DUF3653. Ce dernier est retrouvé dans de nombreux IMEXs. Par des approches de biologie moléculaire j’ai étudié le mécanisme d’action de cette protéine. J’ai reproduit la réaction de recombinaison in vitro et démontré qu’elle active XerD en interagissant directement avec elle. Enfin dans un troisième temps, nous nous sommes intéressés aux disparités observées entre la recombinaison Xer chez E.coli et V.cholerae. En particulier, la recombinaison Xer semble agir seulement sur les dimères chez E.coli alors qu’elle est active également sur les monomères chez V.cholerae. Nous avons démontré que ces divergences de comportement ne viennent pas des Xer elles-mêmes, ni de leurs propriétés d'activations par FtsK. Elles résultent des différentes chorégraphies de ségrégation des chromosomes entre ces deux bactéries et dépendent également des vitesses de croissanceMost of bacteria have a single circular chromosome. During replication of DNA, this circularity can lead to two sister chromatids topologically linked (catenanes and dimers). These topological links have to be solved in order to allow good segregation of genetic information between the two daughter cells during cell division. Bacteria possess a highly conserved machinery: the tyrosine recombinases XerC XerD that are capable to resolve dimers and some catenanes, by catalyzing a crossover at the specific site dif located in the Ter region of the chromosome. During this process they realize two sequentialstrand exchanges.The Xer reaction is spatiotemporally controlled by a protein of the divisome: FtsK. FtsK is a pump that translocates DNA through the septum of division. When FtsK meets a synapse that consists of two dif loaded by XerC and XerD, it activates XerD catalysis that initiates first strand exchange. Secondly XerC catalyzes a second strand exchange independently of FtsK. To date the activation mechanism of XerD is not well understood. Some mobile elements solve their multimeric states (like plasmids) or integrate their genome into the chromosome of their host by using XerCD recombinases. Such integrative elements are named IMEXs (Integrative Mobile Element using Xer). The mobile elements studied before my thesis all used recombination pathways initiated by catalysis of XerC and not requiring activation of XerD .During my PhD I studied at first the integration mechanism / excision of a new class IMEXs using as a model the TLC phage Vibrio cholerae, the bacterium responsible for cholera. By genetic approaches I demonstrated that TLCphi uses a recombination pathway initiated by XerD catalysis and independently of FtsK. My work has also shown that the phage excision participates in the evolution of pandemic strains of V. cholerae. In the second part, I identified a phage factor that allows TLC to bypass the activation of XerD by FtsK. This factor was a protein of unknown function with a HTH domain and a DUF3653 domain. DUF3653 are found in many IMEXs. Using molecular biology approaches, I studied the mechanism of action of this protein. I reproduced the recombination reaction in vitro and demonstrated that this factor activates XerD by directly interacting with it. Finally, we were interested to study disparities between Xer recombination in E.coli and V.cholerae. In particular, the Xer recombination seems to act only on dimers in E.coli while it is also active on monomers in V.cholerae. We have demonstrated that these differences in behaviors do not come from Xer themselves or their activation by FtsK. They result from different choreographies of chromosome segregation between these two bacteria and are also dependent on growth rates
31
Yam, Wing-cheong. "Molecular epidemiology of enterotoxigenic escherichia coli and vibrio cholerae in Hong Kong /". [Hong Kong : University of Hong Kong], 1990. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12966381.
Texto completo da fonte
32
Ha, Thi Quyen, e Duy Khang Dinh. "The changes in antigenic components of Vibrio cholerae strains isolated in Vietnam: Research article". Technische Universität Dresden, 2014. https://tud.qucosa.de/id/qucosa%3A29114.
Texto completo da fonteResumo:
Whole cells of Vibrio cholerare serotype Inaba and serotype Ogawa (strains I389 and O395) were injected into rabbits to obtain antiserum. The antiserums were used for immune reaction with antigenic components of 25 strains of V.cholerae isolated from five provinces of Vietnam and the two standard strains I389 and O395 by Western-blot technique. Analysis of immune hybrid results showed that there were 11 antigenic components with molecular weights approximately 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa and 20kDa. In which the antigens of 45kDa, 42kDa, 31kDa and 20kDa were similar to OmpT, OmpS, Omp-31kDa and TcpA that have been considered as vaccine-candidate antigens. Among 25 V.cholerae strains, there were 6 antigenic components in common including 79kDa, 62kDa, 45kDa, 35kDa, 31kDa and 20kDa. 23/25 strains contained 42kDa antigen; 5/25 strains contained 38kDa and 23kDa antigens; 11/25 had 26kDa antigen. In addition, 7/25 strains contained antigens identical to V.cholerae I389 serotype Inaba; 6/25 strains contained antigens of I389 and O395; 12/25 strains had changes of antigenic components. These changes were actually the lack of antigens, not appearing new antigens. These results are considered as basis for researches about immune response and prevention of cholera disease.Toàn bộ tế bào của các chủng Vibrio cholerare typ huyết thanh Inaba và typ huyết thanh Ogawa (chủng I389 và O395) được sử dụng để gây miễn dịch trên thỏ để thu kháng huyết thanh. Các kháng huyết thanh được dùng để thực hiện phản ứng miễn dịch với các thành phần kháng nguyên của 25 chủng V.cholerae phân lập từ 5 tỉnh thành của Việt Nam và hai chủng chuẩn I389 và O395 bằng kỹ thuật Western-blot. Phân tích kết quả lai miễn dịch cho thấy, có tổng số 11 thành phần kháng nguyên có kích thước khoảng 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa và 20kDa. Các kháng nguyên này chủ yếu là các protein màng ngoài (Omp) và kháng nguyên lông (TcpA). Trong đó các kháng nguyên 45kDa, 42kDa, 31kDa và 20kDa trùng với các kháng nguyên OmpS, OmpT, Omp-31kDa và TcpA được xem là những kháng nguyên dự tuyển vacxin tả. Có 6 kháng nguyên chung giữa 25 chủng với kích thước 79kDa, 62kDa, 45kDa, 35kDa, 31kDa và 20kDa. 7/25 chủng có các kháng nguyên giống với kháng nguyên của chủng V. cholerae I389 typ huyết thanh Inaba; 6/25 chủng có các kháng nguyên giống với kháng nguyên của cả hai chủng V.cholerae I389 và O395; 12/25 chủng có sự biến đổi thành phần kháng nguyên. Tuy nhiên, sự biến đổi này thực chất là sự thiếu hụt chứ không phải là sự xuất hiện các thành phần kháng nguyên mới. Các kết quả nghiên cứu này có thể được xem là nền tảng ban đầu cho các nghiên cứu về miễn dịch và dự phòng bệnh tả.
33
David, Ariane. "Chorégraphie de ségrégation des deux chromosomes de Vibrio cholerae". Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-00921394.
Texto completo da fonteResumo:
L'objectif de cette thèse est de définir la chorégraphie de ségrégation des deux chromosomes circulaires de Vibrio cholerae, c'est à dire le positionnement de l'information génétique au cours de la croissance de la cellule, ainsi que les mécanismes dirigeant ces ségrégations. Il a longtemps été supposé que les bactéries étaient trop petites pour avoir une organisation intra-cellulaire, et le manque de techniques appropriées ne permettait pas d'infirmer cette hypothèse. Or la taille des chromosomes comparée à celle de la bactérie impose une compaction et aujourd'hui, de nouvelles techniques de microscopie et d'analyse génétique permettent d'affirmer que les chromosomes bactériens étudiés jusqu'à maintenant ont tous une organisation et une chorégraphie de ségrégation précises et différentes selon les espèces. Toutes les espèces étudiées à ce jour ont un chromosome circulaire unique : la réplication du chromosome commence à une origine unique bidirectionnelle, les deux fourches de réplication se déplacent le long des deux bras de réplication (ou réplichores) et finissent la réplication au terminus, diamétralement à l'opposée de l'origine de réplication sur la carte du chromosome. Peu d'espèces ont été étudiées, et Vibrio cholerae émerge progressivement comme un nouveau modèle : son génome est réparti sur deux chromosomes, et la chorégraphie de plusieurs chromosomes dans une cellule n'a jamais été décrite. De plus, cette espèce semble être au croisement évolutif entre Caulobacter crescentus et Escherichia coli : Vibrio cholerae a d'une part une morphologie en croissant, des systèmes de partition aux origines et un positionnement de l'origine du chromosome I, semblables à C. crescentus, et d'autre part un système de compaction du terminus et un set de gènes impliqués dans la maintenance du chromosome ayant co-évolué, qu'on ne retrouve que dans peu d'espèces proches d'E. coli. Une autre caractéristique intéressante de V. cholerae est que le chromosome II semble avoir été acquis récemment et n'est donc peut être pas gouverné par les mêmes mécanismes que le chromosome I, comme en témoignent le positionnement de son origine et son terminus, inédits pour des chromosomes bactériens. Parmi les Vibrios (environ 60 espèces principalement retrouvées dans les environnements aquatiques), certaines espèces sont des pathogènes dévastateurs pour les poissons, le corail, les crustacés ou les fruits de mer. Mais la plus documentée est Vibrio cholerae, car elle provoque chez l'Humain une maladie provoquée par l'ingestion d'eau contaminée qui peut être mortelle si le patient n'est pas réhydraté à temps. Bien que facilement traitable, le choléra fait encore de nombreuses victimes dans les pays en développement où les structures de santé et les règles d'hygiène font parfois défaut. Ainsi l'étude de Vibrio cholerae présente un intérêt médical, mais également par extension aux autres Vibrios, un intérêt environnemental non négligeable.
34
O'Neal, Claire J. "Structural studies of the cholera toxin catalytic subunit /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/8592.
Texto completo da fonte
35
Toribio, Isaías Luis Daniel. "Signal Transduction proteins in Streptococcus pneumoniae and Vibrio cholerae". Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668345.
Texto completo da fonteResumo:
The aim of this project is to structurally characterize proteins involved in bacterial signal transduction systems by applying X-ray crystallography.
Bacteria use signal transduction systems to react in response to any environmental changes detected. Bacterial signal transduction is divided into two categories, one- component systems and two-component systems. Two-component systems are composed by a Response Regulator (RR) and a Histidine Kinase (HK); the Histidine Kinase auto phosphorylates an inner domain, and soon after, it phosphorylates the receiver domain on the Response Regulator, activating the output domain; usually producing a physiological effect in the cell by activating a specific gene. While in one-component systems, one protein has both, a sensory and an output domain. An example of the one-component systems would be ToxR, and an example of the two- component systems would be ComD-ComE.
Bacterial transformation is a type of Horizontal Gene Transfer (HGT), which is a rapid evolutive mechanism in which entire genes can be transferred among bacterial cells. HGT is commonly deemed responsible for the appearance of antibiotic resistance, virulence factors and serotype switching.
Competence for genetic transformation in Streptococcus pneumoniae is a transient physiological state whose development is coordinated by a peptide pheromone (Competence Simulating Peptide or CSP) and its receptor, which activates transcription of two downstream genes, comX and comW, and 15 other “early” genes. ComD (HK) and ComE (RR) are involved in the quorum-signaling pathway that synthesizes the CSP. They help modulate the mechanism in which bacterial transformation occurs, by allowing the inclusion of naked DNA from the environment. We have successfully formed the binary (ComE+DNA) and ternary (ComD+ComE+DNA) complexes and characterized them in the attempt of obtaining crystals to solve their 3-D structure.
On the other hand, to elaborate on one-component systems, like ToxR we can discuss cholera. Cholera is caused by the causative agent Vibrio cholerae. It is estimated that there are from 1.3 to 4.0 million cases out of which up to 143,000 result in cholera deaths annually. After ingesting the V. cholerae, it travels to the small intestine
colonizing it and producing the cholera toxin. ToxR is a membrane-localized transcription factor that regulates the toxT promoter. The activation of the toxT promoter triggers the virulence cascade that leads to the secretion of toxin-coregulated pilus (TCP) and the expression of cholera toxin (CTX).
In recent years, our lab solved the crystal structure of the cytoplasmic domain of ToxR+20DNA, proposing molecular interactions between ToxR and the toxT promoter (Simone Pieretti’s PhD Thesis). In this study, we want to determine the crystallographic structure of three mutants of the cytoplasmic domain of ToxR bound to the toxT promoter. According to biochemical data from our collaborator (Professor Eric Krukonis, from the university of Detroit), these mutations down regulate the activation of ToxR and we aim to analyze the structural changes that these mutants suppose. Using X-ray crystallography we solved the structure of three complexes; ToxRQ78A+20DNA, ToxRS81A+20DNA and ToxRP101A+20DNA at 2.55, 2.95 and 2.95 Å resolution, respectively.
We have compared the final mutant structures with the wildtype, unveiling how the structural changes result in the decrease in activation of the toxT promoter.
36
Choopun, Nipa. "The population structure of Vibrio cholerae in Chesapeake Bay". College Park, Md. : University of Maryland, 2004. http://hdl.handle.net/1903/1686.
Texto completo da fonteResumo:
Thesis (Ph. D.) -- University of Maryland, College Park, 2004.Thesis research directed by: Marine-Estuarine-Environmental Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
37
Humphreys, Sue. "Isolation and characterisation of a Vibrio cholerae ompR homologue". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30363.
Texto completo da fonteResumo:
Vibrio cholerae is the pathogenic agent of the diarrhoeal disease cholera and the major determinant of the disease is the elaboration by the bacteria of the potent enterotoxin cholera toxin (CT). In order to successfully colonise a host V. cholerae must co-ordinately regulate the expression of genes necessary for survival and virulence. ToxR regulates the expression of 17 virulence genes including CT in response to environmental signals like temperature, pH and osmolarity. The change in environment from the external to the human host activates ToxR and the expression of virulence genes under its control. Although this regulon is well characterised it is possible that other regulators are involved. Two-component regulators are a family of proteins that have been isolated from different bacteria which control gene expression in response to environmental signals. The proteins in the family share a high degree of similarity which was exploited in the design of degenerate primers that were used successfully to amplify four response regulator gene fragments from the V. cholerae chromosome. The complete sequence of one of the response regulator fragments has been cloned and shares 80% identity to ompR from E. coli. The sequence of a sensor gene 40% similar to envZ from E. coli has been identified downstream of the V. cholerae gene indicating that the two genes may form part of a two-component regulatory system. The two genes complement E. coli ompR and envZ mutants by altering the expression of E. coli porins indicating that they share functional similarity. Preliminary studies in V. cholerae however, show that the genes do not control porin expression under the conditions analysed. Mutation of the V. cholerae ompR/ envZ homologues will show what proteins are regulated by this system in response to varying environmental signals and whether they play any role in virulence.
38
Sabharwal, Dharmesh. "Regulatory roles of sRNAs in pathogenesis of Vibrio cholerae". Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100528.
Texto completo da fonteResumo:
The Gram-negative pathogen Vibrio cholerae uses variety of regulatory molecules to modulate expression of virulence factors. One important regulatory element of microorganisms is small non-coding RNAs (sRNAs), which control various cell functions such as expression of cell membrane proteins, mRNA decay and riboswitches. In this thesis studies, we demonstrated the roles of the sRNAs VrrA in regulation of outer membrane protein expression, biofilm formation and expression of ribosome binding proteins. In addition, we showed that VrrB, a newly discovered sRNA, played a role in amino acid dependent starvation survival of V. cholerae and might functioned as a riboswitch. VrrA, a 140-nt sRNAs in V. cholerae, was controlled by the alternative sigma factor σE. The outer membrane protein, OmpT is known to be regulated by environmental signals such as pH and temperature via the ToxR regulon and carbon source signals via the cAMP–CRP complex. Our studies provide new insight into the regulation of OmpT by signals received via the σE regulon through VrrA. We demonstrated that VrrA down-regulate ompT translation by base-pairing with the 5′ region of the ompT mRNA in a Hfq (RNA chaperone protein) dependent manner. V. cholerae biofilms contain three matrix proteins—RbmA, RbmC and Bap1—and exopolysaccharide. While much is known about exopolysaccharide regulation, little is known about the mechanisms by which the matrix protein components of biofilms are regulated. In our studies, we demonstrated that VrrA negatively regulated rbmC translation by pairing to the 5' untranslated region of the rbmC transcript and that this regulation was not stringently dependent on Hfq. In V. cholerae, VC0706 (Vrp) and VC2530 proteins are homologous to ribosome-associated inhibitor A (RaiA) and hibernation promoting factor (HPF) of Escherichia coli, respectively. HPF facilitates stationary phase survival through ribosome hibernation. We showed that VrrA repressed Vrp protein expression by base-pairing to the 5´ region of vrp mRNA and that this regulation required Hfq. We also showed that Vrp was highly expressed during stationary phase growth and associated with the ribosomes of V. cholerae. We further demonstrated that Vrp and VC2530 were important for V. cholerae starvation survival under nutrient-deficient conditions. While VC2530 was down-regulated in bacterial cells lacking vrrA, mutation of vrp resulted in increased expression of VC2530. Riboswitches are an important class of regulators in bacteria, which are most often located in the 5' untranslated region (5´ UTR) of bacterial mRNA. In this study, we discovered the novel non-coding sRNA, VrrB located at the 5´ UTR of a downstream gene encoding Vibrio auxotropic factor A (VafA) for phenylalanine. In V. cholerae, reduced production of VafA was observed in the presence of phenylalanine and phenylpyruvate in the culture media. Some analogs of phenylalanine and phenylpyruvate could also modulate the expression of VafA. Furthermore, bacterial cells lacking the vrrB gene exhibited high production of VafA, suggesting that VrrB might function as a riboswitch that controls VafA expression.
39
Massam-Wu, Teresa. "Characterisation of the Vibrio cholerae antibiotic resistance var operon". Thesis, Durham University, 2007. http://etheses.dur.ac.uk/2562/.
Texto completo da fonteResumo:
The discovery and use of antibiotics in the chemotherapy of bacterial infections has revolutionised medicine as it is today. Unfortunately, the progressive use of antibiotics has promoted the evolution of bacterial defences against these mediators and thus the emergence of antibiotic resistance. Multidrug resistance (MDR) in bacterial pathogens has grown with such rapid progression that it now threatens to compromise the effective chemotherapy of a plethora of diseases. This thesis aspires to elucidate the molecular resistance mechanisms adopted by these bacteria, in order to expand our knowledge and to assist in the development of new therapeutic approaches to circumvent these mechanisms. On this basis, this thesis presents insights into a novel Vibrio cholerae antibiotic resistance, var, operon that encodes a metallo- β -lactamase (Mßl), VarG, and a tripartite ATP-binding cassette-type (ABC-type) transport system, VarACDEF that has substrate specificities for antimicrobial peptides and macrolide antibiotics. Mßls are fast emerging as a primary resistance mechanism, possibly as a consequence of the introduction of newer ß-lactam antibiotics such as the carbapenems in response to increasing Gram-negative bacterial resistance. Fascinatingly, the ABC transporter, through secondary structure predictions, has been envisaged to adopt a tripartite structure similar to the MDR transporter, AcrAB-TolC, from the resistance nodulation and cell division (RND) family. The structural characterisation of this system would be the first such tripartite system to be elucidated and may bring new insights into how Gram-negative bacteria may have evolved to tackle the issue that threatens its existence. The resistance mechanisms in the var Operon are believed to be under the control of a LysR-type transcriptional regulatory protein (LTTR), VarR. LTTR proteins form one of the largest transcriptional regulatory families with extremely diverse functions ranging from amino acid biosynthesis to CO(_2) fixation. VarR binds to three distinct promoter regions, varRG, varGA and varBC located upstream and adjacent to VarG, VarA an AcrA-like membrane fusion protein and VarC a TolC-like outer membrane protein, respectively. VarR has also been shown to act as a repressor at the varRG promoter region in the absence of its substrate. Interestingly, the mechanism of regulation by VarR is strikingly similar to the well documented LTTR, AmpR and serine ß-lactamase AmpC system that are found in many pathogenic bacteria. It could be that V. cholerae has evolved from this regular system and developed a ß-lactamase that would prove more beneficial in light of current selective pressures. Contrary to LTTRs being notoriously recalcitrant to purification due to their low solubility, this thesis reports the successful purification and crystallisation of full-length VarR in the presence and absence of its cognate promoter DNA. Elucidating the structural characteristics of VarR would be the first such regulator associated with MDR in the LTTR family. This would advance the knowledge on the only currently existing full-length crystal structure of a LTTR, CbnR, and will provide further insights into how structural conformations may lead to dissociation from the promoter and induction of gene expression. Understanding the mechanism by which VarR induces expression of these resistance mechanisms is paramount for future strategies to prevent the emergence of MDR microorganisms. Although these mechanisms of MDR maybe elucidated in V. cholerae, the evolutionary relatedness and conservation of structure and function in all families will enable this information to be related to similar systems in alternative bacterial species.
40
Bomchil, Natalia. "Régulation de la formation de biofilms chez Vibrio cholerae". Paris 7, 2002. http://www.theses.fr/2002PA077030.
Texto completo da fonte
41
Mitchell, Daniel David. "Cholera toxin inhibition and EpsF from its secretion system /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/9210.
Texto completo da fonte
42
Franzon, Vicki L. "Haemagglutinins of Vibrio cholerae : molecular characterization of the mannose-fucose resistant haemagglutinin (MFRHA) /". Title page, abstract and contents only, 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phf837.pdf.
Texto completo da fonte
43
Antonova, Elena S. "The regulatory network controlling natural competence for DNA uptake in Vibrio cholerae". Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47626.
Texto completo da fonteResumo:
The bacterial pathogen Vibrio cholerae is responsible for ongoing cholera outbreaks in Haiti and elsewhere. Association of V. cholerae with the human host is responsible for fatal disease, but the bacteria also reside as natural inhabitants of aquatic environments, commonly attaching as biofilms to chitinous surfaces of copepods and crabs. Prior studies in V. cholerae demonstrated that competence for genetic transformation, a mechanism of horizontal gene transfer (HGT), requires the TfoX regulator protein that is triggered by chitin, and the HapR transcription factor that is made in response to quorum sensing (QS) signals produced by V. cholerae and Vibrios. To define regulatory components connecting extracellular signals to natural competence, I first demonstrated that QS molecules produced by Vibrios within multi-species chitinous biofilms are required for DNA uptake by V. cholerae, confirming the critical role of QS signals in HGT. Second, I identified by transposon-mutagenesis a new positive regulator of competence, CytR (cytidine repressor), only studied prior in E. coli as a regulator of nucleoside scavenging. Specific mutations in V. cholerae CytR impaired expression of competence genes and halted DNA uptake; and the addition of exogenous cytidine had similar affects as predicted in E. coli. V. cholerae and other competent Vibrios encode TfoX, HapR, and CytR, although none of these regulators directly controls genes coding for the DNA uptake apparatus. Thus, these results have uncovered a regulatory network, likely used by many Vibrios, that contains additional factors linking several extracellular chemical molecules (cytidine, chitin, and QS signals) to DNA uptake. My study has begun to define a molecular mechanism by which both environment and genetics contribute to genome evolution for this important marine pathogen.
44
Yáñez, Marissa Elena. "Structural and functional studies of minor pseudopilins from the type 2 secretion system of Vibrio cholerae /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8086.
Texto completo da fonte
45
Lin, Po-Chi. "Na⁺-translocating NADH:Quinone oxidoreductases from Vibrio cholerae and Yarrowia lipolytica /". Zürich : ETH, 2007. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17541.
Texto completo da fonte
46
Farfán, Sellarés Maribel. "Estudio de la estructura genética de poblaciones de "Vibrio cholerae"". Doctoral thesis, Universitat de Barcelona, 2002. http://hdl.handle.net/10803/2415.
Texto completo da fonteResumo:
Se ha estudiado la variabilidad genética de poblaciones de V. cholerae procedentes de distintas fuentes y orígenes geográficos, que agrupan diferentes serogrupos y biotipos de esta especie. Se ha analizado la variabilidad genética a dos niveles: a un nivel proteico, aplicando la técnica de electroforesis de aloenzimas multilocus (MLEE), y a un nivel génico, realizando el análisis de secuencias multilocus (MLST). Con ello, se ha intentado determinar la relación genética existente entre las distintas cepas estudiadas, considerando los datos obtenidos globalmente y por subgrupos de poblaciones, para establecer la estructura poblacional y la diversidad génica que presenta V. cholerae.Un total de 107 cepas de V. cholerae, incluyendo 29 cepas pertenecientes al serogrupo O139, fueron estudiadas aplicando la técnica de electroforesis de aloenzimas multilocus (MLEE) para determinar la variación alélica de 15 enzimas "housekeeping". Todos los loci fueron polimórficos y se identificaron 99 ETs para el total de la muestra. No se detectó una asociación significativa de las cepas en función de su serogrupo u origen geográfico. Se obtuvo el valor de diversidad génica media (H=0,50) más alto descrito para esta especie. El análisis del desequilibrio de ligamiento mostró una estructura clonal para el conjunto de la población, pero cuando se estudiaron subgrupos de esta población hubo excepciones, que hacen pensar en la existencia de un cierto grado de recombinación. Estos resultados sugieren que la población estudiada presenta una estructura poblacional epidémica.
Para una colección de 29 cepas del serogrupo O139 se ha realizado el análisis comparativo de fragmentos internos de 6 genes "housekeeping", aplicando la metodología de análisis de secuencias multilocus (MLST). Los resultados obtenidos muestran la existencia de al menos 3 clones distintos entre las cepas analizadas, contradiciendo la actual hipótesis monoclonal de este serogrupo. También se detectaron dos grupos muy distintos de cepas del serogrupo O139, ST1 y ST4, que exhibieron diferencias en el perfil alélico para los 6 loci analizados.
47
Rawlings, Tonya Kafi. "Interactions of Vibrio cholerae serogroups O1 and O139 and copepods". College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2865.
Texto completo da fonteResumo:
Thesis (Ph. D.) -- University of Maryland, College Park, 2005.Thesis research directed by: Marine-Estuarine-Environmental Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
48
Iredell, J. R. "Molecular export and pilin assembly : TCP biogenesis in Vibrio cholerae /". Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phi648.pdf.
Texto completo da fonte
49
Resch, Craig. "Biochemistry and physiology of NhaP-type antiporters in Vibrio cholerae". Elsevier, 2010. http://hdl.handle.net/1993/31098.
Texto completo da fonteResumo:
Antiporters that exchange alkali cations (Na+ or K+) for protons play an important role in the physiology of all known bacterial species. They are involved in regulating intracellular pH and maintaining cellular volume as well as the formation of a chemical Na+ gradient across the membrane, which is important to many bacteria as an energy source for processes such as accumulation of substrates, ATP synthesis, and flagellar rotation. Another important role of cation/proton antiporters is homeostasis of intracellular cation content. The situation of a thermodynamic equilibrium of Na+ or K+ on the membrane would result in toxic intracellular levels of these cations, so bacteria have cation/proton antiporters, which expel excess of alkali cations at the expense of the proton motive force.
Of many antiporters described to date, the NhaP-type family is one of the most interesting groups. Its members collectively demonstrate a great diversity of their features. There are three antiporters of NhaP type encoded in the genome of the dangerous human pathogen, Vibrio cholerae. Phenotype analysis of engineered chromosomal VcnhaP1, VcnhaP2 and VcnhaP3 deletion mutants has proven the three NhaP paralogues to be essential for V. cholerae growth at low pH in the presence of high or low concentrations of K+.
Genes encoding Vc-NhaP1-3 were cloned and antiporters expressed in their functional form in an antiporter-less strains of Escherichia coli. Although initially annotated as Na+/H+ antiporters, when assayed in everted membrane vesicles, all three isoforms of Vc-NhaP were shown to be K+/H+ antiporters with only limited ability to Na+/H+ antiport. None of three proteins was able to mediate Li+/H+ exchange. Overall, the three antiporters differed in their biochemical profiles, predicted topology, and their phenotypic manifestations.February 2016
50
Alm, Richard A. "Molecular characterization of the haemolysin determinant of Vibrio cholerae O1 /". Title page, contents and abstract only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha444.pdf.
Texto completo da fonteResumo:
Thesis (Ph. D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1990.Includes an appendix of author's previously published papers. Includes bibliographical references (leaves 123-160).