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Prele, Cecilia Marie Antoinette. "Vesicular trafficking in osteoblasts." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271058.
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Bishop, Carolyn Wagoner 1947. "Hydraulic properties of vesicular basalt." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/291554.
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Laboratory experiments were conducted on vesicular basalt cores to estimate hydraulic properties. Properties included dry bulk density, effective porosity, skeletal density, saturated hydraulic conductivity and determination of moisture characteristic curves. Unsaturated hydraulic properties estimated included hydraulic conductivity and diffusivity as a function of matrix suction. Infiltration tests were run on a larger block of the same basalt. Infiltration curves were developed and saturated hydraulic conductivity estimated.
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Kremer, Katrin. "Vesicular trafficking in Toxoplasma gondii." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4753/.
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Toxoplasma gondii is an obligate intracellular protozoan parasite with a worldwide prevalence. Together with the causative agent of malaria (Plasmodium falciparum) and other medically important pathogenic parasites it belongs to the phylum of the Apicomplexa. Besides identifiable eukaryotic organelles, apicomplexan parasites differ from other eukaryotic cells by an extra set of specialised secretory organelles (micronemes, rhoptries and dense granules), that are sequentially secreted during invasion of the host cell. Upon host cell contact the apically located micronemes are the first organelles to be released and contain crucial virulence factors that are secreted. In order to systematically analyse vesicular traffic with a special focus on the secretory pathway of rhoptry and microneme proteins the ddFKBP system was used to perform a systematic analysis of Rab proteins in Toxoplasma gondii. Rab proteins are small GTP- binding proteins that are involved in targeting and fusion of vesicles from a donor to an acceptor membrane. Whereas higher eukaryotes like human cells encode more than 60 different Rab proteins apicomplexan parasites possess only a reduced core set of Rab proteins. Performing co-localisation studies with generated parasite lines expressing ddFKBPmyc-tagged versions of Rab1A, 1B, 2, 4, 5A, 5C, 7, 18 and Rab5B-ddFKBPHA revealed, that all these Rabs localise to the early secretory pathway (Rab1B, 2 and 18), the Golgi (Rab4), or the late secretory pathway (Rab5A, Rab5B, Rab5C and Rab7). No exact localisation could be defined for Rab1A. Rab5A and Rab5C, normally involved in endocytic uptake, were identified as important regulators of traffic to micronemes and rhoptries in Toxoplasma gondii, using an overexpression screen of Rabs and the analysis of trans-dominant mutants of promising candidates. Intriguingly, some microneme proteins could be found to traffic independently on functional Rab5A and Rab5C, indicating the existence of independent transport routes to micronemes, which again indicates that apicomplexans have remodelled Rab5-mediated vesicular traffic into a secretory system that is essential for host cell invasion. By using two-colour super-resolution stimulated emission depletion (STED) microscopy, distinct localisations of independent microneme proteins could be verified. This demonstrated that micronemal organelles are organised in distinct subsets or subcompartments. Given these results, it can be assumed that apicomplexan parasites modify classic regulators of the endocytic system to carry out essential parasite-specific roles in the biogenesis of their unique secretory organelles.
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Hassan, Hanna. "Proteomic profiling of vesicular organelles." Thesis, KTH, Skolan för bioteknologi (BIO), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215028.
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Roberts, Marnie. "The regulation of integrin vesicular trafficking." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29673.
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Growth factors are able to influence cell adhesion and migration by regulating the function of integrins. Integrins engage in endo/exocytic cycling and I have investigated the possibility that growth factors influence integrin function by controlling their endocytosis and/or recycling. In serum starved mouse fibroblasts avb3 and a5b1 integrins are internalised, trafficked to the perinuclear recycling compartment, and then returned to the cell surface in a Rab11-dependent fashion. In contrast, following addition of PDGF, avb3 integrin (but not a5b1) was returned directly from the early endosomes to the plasma membrane via a pathway dependent on Rab4, and not Rab11. Moreover, growth factor regulated integrin recycling was not restricted to fibroblasts, but occurred in human endothelial cells in response to VEGF. Inhibition of avb3 recycling using dominant negative Rab4 mutants compromised cell adhesion and spreading on vitronectin (a ligand for avb3), but adhesion to fibronectin (a ligand for a5b1 and avb3) was unchanged indicating that Rab4-depdnent recycling is essential for avb3 function. PDGF and VEGF are known to activate the PI(3)K/ PKB/Akt signalling axis and recent evidence indicates that this pathway is involved in modulating integrin function. Recycling of both avb3 and a5b1 was inhibited by expression of dominant negative PKB and, furthermore, constitutively active PKB stimulated the flux of avb3 from the early endosome to the plasma membrane. Blockade of PKB/Akt by dominant negative mutants compromised cell spreading on vitronectin and fibronectin, consistent with a requirement for recycling in the function of both avb3 and a5b1 integrins. To gain insight into the biochemical events occurring during integrin activation I looked for active signalling molecules that are recruited to avb3 following PDGF treatment. A 44kDa protein rich in phosphotyrosine and phosphothreonine coimmunoprecipitated with avb3 integrin and western blotting revealed this protein to be active pp44 ERK1.
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Edelmann, Sophia [Verfasser]. "Human and zoonotic Chlamydia species interact with Golgi-dependent vesicular and non-vesicular trafficking pathways / Sophia Edelmann." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/110293349X/34.
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Barmark, Gunilla. "Functional studies of vesicular transport in yeast /." Uppsala : Dept. of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, 2005. http://epsilon.slu.se/2005110.pdf.
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Banbury, David N. "New monoclonal antibodies to visualise vesicular compartments." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259782.
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Nijhar, Sukhvinder Kaur. "Antigenic characterisation of swine vesicular disease virus." Thesis, University of Hertfordshire, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363501.
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Davidson, Kent. "Genetic studies of vesicular-arbuscular mycorrhizal fungi." Thesis, University of Bristol, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279742.
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Zylbersztejn, Kathleen. "Role of vesicular traffic in axon guidance." Paris 7, 2011. http://www.theses.fr/2011PA077146.
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Lors du développement, les molécules de guidage attractives et répulsives, telles que les Sémaphorines (Sema), sont responsables de la formation du réseau neuronal des axones et des dendrites. Les molécules de guidage extracellulaire se lient à des récepteurs qui activent les voies de signalisation intracellulaire et remodèlent le cône de croissance. Le rôle du trafic membranaire dans le guidage axonale est encore largement inconnu. Le trafic membranaire nécessite les protéines SNARE pour la fusion membranaire. La SNARE vésiculaire Synaptobrévine2 (Syb2) est connue pour son rôle dans la libération des neurotransmetteurs dans les neurones matures tandis que TI-VAMP est principalement connue pour son rôle dans la croissance axonale. Leurs rôles potentiels dans le guidage axonale demeurent inconnus. J'ai montré que Syb2 est nécessaire pour la répulsion SemaSA-dépendante, mais pas pour l'attraction SemaSC-dépendante dans des neurones en culture et dans le cerveau murin. Syb2 interagit aussi avec Neuropilinel et PlexinAl, les deux éléments du récepteur à la SemaSA, via son domaine juxta-transmembranaire. Nous concluons que signalisation et la répulsion axonale SemaSA-dépendante nécessitent le trafic vésiculaire Syb2-dépendante. Nous proposons donc un modèle dans lequel la répulsion induite par la SemaSA requiert une endocytose locale accrue et une diminution de l'exocytose. La SemaSA est également impliquée dans le guidage de cellules non neuronales. Certaines de nos observations ont été obtenues dans des cellules non neuronales, suggérant que nos conclusions peuvent s'appliquer généralement à la signalisation de la SemaSADuring development, attractive and repulsive guidance molecules, such as semaphorins (Sema), are responsible for proper wiring of axons and dendrites. Attractive and repulsive external guidance cues bind to receptors which activate intracellular signalling pathways and reshape the growth cone. The role of vesicular traffic in axonal guidance is still largely unknown. Vesicular traffic requires SNAREs proteins for membrane fusion. The exocytic vesicular SNARE Synaptobrevin2 (Syb2) mediates neurotransmitter release in mature neurons while TI-VAMP is mainly known for mediating axon growth. Their potential roles in axon guidance remain elusive. According to a previous model, attraction would rely solely on Syb2-dependent exocytosis while repulsion would exclusively require endocytosis. However, my PhD work has hinted a more complex view on guidance mechanisms. I showed that Syb2 is required for SemaSA-dependent repulsion but not SemaSC-dependent attraction in cultured neurons and in the mouse brain. Syb2 associates with Neuropilinl and PlexinAl, two essential components of the SemaSA receptor, via its juxta-transmembrane domain. We concluded that SemaS A-mediated signalling and axonal repulsion require Syb2-dependent vesicular traffic. We thus propose a model in which SemaSA-induced repulsion is mediated by local increased endocytosis and decreased exocytosis. SemaSA is also involved in non neuronal cell navigation, Some of our observations were obtained in non-neuronal cells further suggesting that our conclusions may more generally apply to SemaSA signaling
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Lin, Fengsheng. "The duration of infection in swine vesicular disease." Thesis, Royal Veterinary College (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300624.
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Bhangu, P. S. "Vesicular 'pre-synaptic' glutamatergic signalling mechanisms in bone." Thesis, University of York, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288814.
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Leme, Raquel de Arruda. "Senecavirus A : virose vesicular emergente na suinocultura brasileira." Universidade Estadual de Londrina. Centro de Ciências Agrárias. Programa de Pós-Graduação em Ciência Animal, 2017. http://www.bibliotecadigital.uel.br/document/?code=vtls000214355.
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As doenças vesiculares são de grande importância para a Medicina Veterinária. A febre aftosa, a doença vesicular suína, o exantema vesicular suíno e a estomatite vesicular são doenças vesiculares clássicas de etiologia viral. Na família Picornaviridae estão incluídos o vírus da febre aftosa e o vírus da doença vesicular suína que ocasionam lesões vesiculares em suínos. Entretanto, dois estudos realizados no Canadá e nos EUA a partir de 2008 identificaram uma nova espécie de picornavírus, denominada Senecavirus A, como o mais provável agente etiológico de doença vesicular, similar à febre aftosa, em suínos. No final de 2014 e início de 2015 houve diversos relatos de doença vesicular em suínos nas fases de creche e terminação, além do aumento da incidência de doença multissistêmica em leitões, com altas taxas de mortalidade, nos principais estados brasileiros produtores de suínos. O objetivo deste estudo foi investigar a infecção natural pelo Senecavirus A em suínos de diferentes categorias de produção provenientes de granjas dos estados brasileiros de maior importância para a suinocultura. Para isso foram realizados três estudos. O primeiro estudo teve como objetivo investigar a infecção pelo Senecavirus A em surtos de doença vesicular de origem desconhecida em suínos das categorias de creche e adultos. Um conjunto de primers específico para amplificar um produto de 542 pb da região VP3/VP1 do genoma do vírus foi desenhado para ser utilizado na técnica de RT-PCR. Amostras clínicas de suínos foram coletadas em oito granjas com surto da doença vesicular, incluindo fluido vesicular (n=4), swabs de vesículas rompidas (n=7) e raspados de lesões ulcerativas (n=5). Foram também analisadas raspados de pele (n=52) de suínos assintomáticos provenientes de granjas com e sem histórico da doença. Os agentes virais de doenças vesiculares clássicas foram investigados e não foram detectados. O RNA do Senecavirus A foi detectado em todas as amostras (16/16) provenientes de animais acometidos pela doença vesicular, enquanto nenhuma das amostras de animais assintomáticos foram positivas para o vírus. O segundo e o terceiro estudos descrevem, respectivamente, novas manifestações clínicas associadas ao Senecavirus A assim como os achados patológicos, imunohistoquímicos e moleculares associados à infecção, ambos em leitões neonatos com 1 a 5 dias de idade. No segundo estudo, foram analisadas amostras de órgãos/tecidos (n=81) e de fezes (n=6) de 10 leitões, provenientes de cinco granjas dos estados do Paraná, Santa Catarina e Mato Grosso do Sul. O terceiro estudo é complementar ao segundo e foram incluídas amostras clínicas de mais dois leitões provenientes dos estados de São Paulo e Santa Catarina, totalizando 102 amostras de órgãos/tecidos e 8 amostras de fezes. Todos os leitões incluídos nos estudos manifestaram sinais clínicos de fraqueza, letargia, salivação excessiva, hiperemia cutânea, sinais neurológicos, diarreia e/ou morte espontânea. Em conjunto, os resultados desses dois estudos revelaram que os achados de necropsia mais comuns foram impressão das costelas em pulmões (n=9), glossite diftérica (n=6) e lesões ulcerativas na banda coronária (n=5). A histopatologia revelou pneumonia intersticial (n=12), miocardite (n=6), glossite diftérica (n=3), encefalite (n=3) e atrofia das vilosidades intestinais com vacuolização das células epiteliais superficiais (n=6). A imunohistoquímica com anticorpos monoclonais específicos para Senecavirus A demonstrou imunorreatividade no plexo coróide do cérebro, epitélio degenerado de lesões ulcerativas da língua, uroepitelio do rim e vesícula urinária e nas células superficiais do intestino e em vários tecidos dos leitões; os ensaios moleculares para os outros vírus avaliados apresentaram resultados negativos. Os estudos descrevem pela primeira vez a infecção pelo Senecavirus A fora da América do Norte e sugerem que o vírus seja o agente causal dos surtos de doença vesicular descritos no Brasil, bem como a participação do vírus em múltiplas lesões observadas em leitões neonatos, caracterizando-se como um vírus pantrópico capaz de causar doença multissistêmica em suínos infectados precocemente.Vesicular diseases are of great importance for Veterinary Medicine. Foot-and-mouth disease, swine vesicular disease, vesicular exanthema of swine, and vesicular stomatitis are classical vesicular diseases of viral etiology. In the Picornaviridae family are included the foot-and-mouth disease virus and swine vesicular disease virus that cause vesicular lesions in pigs. However, two studies conducted in Canada and in the United States from 2008 identified a new species of picornavirus, known as Senecavirus A, as the most likely etiological agent of vesicular disease, similar to foot-and-mouth disease, in swine. At the end of 2014 and early 2015 there were several reports of vesicular disease in pigs at nursery and finishing ages, as well as an increasing in the incidence of multisystemic disease in piglets with high mortality rates in the major Brazilian pig-producing states. The objective of this study was to investigate the natural infection by Senecavirus A in pigs of different production categories from herds of the Brazilian states of greater importance for pork industry. Three studies were carried out. The first study aimed to investigate the Senecavirus A infection in outbreaks of vesicular disease of unknown etiology in weaned and adult pigs. A specific primer set for amplifying a 542 bp product from the VP3/VP1 region of the virus genome was designed for use in the RT-PCR technique. Clinical samples of pigs were collected from eight farms with vesicular disease outbreak, including vesicular fluid (n=4), swabs of ruptured vesicle (n=7), and scrapping of ulcerative lesions (n=5). Cutaneous scrappings (n=52) of asymptomatic pigs from farms with and without vesicular disease history were also analyzed. The viral agents of classic vesicular diseases were investigated and were not detected. Senecavirus A RNA was detected in all samples (16/16) of vesicular disease-affected animals, while none of the samples from asymptomatic pig were positive for the virus. The second and third studies describe, respectively, new clinical manifestations associated with Senecavirus A and pathological, immunohistochemical, and molecular findings associated with infection, both in neonatal piglets at 1 to 5 days of age. In the second study, organ/tissue samples (n=81) and feces (n=6) of 10 piglets from five herds of the states of Paraná, Santa Catarina, and Mato Grosso do Sul were analyzed. The third study is complementary to the second, and clinical samples of two more piglets from the states of São Paulo and Santa Catarina were included, totalizing 102 organ/tissue samples and 8 fecal samples. All piglets included in the studies showed clinical signs of weakness, lethargy, excessive salivation, cutaneous hyperemia, neurological signs, diarrhea, and/or spontaneous death. Overall, the results of these two studies revealed that the most common necropsy findings were faint rib impressions on the pleural surface of the lungs (n=9), diphtheritic glossitis (n=6), and ulcerative lesions at the coronary band (n=5). Histopathology revealed interstitial pneumonia (n=12), myocarditis (n=6), diphtheritic glossitis (n=3), encephalitis (n=3), and atrophy of intestinal villi with vacuolation of the superficial epithelial cells (n=6). Immunohistochemistry with monoclonal antibodies specific for Senecavirus A demonstrated immunoreactivity of the choroid plexus of the cerebrum, degenerate epithelium of ulcerative lesions of the tongue, the urothelium of the kidney and urinary bladder, and the superficial cells of the intestine and in various tissues of the piglets. The molecular tests for the other viruses evaluated showed negative results. The studies describe for the first time the infection by Senecavirus A outside of North America and suggest that the virus is the causative agent of the outbreaks of vesicular disease described in Brazil, as well as the participation of the virus in multiple lesions observed in neonatal piglets, characterizing as a pantropic virus able to produce a multisystemic disease entity in pigs infected at an early age.
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Gallo, Alessandra. "Role of non-vesicular secretion in neuronal development." Thesis, Université de Paris (2019-....), 2019. https://theses.md.univ-paris-diderot.fr/GALLO_Alessandra_va.pdf.
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La croissance des neurites au cours du développement neuronal nécessite une expansion de la membrane plasmique (MP) via l’insertion de nouveaux lipides et protéines. Cet événement se produit à la suite de la fusion des vésicules de sécrétion avec la MP. Cependant, plusieurs études ont montré que le transfert non-vésiculaire de lipides au niveau des sites de contact entre le réticulum endoplasmique (RE) et la MP joue aussi un rôle dans la croissance des cellules. Des membres de la famille de synaptotagmines étendues (E-Syts) ont été identifiés comme protéines de transfert des lipides dépendantes du Ca2+ au niveau des jonctions RE-MP.Nous avons découvert qu’un nouveau complexe SNARE aux sites de contact RE-MP, composé par Sec22b et Stx1, est impliqué dans la croissance des neurites bien qu’il soit incapable de favoriser la fusion membranaire. Cependant, la manière dont ce complexe participe à l’extension des neurites reste à élucider. Chez la levure, Sec22 interagit avec les protéines de transfert des lipides de la famille OSH, enrichis aux sites de contact RE-MP.Sur la base de ces observations, notre hypothèse est que le transfert non-vésiculaire de lipides induit par E-Syts au niveau des jonctions RE-MP contenant Sec22b pourrait contribuer à la croissance neuronale. L’objectif de ma thèse était d’explorer cette hypothèse. Nous montrons que Sec22b interagit avec E-Syt2 et Stx1 dans les cellules PC12 et avec E-Syt2, E-Syt3 et Stx3 dans les cellules HeLa. L’interaction Sec22b/E-Syt2 dépend du domaine Longin de Sec22b. La surexpression des E-Syts stabilise l’association Sec22b/Stx1, alors que l’inactivation des E-Syts provoque l’effet inverse. La surexpression de E-Syt2 de type sauvage, mais pas des mutants incapables de transférer les lipides ou non fixés au RE, augmentent la formation de filopodes axonaux et la ramification de neurites dans les neurones en développement. Cet effet est inhibé par une neurotoxine clostridiale clivant Stx1, par l’expression du domaine Sec22b Longin et par un mutant Sec22b ayant une extension entre les domaines SNARE et transmembranaire.En conclusion, mes résultats soutiennent l’idée que les sites de contact Sec22b/Stx1 contribuent à l’expansion de la MP via une interaction avec des protéines de transfert de phospholipides comme E-SytsThe growth of neurites during neuronal development requires a massive increase of surface area via the insertion of new proteins and lipids. This event occurs through the fusion of secretory vesicles with the plasma membrane (PM), the final step of the secretory pathway. Recently, non-vesicular transfer of lipids at contacts between endoplasmic reticulum (ER) and PM was shown to contribute to membrane expansion. Members of the ER-integral membrane protein Extended-Synaptotagmin (E-Syt) family have been identified as Ca2+-dependent lipid transfer proteins at ER-PM contact sites, and shown to transfer glycerophospholipids via their lipid binding domains. The laboratory previously found that a novel ER-PM SNARE complex, composed of the ER-resident Sec22b and the neuronal plasmalemmal Stx1, is involved in neurite growth despite being unable to mediate membrane fusion. However, how this complex participates to neurite extension remained to be elucidated. In yeast, Sec22 interacts with lipid transfer proteins of the OSH family, enriched at the ER- PM contacts, supporting a role for Sec22b-populated ER- PM junctions in non-vesicular lipid transport between these bilayers. Based on these observations, our starting hypothesis was that E-Syts-mediated non-vesicular lipid transfer at Sec22b-populated ER-PM contacts, might contribute to neurite growth. The goal of my PhD was to explore this hypothesis with two specific questions: 1-What are the partners of Sec22b complexes which might be involved in the unconventional mechanisms of membrane expansion? 2-What is the mechanism whereby the non-fusogenic SNARE Sec22b/Stx1 complex acts in neuronal development?Here we show that Sec22b interacts with E-Syt2 and Stx1 in PC12 cells and with E-Syt2, E-Syt3 and Stx3 in HeLa cells. Overexpression of E-Syt2 stabilized Sec22b-Stx3 association, whereas silencing of E-Syt2 had the opposite effect. Overexpression of E-Syt2 full length, but not the mutant forms which are unable to transfer lipids or attach to the ER, increased the formation of filopodia particularly in the growing axon. Finally, this effect was inhibited by a clostridial neurotoxin cleaving Stx1, by the expression of Sec22b Longin domain and a by a Sec22b mutant with extended linker between SNARE and transmembrane domains.In conclusion, these results support the hypothesis that Sec22b/Stx1 junctions may contribute to membrane expansion via an interaction with phospholipid transfer proteins like E-Syts
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Presloid, John B. "Characterization of Vesicular Stomatitis Virus Strains with Adaptability." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1225313889.
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Soh, Timothy Kinshiong. "Single particle studies of vesicular stomatitis virus assembly." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17464089.
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The formation of viral particles requires the coordinated assembly of both nucleic acids and proteins. In the case of Rhabdoviruses, such as vesicular stomatitis virus (VSV), the particles display a characteristic bullet-shape. VSV virions consist of the matrix protein (M), glycoprotein (G), and viral ribonucleoprotein (RNP), which contains the nucleocapsid protein (N) coated RNA bound to the large polymerase protein (L) through the phosphoprotein (P). During assembly, these components are recruited to the plasma membrane where the viral RNP undergoes condensation by M and envelopment with G containing membranes. To address whether formation of the bullet-shape requires a consistent packaging of the viral proteins, the composition of single virions was measured with fluorescence microscopy. We generated autonomously replicating VSV bearing up to 3 fluorescent protein fusions in the disordered N-terminal region of M and N-terminus of P and G. Quantification of single particles reveals that VSV assembles with a range of M, P, and G molecules, suggesting a flexible packaging mechanism. The maintenance of the bullet-shape with significantly less M proposes that condensation does not require the particle to be saturated with M. Our fluorescent VSV clones permit the tracking of viral components in live cells. We observed that assembly of M into particles requires ~2 min and can be broken into 4 stages. First, M forms a small preassembly complex. Second, M rapidly assembles into particles where its incorporation initiates before P, although they are packaged concurrently. This is followed by a delay before final release of particles into the supernatant. Late domains in M were thought to only recruit the endosomal sorting complexes required for transport (ESCRT) pathway to mediate fission. However, using our M fusions we demonstrate that these motifs are required for efficient competition into released particles and a step in assembly prior to pinching off. These constructs have permitted the study of viral assembly at the single particle level and are useful tools for studying viral entry and egress. Specifically, VSV containing M-eGFP and the lassa virus glycoprotein instead of G was used to demonstrate the requirement of a host factor for lassa virus fusion.Medical Sciences
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Walker, Angela. "Electrochemical study of vesicular release in bovine chromaffin cells." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23431.
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The time course of the spontaneous current spikes produced by the release of the catecholamines from individual vesicles was examined in bovine chromaffin cells by using the carbon filament technique in the amperometric mode.Frequency histograms of the rise and decay times of the current spikes showed a paucity of very short duration events. Scatterograms of the rise and decay times consistently showed a positive relation, and the best fitted lines intercepted the ordinate (the axis of the decay time) at: 16.06 $ pm$ 6.45 msec (n = 11).
The effect of temperature changes upon the time course of release of content of individual vesicles in chromaffin cells was also examined. The amplitudes of the current spikes did not change significantly, whereas the rise times and the decay times diminished from (23.2 $ pm$ 11.6 to 11.9 $ pm$ 2.7 msec, and from 76.6 $ pm$ 25.4 to 47.3 $ pm$ 9.3 msec respectively) as the temperature was raised from 15$ sp circ$C to 35$ sp circ$C (n = 5). Nevertheless, the Q$ sb{10}$ values of the rise and decay times were surprisingly low.
The experimental findings suggest that in bovine chromaffin cells the duration of the release of content of single vesicles is much longer than in synapses. The results also suggest that this mechanism does not involve processes that are strongly temperature sensitive.
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Sukarno, Nampiah. "Effects of selected fungicides on vesicular-arbuscular mycorrhizal symbiosis." Title page, contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phs948.pdf.
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Musandu, Amos Omonge Absalom. "Vesicular-arbuscular mycorrhiza and phosphorus availability in Kenyan soils." Thesis, Imperial College London, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416441.
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Quinn, T. G. "Characterisation of the vesicular monoamine transporters 1 and 2." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368550.
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Amijee, F. "Colonization of root systems by vesicular-arbuscular mycorrhizal fungi." Thesis, University of Leeds, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374170.
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Hansson, Stefan R. "The serotonin transporter and vesicular monoamine transporters during development." Lund : Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945023.html.
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Hodges, Erin Nicole. "Characterization of the S2 isolate of vesicular stomatitis virus." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12781.
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Thesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.Vesicular stomatitis virus is a prototype nonsegmented, negative-sense RNA virus that has been widely used to study common aspects of RNA virus replication. Attenuated mutants of VSV have led to important discoveries about viral function, particularly genome replication and mRNA transcription. S2 VSV is small plaque isolate of VSV initially described to be attenuated in vivo but still able to induce a robust interferon response. Detailed characterization of the attenuated VSV isolate S2 has verified that this isolate is attenuated and is able to induce a blocking antibody response in vivo. Further characterization showed that this isolate is antigenically and phylogenetically distinct from related wild-type VSV isolates. Sequencing of the virus shows that there are more than three hundred nucleotide changes from the standard VSV laboratory strain, San Juan. Characterization of the RNA products produced in S2 VSV infected cells has led to the discovery of a non-interfering subgenomic particle that is carried along with S2 VSV infection. Additionally, characterization of the attenuated phenotype showed that S2 VSV has markedly different transcription gradient when compared with San Juan VSV. S2 shows a steeper gradient of polymerase transcription than wild-type virus and a decline in total transcription after 4 hpi. As expected, this decline in active transcription leads to lower level of mRNA accumulation in S2 VSV infected cells. In a coinfection with wild-type VSV, the S2 pattern of transcription is completely dominant at all times in infection, and this altered transcription phenotype of S2 is not due to an innate cellular response, as transcription in vitro duplicates the phenotype seen in cells. S2 VSV is the first demonstrated viral mutant with a steeper gradient of transcription that is not dependent on RNA template sequence or host response. The attenuation and ability of S2 VSV to inhibit wild-type virus suggests that S2 VSV would be a good candidate vector for VSV-based vaccines. In addition, the mechanism behind the altered transcriptional profile of S2 VSV has led to new understanding of the role of the polymerase complex in the unique mechanism of transcriptional control by the nonsegmented, negative-sense RNA viruses.
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Zimmermann, Johannes [Verfasser]. "Regulation of neurotransmitter release by essential vesicular proteins / Johannes Zimmermann." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1073869059/34.
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Kraus, Tobias. "Distribution of vesicular glutamate transporter 1 in the mouse esophagus /." Erlangen, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000252730.
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Sulistyowati, Emy. "Development of molecular probes to distinguish vesicular-arbuscular mycorrhizal fungi." Title page, Summary and Contents only, 1995. http://web4.library.adelaide.edu.au/theses/09A/09as949.pdf.
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Bibliography: leaves 71-79. Almost 80 percent of plant taxa develop vesicular-arbuscular mycorrhizae (VAM) which are symbiotic associations between plant roots and soil fungi. The fungi are biotropic-obligate symbionts. Identification of VAM fungi is currently based on spore characteristics. Molecular techniques provide tools for better and more accurate identification of species, as well as for the examination of genetic variability occuring between individual spores of a single species.
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Guo, Jing. "PHYSICO-CHEMICAL STUDIES OF THE VESICULAR GLUTAMATE TRANSPORTER 1 (VGLUT1)." The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-01122009-152821/.
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The vesicular glutamate transporter 1 (VGLUT1) is an important membrane protein located in glutamatergic synaptic vesicles. It is responsible for the storage and release of the excitatory neurotransmitter glutamate. VGLUT1 is a highly hydrophobic integral membrane protein with a molecular weight around 61 kD. The tertiary structure of VGLUT1 is still unknown. In our study, recombinant VGLUT1 was expressed in Pichia pastoris and purified using either a nickel chelating column or cobalt-coated Dynabeads. The HiTrapTM nickel chelating column proved to be more efficient in purification of recombinant VGLUT1 than Dynabeads. To study the physico-chemical properties and structure of VGLUT1 and advance our understanding of the membrane topology, FITC was used to modify VGLUT1 in solution. On average, 5.35 ¡À 1.10 lysines were labeled with FITC in each VGLUT1 molecule. Trypsin, endoproteinase Glu-C and Arg-C were used to digest FITC labeled VGLUT1 for mass spectrometry analysis. Mass spectrometry and other proteomics techniques were applied to identify labeled residues. Nine lysine residues were revealed to be labeled by FITC in total, among which 8 lysines (K10, K25, K140, K196, K272, K339, K378, and K507) are from native VGLUT1 and one is located at myc epitope (K569).
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Linden, James Francis. "Towards the establishment of the vesicular proteome of porcine retina." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426706.
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Sanders, Ian Robert. "Seasonality, specificity and selectivity of vesicular-arbuscular mycorrhizas in grasslands." Thesis, University of York, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280447.
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Facelli, Evelina. "The role of mycorrhizal symbiosis in plant intraspecific competition and population structure." Title page, Contents and Abstract only, 1998. http://hdl.handle.net/2440/37773.
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The overall objective of this project was to investigate the effects of the symbiotic association of plants with vesicular - arbuscular mycorrhizal fungi on the intensity of intraspecific competition and its consequences on population structure I performed four main glasshouse experiments using a non - cultivated species, Rhodanthe chlorocephala ssp rosea, or a cultivated species, Trifolium subterraneum. I grew the plants at different plant densities, under different levels of resources ( phosphorus and / or light ), in environments with homogeneous and / or patchy distribution of phosphorus ( P ). In pots with homogeneous distribution of P, the addition of P to R. chlorocephala and mycorrhizal infection in T. subterraneum increased plant biomass of single plants. However, these beneficial effects were reduced by increasing plant density. Shading of plants of T. subterraneum did not generally alter these effects. Mycorrhizal symbiosis and the addition of P always increased the intensity of plant intraspecific competition. In trays with patchy or homogeneous distribution of P, mycorrhizal infection and patchy distribution of P increased the total biomass and size inequality of populations of plants of T. subterraneum. Individual biomass was determined by the local soil P concentration in patchy environments and by mycorrhizal infection in low density treatments. Mycorrhizal infection, but not patchy P distribution, increased relative competition intensity. Asymmetric or symmetric distribution of resources between plants will change these size hierarchies. The distinction between these two types of distributions has lead to two different models explaining the interaction between competition and size inequality ( degree to which the biomass is concentrated within a small fraction of the population &# 40 Weiner and Thomas 1986 ) ) the resource depletion and resource pre - emption models ( Weiner and Thomas 1986, Weiner 1988b ). In the first model ( resource depletion ) competition reduces the relative growth rate of all the individuals by the same proportion, reduces variance of growth rates and reduces variation in sizes. Thus, in this model resource acquisition is proportional to plant size ( Weiner 1990 ). This model is also called symmetric or two - sided competition and applies when competition for nutrients predominates. It predicts that at high density, plants will be smaller but the population will have less inequality than at low density ( Weiner and Thomas 1986 ). In the second model ( resource pre - emption ), competition increases the variation in relative growth rates and increases variation in sizes. Large plants obtain a more than proportional share of the resources ( relative to sizes ) ( Weiner 1990 ) and this increases their competitive ability which results in a positive feedback on plant size. This phenomenon is also called snowball cumulation, asymmetric or one - sided competition and it was observed only when competition for light was predominant ( Wilson 1988a ). This second model predicts that at high density plant populations will have more inequality than at low density ( Weiner and Thomas 1986 ). Although these two models are generally accepted, alternative analyses and recent experiments show that the degree of asymmetry of the interaction depends on the spatial and temporal distribution of the resource, the spatial distribution of the individuals in the population, neighbourhood competition and the mobility of the resource ( Huston 1986 ; Miller and Weiner 1989, Weiner 1990, Bonan 1991 ). Weiner ( 1990 ) suggested that if nutrients are distributed homogeneously and the uptake is proportional to root size, the competitive interaction will be more symmetric, whereas if patches with more nutrients can be reached by large individuals, asymmetric competition will predominate. This hypothesis has not been tested yet. Turner and Rabinowitz ( 1983 ) found that populations with an initial random spatial distribution of individuals had an unexpected increase in size inequality. My results emphasise that the main effects of mycorrhizas at the individual level cannot be expected to be apparent at the population level, because of the influence of density - dependent processes. However, infected individuals with a strong response to the symbiosis would have an advantage in situations of competition. This scenario can explain the maintenance of the symbiotic ability even under conditions such as dense populations, where there is no obvious advantage of the symbiosis at the population level.Thesis (Ph.D.)--Department of Soil and Water, 1998.
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Amerian, Mohammad Reza. "Effects of VA mycorrhizae and drought on the physiology of maize and bean grown singly and intercropped." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247833.
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Hume, Alistair N. "The molecular genetics of endocytosis and growth control in fission yeast." Thesis, University of Sussex, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310260.
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Célia, Barbosa Lins Aroucha Dayse. "Alterações morfológicas e função motora da vesícula biliar na esquistossomose mansônica." Universidade Federal de Pernambuco, 2002. https://repositorio.ufpe.br/handle/123456789/6999.
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Previous issue date: 2002Com o objetivo de estudar as características ultrassonográficas da vesícula biliar na esquistossomose mansônica e sua função motora foram avaliados 29 pacientes portadores de esquistossomose, 5 na forma hepatointestinal e 24 hepatoesplênicos, e 29 individuos sadios, sem esquistossomose. Procurou-se verificar a ocorrência de alterações do volume e da fração de ejeção da vesícula biliar e relacioná-las com o grau de fibrose hepática a intensidade da fibrose perivesicular, e os sinais ultrassonográficos de hipertensão porta, comparando-se os resultados nos três grupos estudados. A ultrassonografia foi realizada seguindo protocolos estabelecidos pela Organização Mundial da Saúde, protocolos do Cairo e Niamey, que definem o grau e padrão da fibrose hepática, os aspectos ultrassonográficos da hipertensão porta e as alterações da parede vesicular. O volume da vesícula biliar foi avaliado em jejum e apõs 30 e 60 minutos de uma refeição gordurosa padronizada segundo Damião et al, 1997, a fim de calcular a fração de ejeção. Para o cálculo do volume utilizou-se a fórmula: volume = comprimento longitudinal x transversal x anteroposterior x 0,52. Foi encontrada correlação significativa entre a espessura da parede vesicular avaliada por meio da ultrassonografia com as formas clínicas da esquistossomose. Observou-se também relação estatisticamente significativa entre a espessura da parede vesicular com o grau de fibrose hepática, havendo progressão da espessura vesicular com o aumento do grau de fibrose hepática. Não houve diferença entre o volume de jejum, volume residual e fração de ejeção da vesícula biliar entre os pacientes esquistossomóticos e os controles.Esses achados nos levam a concluir que as alterações morfológicas presentes na vesícula biliar dos pacientes esquistossomóticos não foram suficientes para comprometer a função motora da vesícula avaliada por meio da ultrassonografia
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Sancayaningsih, Retno Peni. "Studies of vesicular-arbuscular mycorrhiza in Wanagama I Forest Research Center, Yogyakarta, Indonesia." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30315.
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Three studies were conducted on VA mycorrhiza in Wanagama Forest Research Center, Yogyakarta, Indonesia. The first was on VA mycorrhizal status of four forest species (Acacia mangium, Acacia holosericea, Tectona grandis, and Swietenia macrophylla) plantations and nurseries of Acacia mangium and Tectona grandis. Samples from the field were only taken during the dry season, June 1988. These four six-year old forestry species were mycorrhizal. Nursery plants had higher VAM colonization than the plantation roots and both Acacia species have higher percent colonization than the other two species. Available phosphorus in calcareous soils is low and seems not to be a major contribution to the variation of VAM colonization. Potassium and sodium were more important in this case even though their role could not be determined in this study.
The second study was conducted to determine VAM fungal species associated with the plant species. There were 16 different spore types belonging to the genera Glomus, (the most common found), Sclerocystis, Scutellispora, and probably Acaulospora. Type of inoculum and host compatibility were suggested as important factors in the success of pot culture study.
The third study was carried out in a growth chamber to determine Acacia spp. response to single VAM fungal species and mixed species inoculum. Single species inoculum in both Acacia was observed to improve biomass and plant growth better than the mixed inoculum. Acacia mangium performed better with Glomus versiforme than did A. holosericea. Host compatibility, effectiveness of VAM spore inoculant, infectivity and environmental factors have major effects on plant growth responses.
Study of tropical VAM requires further basic research, including taxonomy. Experimental procedures such as pot culture technique, type of inoculum, growth media and host plant specificity along with evaluation of appropriate soil chemical analysis also requirefurther elaboration. These types of studies are needed to understand the relationship between VAM and the environment and in the application studies in agriculture and forestry. This information is especially important in tropical countries, where little research results and limited resources, such as for fertilizers, are available.Land and Food Systems, Faculty of
Graduate
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Varela, Fernández Liza Fernanda, and Chimal Marco Antonio Mondragón. "“FACTORES DE RIESGO ASOCIADOS AL DESARROLLO DE COLECISTITIS LITIASICA. HOSPITAL MUNICIPAL DE TENANGO DEL VALLE MARIANO MATAMOROS BICENTENARIO, ISEM; 2010- 2011”." Tesis de Licenciatura, Medicina-Quimica, 2013. http://ri.uaemex.mx/handle/123456789/14032.
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El estudio realizado aporta información acerca de los factores de riesgo
asociados al desarrollo de la Colecistitis Crónica así mismo, conocer su
comportamiento epidemiológico, para establecer programas de prevención,
diagnóstico y atención oportuna,
Objetivo. Identificar los factores de riesgo asociados al desarrollo de Colecistitis
Litiásica en pacientes del Hospital General de Tenango, ISEM; durante los años
2010 y 2011.
Material y método. Se incluyeron 50 expedientes de pacientes con diagnóstico
de Colecistitis Litiásica ingresados en el Hospital Municipal de Tenango del Valle
durante el periodo de estudio 2010 y 2011 clasificando los datos recabados y
tabulando en cuadros y graficas para realizar el análisis estadístico de los
mismos.
Resultados. Se revisaron expedientes del archivo del Hospital Municipal de
Tenango del Valle, seleccionando 50. Se encontró que el grupo etáreo
mayoritario fue de los 36 a los 45 años (38%). Con respecto al género se
encontró una relación del sexo femenino 6:1 con respecto al sexo masculino. Se
encontró que 40 casos (80%) cuentan con un Índice de Masa Corporal por arriba
de lo normal en un 38%. En cuanto a los signos y síntomas, se reportó en 90%
de los casos dolor abdominal en hipocondrio derecho como la principal
manifestación clínica. En relación al tratamiento quirúrgico; se realizó en un 82%
colecistectomía abierta y sólo 18% pacientes fueron sometidos a
colecistectomía laparoscópica observando complicaciones como sangrado
mientras que otras complicaciones en un 2%.
Conclusiones. Durante el estudio los factores de riesgo asociados fueron edad,
sexo femenino, obesidad, y multiparidad encontrando además que las
complicaciones son más frecuentes que lo reportado en la literatura.
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Griffiths, Genevieve S. "Investigating the impact and mechanism of vesicular and non-vesicular mediated GPI-linked protein transfer from reproductive luminal fluids to sperm, using SPAM1 as a model." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 119 p, 2007. http://proquest.umi.com/pqdweb?did=1397900391&sid=22&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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Scheu, Bettina. "Understanding silicic volcanism: Constraints from elasticity and failure of vesicular magma." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-44019.
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Burkhart, Christoph. "Characterization of the T helper cell response to vesicular stomatitis virus /." Zürich, 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10799.
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Evans, Timothy Martin. "Molecular events in hedgehog signalling : regulation by vesicular trafficking and sterols /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18704.pdf.
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Murphy, Phillip James. "Plant-fungal interactions during vesicular-arbuscular mycorrhiza development : a molecular approach." Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phm9778.pdf.
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Bibliography: leaves 153-185. Vesicular-arbuscular (VA) mycorrhiza formation is a complex process which is under the genetic control of both plant and fungus. This project aims to develop a model infection system in Hordeum vulgare L. (barley) suitable for molecular analysis; to identify host plant genes differentially expressed during the early stages of the infection process; and to screen a mutant barley population for phenotypes which form abnormal mycorrhizas.
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Choi, Woo-Young. "Molecular biological characterization of defective interfering particles of vesicular stomatitis virus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq26110.pdf.
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Mire, Chad Edward. "Investigation of the vesicular stomatitis virus matrix protein uncoating and assembly /." View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/abstracts/2008-035-Mire-index.html.
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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2008.Title from title page screen (viewed on September 9, 2008). Research advisor: Michael A. Whitt, Ph.D. Document formatted into pages (xi, 119 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 104-119).
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Jethwa, Susanna Anjali. "Exosomes : vesicular carriers of autotaxin, a novel mechanism of LPA signalling." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608189.
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Blackmore, Colin Giles. "Modulation of intravesicular pH and progastrin processing by vesicular monoamine transporters." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366674.
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Dixon, Leigh. "Vesicular systems and solubilisation : drug interactions with lipid monolayers and bilayers." Thesis, University of Strathclyde, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401329.
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McGonigle, T. P. "Vesicular-arbuscular mycorrhizas and plant performance in a semi-natural grassland." Thesis, University of York, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379456.
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Predescu, Sanda. "Plasmalemmal vesicles (caveolae) are special vesicular carriers involved in endothelial transcytosis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9944218.
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Venkatesh, Divya. "Evolution of vesicular transport in kinetoplastids : dynamics and novel gene products." Thesis, University of Cambridge, 2016. https://www.repository.cam.ac.uk/handle/1810/269276.
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The membrane trafficking system mediates delivery of macromolecules and metabolites to discrete intracellular compartments from their site of uptake or synthesis. For many pathogens the trafficking system has a special relevance as it is responsible for maintaining the host-pathogen interface, i.e., the cell surface. Both the surface and the underlying trafficking apparatus are intimately connected with immune evasion in many parasites including those belonging to the highly divergent order Kinetoplastida. Kinetoplastid parasites are etiological agents of several neglected tropical diseases such as African sleeping sickness, Chagas disease, and Leishmaniasis. Newly available sequences of many kinetoplastid genomes were used to reconstruct evolution of trafficking across this lineage, using three central paralogous trafficking families: Rabs, SNAREs and Rab-GAPs, which have defined roles in specific trafficking events. Further, proteomics was used to analyse a representative SNARE complex to explore compositional conservation between kinetoplastids and Opistokhonts. Overall there is little evidence for large scale expansions or contractions of these protein families, excluding a direct association with parasitism or changes to host range, host immunosophistication or transmission mechanisms. The data indicate a stepwise sculpting of the trafficking system where the large repertoire of the basal bodonids is mainly retained by the cruzi group, while extensive lossses characterise other lineages, particularly the African trypanosomes and phytomonads. Kinetoplastids possess several lineage-specific Rabs but all retain a core canonical Rab set; by contrast there is little novelty within the SNARE family even though certain canonical endosomal SNAREs appear to show a considerable degree of sequence divergence. Proteomics suggests that SNARE complex composition is largely conserved. The major changes in Rab and SNARE repertoires are associated with endosomal and late exocytic pathways, which is consistent with the considerable evolution of surface proteomes. Therefore, despite the absence of a transition per se associated with parasitism, adaptation of membrane trafficking is likely under active selection where it meets the host environment.
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Castro, Braulio Marcone de. "Funções motoras em camundongos deficientes do transportador vesicular de acetilcolina (VAChT)." Universidade Federal de Minas Gerais, 2006. http://hdl.handle.net/1843/SMOC-6WMHF8.
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Acetylcholine (ACh)mediated neurotransmission has a crucialrole in the control of movement. Release of ACh depends on its storagein synaptic vesicles, a step controlled by the activity of the VAChT. Wedeveloped a genetically altered strain of mice with reduced expression ofthis transporter. Heterozygous (VAChT KDHET) and homozygous (VAChTKDHOM) knockdown mice have 45 and 65% decrease in VAChT protein.To evaluate whether VAChT deficiency may affect motor functions, weused the following tasks: grip force, wire hang and treadmill. Motorlearning was measured on the rotarod. We were unable to detect anyalteration in the grip force, wire hang and treadmill tests in VAChT KDHETmice; however VAChT KDHOM mice were significantly impaired in allthree tasks. Reduced grip strength in VAChT KDHOM mice was readilyreversed by prior injection of galantamine. Moreover, motor learningperformance on the accelerating rotarod task by VAChT KDHET mice wasworse than for wild type controls. Our results demonstrate that differentlevels of cholinergic hypofunction may causes distinct types of motorabnormality. VAChT KDHOM shows a myastenic profile, while VAChTxi KDHET mice presented a decrease in motor learning with normal motor function. These genetically modified mice may represent a novel model system for investigation of motor control and congenital myasthenic syndromes.A liberação do neurotransmissor Acetilcolina (ACh) depende desua estocagem em vesículas sinápticas, um passo controlado pelaatividade do transportador vesicular de ACh (VAChT). A Neurotransmissão mediada por ACh possui um papel crucial no controle central e periférico do movimento. Camundongos Knock-downheterozigoto (VAChT KDHET) e homozigoto (VAChT KDHOM) para oVAChT apresenntam uma redução de 45% e 65% na expressão doVAChT, respectivamente. Para avaliar o impacto da redução daexpressão do VAChT em funções motoras, utilizamos o teste de força deagarre, o teste wire hang, a esteira motorizada e o teste da locomoçãoforçada em cilindro giratório (Rotarod). Animais VAChT KDHET nãoapresentaram alterações no wire hang, teste de força de agarre e naesteira motorizada, entretanto animais VAChT KDHOM apresentaram uma performance significamente prejudicada em tais tarefas. O déficit na força de agarre observado em animais VAChT KDHOM foitemporariamente revertido pela administração de inibidores da AChEcentrais e periféricos. Apesar da ausência de alterações na forçamuscular e resistência ao exercício, camundongos VAChT KDHETapresentaram uma cinética de aprendiizado motor mais lenta queanimais selvagens. Nossos resultados demonstram que diferentes níveis de hipofunção colinérgica podem causar formas distintas deanormalidade motora. Camundongos VAChT KDHOM apresentaram um x perfil miastênico, enquanto animais VAChT KDHET parecem apresentar um comprometimento de origem predominantemente central. Estes camundongos geneticamente modificados podem representar novos modelos para a investigação da neuroquímica do controle motor, bem como modelos de disfunções motoras geradas por quadros de hipofunção colinérgica.