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Academic literature on the topic 'Type III secretion helper proteins'

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Published: 23 September 2022
Last updated: 28 January 2023

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Journal articles on the topic "Type III secretion helper proteins"

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Holeva, Maria C., Kenneth S. Bell, Lizbeth J. Hyman, Anna O. Avrova, Stephen C. Whisson, Paul R. J. Birch, and Ian K. Toth. "Use of a Pooled Transposon Mutation Grid to Demonstrate Roles in Disease Development for Erwinia carotovora subsp. atroseptica Putative Type III Secreted Effector (DspE/A) and Helper (HrpN) Proteins." Molecular Plant-Microbe Interactions® 17, no. 9 (September 2004): 943–50. http://dx.doi.org/10.1094/mpmi.2004.17.9.943.

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Soft rot Erwinia spp., like other closely related plant pathogens, possess a type III secretion system (TTSS) (encoded by the hrp gene cluster) implicated in disease development. We report the sequence of the entire hrp gene cluster and adjacent dsp genes in Erwinia carotovora subsp. atroseptica SCRI1039. The cluster is similar in content and structural organization to that in E. amylovora. However, eight putative genes of unknown function located within the E. carotovora subsp. atroseptica cluster do not have homologues in the E. amylovora cluster. An arrayed set of Tn5 insertional mutants (mutation grid) was constructed and pooled to allow rapid isolation of mutants for any given gene by polymerase chain reaction screening. This novel approach was used to obtain mutations in two structural genes (hrcC and hrcV), the effector gene dspE/A, and the helper gene hrpN. An improved pathogenicity assay revealed that these mutations led to significantly reduced virulence, showing that both the putative E. carotovora subsp. atroseptica TTSS-delivered effector and helper proteins are required for potato infection.
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Yu, H. B., P. S. Srinivasa Rao, H. C. Lee, S. Vilches, S. Merino, J. M. Tomas, and K. Y. Leung. "A Type III Secretion System Is Required for Aeromonas hydrophila AH-1 Pathogenesis." Infection and Immunity 72, no. 3 (March 2004): 1248–56. http://dx.doi.org/10.1128/iai.72.3.1248-1256.2004.

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ABSTRACT Aeromonas hydrophila is a gram-negative opportunistic pathogen in fish and humans. Many bacterial pathogens of animals and plants have been shown to inject anti-host virulence determinants into the hosts via a type III secretion system (TTSS). Degenerate primers based on lcrD family genes that are present in every known TTSS allowed us to locate the TTSS gene cluster in A. hydrophila AH-1. A series of genome walking steps helped in the identification of 25 open reading frames that encode proteins homologous to those in TTSSs in other bacteria. PCR-based analysis showed the presence of lcrD homologs (ascV) in all of the 33 strains of A. hydrophila isolated from various sources. Insertional inactivation of two of the TTSS genes (aopB and aopD) led to decreased cytotoxicity in carp epithelial cells, increased phagocytosis, and reduced virulence in blue gourami. These results show that a TTSS is required for A. hydrophila pathogenesis. This is the first report of sequencing and characterization of TTSS gene clusters from A. hydrophila. The TTSS identified here may help in developing suitable vaccines as well as in further understanding of the pathogenesis of A. hydrophila.
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Morse, Kaitlyn, Junzo Norimine, Guy H. Palmer, Eric L. Sutten, Timothy V. Baszler, and Wendy C. Brown. "Association and Evidence for Linked Recognition of Type IV Secretion System Proteins VirB9-1, VirB9-2, and VirB10 in Anaplasma marginale." Infection and Immunity 80, no. 1 (October 28, 2011): 215–27. http://dx.doi.org/10.1128/iai.05798-11.

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ABSTRACTLike several other bacterial pathogens,Anaplasma marginalehas an outer membrane that induces complete protection from infection and disease. However, the proteins that confer protective immunity and whether protection requires interacting proteins and/or linked T-cell and immunoglobulin G epitopes are not known. Our goal is to target the conserved type IV secretion system (T4SS) to identify conserved, immunogenic membrane proteins that are interacting and linked recognition candidates. Linked recognition is a process by which a B cell is optimally activated by a helper T cell that responds to the same, or physically associated, antigen.A. marginaleT4SS proteins VirB2, VirB4-1, VirB4-2, VirB6-1, VirB7, VirB8-2, VirB9-1, VirB9-2, VirB10, VirB11, and VirD4 were screened for their ability to induce IgG and to stimulate CD4+T cells from outer membrane-vaccinated cattle. VirB9-1, VirB9-2, and VirB10 induced the strongest IgG and T-cell responses in the majority of cattle, although three animals with major histocompatibility complex class II DRB3 restriction fragment length polymorphism types 8/23, 3/16, and 16/27 lacked T-cell responses to VirB9-1, VirB9-1 and VirB9-2, or VirB9-2 and VirB10, respectively. For these animals, VirB9-1-, VirB9-2-, and VirB10-specific IgG production may be associated with T-cell help provided by responses to an interacting protein partner(s). Interacting protein partners indicated by far-Western blotting were confirmed by immunoprecipitation assays and revealed, for the first time, specific interactions of VirB9-1 with VirB9-2 and VirB10. The immunogenicity and interactions of VirB9-1, VirB9-2, and VirB10 justify their testing as a linked protein vaccine againstA. marginale.
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Misselwitz, Benjamin, Saskia K. Kreibich, Samuel Rout, Bärbel Stecher, Balamurugan Periaswamy, and Wolf-Dietrich Hardt. "Salmonella entericaSerovar Typhimurium Binds to HeLa Cells via Fim-Mediated Reversible Adhesion and Irreversible Type Three Secretion System 1-Mediated Docking." Infection and Immunity 79, no. 1 (October 25, 2010): 330–41. http://dx.doi.org/10.1128/iai.00581-10.

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ABSTRACTThe food-borne pathogenSalmonella entericaserovar Typhimurium invades mammalian epithelial cells. This multistep process comprises bacterial binding to the host cell, activation of theSalmonellatype three secretion system 1 (T1), injection of effector proteins, triggering of host cell actin rearrangements, andS. Typhimurium entry. While the latter steps are well understood, much less is known about the initial binding step. Earlier work had implicated adhesins (but not T1) or T1 (but not other adhesins). We have studied here theSalmonellavirulence factors mediatingS. Typhimurium binding to HeLa cells. Using an automated microscopy assay and isogenicS. Typhimurium mutants, we analyzed the role of T1 and of several known adhesins (Fim, Pef, Lpf, Agf, and Shd) in host cell binding. In wild-typeS. Typhimurium, host cell binding was mostly attributable to T1. However, in the absence of T1, Fim (but not Pef, Lpf, Agf, and Shd) also mediated HeLa cell binding. Furthermore, in the absence of T1 and type I fimbriae (Fim), we still observed residual binding, pointing toward at least one additional, unidentified binding mechanism. Dissociation experiments established that T1-mediated binding was irreversible (“docking”), while Fim-mediated binding was reversible (“reversible adhesion”). Finally, we show that noninvasive bacteria docking via T1 or adhering via Fim can efficiently invade HeLa cells, if actin rearrangements are triggeredin transby a wild-typeS. Typhimurium helper strain. Our data show that binding to HeLa cells is mediated by at least two different mechanisms and that both can lead to invasion if actin rearrangements are triggered.
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D'Souza, S., V. Rosseels, M. Romano, A. Tanghe, O. Denis, F. Jurion, N. Castiglione, A. Vanonckelen, K. Palfliet, and Kris Huygen. "Mapping of Murine Th1 Helper T-Cell Epitopes of Mycolyl Transferases Ag85A, Ag85B, and Ag85C from Mycobacterium tuberculosis." Infection and Immunity 71, no. 1 (January 2003): 483–93. http://dx.doi.org/10.1128/iai.71.1.483-493.2003.

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ABSTRACT BALB/c (H-2d ) and C57BL/6 (H-2b ) mice were infected intravenously with Mycobacterium tuberculosis H37Rv or vaccinated intramuscularly with plasmid DNA encoding each of the three mycolyl transferases Ag85A, Ag85B, and Ag85C from M. tuberculosis. Th1-type spleen cell cytokine secretion of interleukin-2 (IL-2) and gamma interferon (IFN-γ) was analyzed in response to purified Ag85 components and synthetic overlapping peptides covering the three mature sequences. Tuberculosis-infected C57BL/6 mice reacted strongly to some peptides from Ag85A and Ag85B but not from Ag85C, whereas tuberculosis-infected BALB/c mice reacted only to peptides from Ag85A. In contrast, spleen cells from both mouse strains produced elevated levels of IL-2 and IFN-γ following vaccination with Ag85A, Ag85B, and Ag85C DNA in response to peptides of the three Ag85 proteins, and the epitope repertoire was broader than in infected mice. Despite pronounced sequence homology, a number of immunodominant regions contained component specific epitopes. Thus, BALB/c mice vaccinated with all three Ag85 genes reacted against the same amino acid region, 101 to 120, that was also immunodominant for Ag85A in M. bovis BCG-vaccinated and tuberculosis-infected H-2d haplotype mice, but responses were completely component specific. In C57BL/6 mice, a cross-reactive T-cell response was detected against two carboxy-terminal peptides spanning amino acids 241 to 260 and 261 to 280 of Ag85A and Ag85B. These regions were not recognized at all in C57BL/6 mice vaccinated with Ag85C DNA. Our results underline the need for comparative analysis of all three Ag85 components in future vaccination studies.
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Lindeberg, Magdalen, Samuel Cartinhour, Christopher R. Myers, Lisa M. Schechter, David J. Schneider, and Alan Collmer. "Closing the Circle on the Discovery of Genes Encoding Hrp Regulon Members and Type III Secretion System Effectors in the Genomes of Three Model Pseudomonas syringae Strains." Molecular Plant-Microbe Interactions® 19, no. 11 (November 2006): 1151–58. http://dx.doi.org/10.1094/mpmi-19-1151.

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Pseudomonas syringae strains translocate large and distinct collections of effector proteins into plant cells via the type III secretion system (T3SS). Mutations in T3SS-encoding hrp genes are unable to elicit the hypersensitive response or pathogenesis in nonhost and host plants, respectively. Mutations in individual effectors lack strong phenotypes, which has impeded their discovery. P. syringae effectors are designated Hop (Hrp outer protein) or Avr (avirulence) proteins. Some Hop proteins are considered to be extracellular T3SS helpers acting at the plant-bacterium interface. Identification of complete sets of effectors and related proteins has been enabled by the application of bioinformatic and high-throughput experimental techniques to the complete genome sequences of three model strains: P. syringae pv. tomato DC3000, P. syringae pv. phaseolicola 1448A, and P. syringae pv. syringae B728a. Several recent papers, including three in this issue of Molecular Plant-Microbe Interactions, address the effector inventories of these strains. These studies establish that active effector genes in P. syringae are expressed by the HrpL alternative sigma factor and can be predicted on the basis of cis Hrp promoter sequences and N-terminal amino-acid patterns. Among the three strains analyzed, P. syringae pv. tomato DC3000 has the largest effector inventory and P. syringae pv. syringae B728a has the smallest. Each strain has several effector genes that appear inactive. Only five of the 46 effector families that are represented in these three strains have an active member in all of the strains. Web-based community resources for managing and sharing growing information on these complex effector arsenals should help future efforts to understand how effectors promote P. syringae virulence.
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Zhao, Yue, Jianjin Shi, Xuyan Shi, Yupeng Wang, Fengchao Wang, and Feng Shao. "Genetic functions of the NAIP family of inflammasome receptors for bacterial ligands in mice." Journal of Experimental Medicine 213, no. 5 (April 25, 2016): 647–56. http://dx.doi.org/10.1084/jem.20160006.

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Biochemical studies suggest that the NAIP family of NLR proteins are cytosolic innate receptors that directly recognize bacterial ligands and trigger NLRC4 inflammasome activation. In this study, we generated Naip5−/−, Naip1−/−, and Naip2−/− mice and showed that bone marrow macrophages derived from these knockout mice are specifically deficient in detecting bacterial flagellin, the type III secretion system needle, and the rod protein, respectively. Naip1−/−, Naip2−/−, and Naip5−/− mice also resist lethal inflammasome activation by the corresponding ligand. Furthermore, infections performed in the Naip-deficient macrophages have helped to define the major signal in Legionella pneumophila, Salmonella Typhimurium and Shigella flexneri that is detected by the NAIP/NLRC4 inflammasome. Using an engineered S. Typhimurium infection model, we demonstrate the critical role of NAIPs in clearing bacterial infection and protecting mice from bacterial virulence–induced lethality. These results provide definitive genetic evidence for the important physiological function of NAIPs in antibacterial defense and inflammatory damage–induced lethality in mice.
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Medina, Eva, Paola Paglia, Thomas Nikolaus, Astrid Müller, Michael Hensel, and Carlos A. Guzmán. "Pathogenicity Island 2 Mutants of Salmonella typhimurium Are Efficient Carriers for Heterologous Antigens and Enable Modulation of Immune Responses." Infection and Immunity 67, no. 3 (March 1, 1999): 1093–99. http://dx.doi.org/10.1128/iai.67.3.1093-1099.1999.

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ABSTRACT The potential use as vaccine delivery system of Salmonella typhimurium strains harboring defined mutations in thesseC (HH104) and sseD (MvP101) genes, which encode putative effector proteins of the type III secretion system ofSalmonella pathogenicity island 2, was evaluated and compared with that of the well-characterized aroA mutant strain SL7207 by using β-galactosidase (β-Gal) as a model antigen. When orally administered to immune-competent or gamma interferon-deficient (IFN-γ−/−) BALB/c mice, both mutants were found to be highly attenuated (50% lethal dose, >109 bacteria). Both strains were also able to efficiently colonize and persist in Peyer’s patches. Immunization with HH104 and MvP101 triggered β-Gal-specific serum and mucosal antibody responses equivalent to or stronger than those observed in SL7207-immunized mice. Although immunoglobulin G2 (IgG2) serum antibodies were dominant in all groups, IgG1 was also significantly increased in mice vaccinated with MvP101 and SL7207. Comparable β-Gal-specific IgA and IgG antibodies were detected in intestinal lavages from mice immunized with the different strains. Antigen-specific CD4+ T-helper cells were generated after vaccination with all vaccine prototypes; however, responses were significantly more efficient when HH104 and MvP101 were used (P < 0.05). Significantly higher levels of IFN-γ were produced by restimulated spleen cells from mice immunized with HH104 than from those vaccinated with the MvP101 or SL7207 derivatives (P ≤ 0.05). Interestingly, the three strains induced major histocompatibility complex class I-restricted CD8+ cytotoxic T cells against β-Gal; however, cytotoxic T-lymphocyte responses were significantly stronger after immunization with HH104 (P < 0.05). These novel S. typhimurium attenuated strains constitute promising delivery systems for vaccine antigens. The qualitative differences observed in the obtained responses with different carriers may be useful for those applications in which a targeted immunomodulation is required.
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Piazza, Roxane M. F., Sabine Delannoy, Patrick Fach, Halha O. Saridakis, Margareth Z. Pedroso, Letícia B. Rocha, Tânia A. T. Gomes, Mônica A. M. Vieira, Lothar Beutin, and Beatriz E. C. Guth. "Molecular and Phenotypic Characterization of Escherichia coli O26:H8 among Diarrheagenic E. coli O26 Strains Isolated in Brazil." Applied and Environmental Microbiology 79, no. 22 (August 23, 2013): 6847–54. http://dx.doi.org/10.1128/aem.01693-13.

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ABSTRACTEscherichia colistrains of serogroup O26 comprise two distinct groups of pathogens, characterized as enteropathogenicE. coli(EPEC) and enterohemorrhagicE. coli(EHEC). Among the several genes related to type III secretion system-secreted effector proteins,espKwas found to be highly specific for EHEC O26:H11 and itsstx-negative derivative strains isolated in European countries.E. coliO26 strains isolated in Brazil from infant diarrhea, foods, and the environment have consistently been shown to lackstxgenes and are thus considered atypical EPEC. However, no further information related to their genetic background is known. Therefore, in this study, we aimed to discriminate and characterize these Brazilian O26stx-negative strains by phenotypic, genetic, and biochemical approaches. Among 44 isolates confirmed to be O26 isolates, most displayed flagellar antigen H11 or H32. Out of the 13 nonmotile isolates, 2 tested positive forfliCH11, and 11 werefliCH8positive. The identification of genetic markers showed that several O26:H11 and all O26:H8 strains tested positive forespKand could therefore be discriminated as EHEC derivatives. The presence of H8 among EHEC O26 and itsstx-negative derivative isolates is described for the first time. The interaction of three isolates with polarized Caco-2 cells and with intestinal biopsy specimen fragmentsex vivoconfirmed the ability of the O26 strains analyzed to cause attaching-and-effacing (A/E) lesions. The O26:H32 strains, isolated mostly from meat, were considered nonvirulent. Knowledge of the virulence content ofstx-negative O26 isolates within the same serotype helped to avoid misclassification of isolates, which certainly has important implications for public health surveillance.
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Coburn, Bryan, Inna Sekirov, and B. Brett Finlay. "Type III Secretion Systems and Disease." Clinical Microbiology Reviews 20, no. 4 (October 2007): 535–49. http://dx.doi.org/10.1128/cmr.00013-07.

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SUMMARY Type III secretion systems (T3SSs) are complex bacterial structures that provide gram-negative pathogens with a unique virulence mechanism enabling them to inject bacterial effector proteins directly into the host cell cytoplasm, bypassing the extracellular milieu. Although the effector proteins vary among different T3SS pathogens, common pathogenic mechanisms emerge, including interference with the host cell cytoskeleton to promote attachment and invasion, interference with cellular trafficking processes, cytotoxicity and barrier dysfunction, and immune system subversion. The activity of the T3SSs correlates closely with infection progression and outcome, both in animal models and in human infection. Therefore, to facilitate patient care and improve outcomes, it is important to understand the T3SS-mediated virulence processes and to target T3SSs in therapeutic and prophylactic development efforts.
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Dissertations / Theses on the topic "Type III secretion helper proteins"

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Demirjian, Choghag. "Deciphering Arabidopsis thaliana responses to Ralstonia solanacearum virulence factors through the study of plant natural variation." Thesis, Toulouse 3, 2022. http://www.theses.fr/2022TOU30109.

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Ralstonia solanacearum, l'agent causal du flétrissement bactérien, est considéré comme l'un des agents pathogènes bactériens les plus importants au monde. Le pouvoir pathogène de cette bactérie du sol est principalement basé sur son système de sécrétion de type III (SST3) et ses effecteurs de type III (ET3s), provoquant la maladie sur plus de 250 espèces végétales. R. solanacearum injecte ses ET3s à travers cette seringue moléculaire directement à l'intérieur de la plante hôte. Ces ET3s détournent les réponses de défense de la plante, soit dans le cytoplasme, soit dans le noyau, afin de supprimer l'immunité de la plante et de favoriser la multiplication bactérienne. La sécrétion des ET3s est finement contrôlée au niveau post-traductionnel par des protéines associées au contrôle de la sécrétion de type III, et par des protéines chaperonnes de type III.A ce jour, la fonction in planta de ces effecteurs et protéines chaperonnes, et la manière dont R. solanacearum module l’immunité de la plante en sa faveur restent mal comprises. Mon projet de thèse visait à mieux comprendre le rôle des déterminants de la pathogénicité de R. solanacearum en identifiant certaines des cibles d’A. thaliana, directes ou indirectes, modulées par la bactérie. Pour ce faire, j'ai utilisé des populations naturelles d'A. thaliana à deux échelles géographiques et adopté l'approche consistant à confronter des populations naturelles à des mutants de R. solanacearum dans lesquels des déterminants majeurs de pathogénie sont mutés. Cette approche est nouvelle puisque à ce jour les études d’association pangénomique (GWAS) menées sur les interactions plantes-agents pathogènes utilisent des souches sauvages de phytopathogènes. En outre, cette approche a permis de découvrir une diversité de réponses qui n'avaient pas été détectées auparavant. Dans la première partie de mon projet de thèse, j'ai identifié des QTLs impliqués dans la résistance quantitative à la maladie en réponse à des mutants simples de R. solanacearum, et j'ai validé fonctionnellement ces QTLs (Quantitative Trait Loci) comme facteurs de sensibilité. Dans la deuxième partie de ma thèse, nous avons étudié un gène codant pour une protéine de type NLR que nous avons appelé Bacterial Wilt Susceptibility 1 (BWS1). Nous avons montré que BWS1 agissait comme un facteur de sensibilité quantitatif, ayant un rôle de régulateur négatif dans une réponse immunitaire dépendante de SGT1.)
Ralstonia solanacearum, the causal agent of bacterial wilt, is considered one of the world’s most important bacterial pathogens. This soil-borne bacterium relies mainly on its type III secretion system (T3SS) and type III effectors (T3Es) in order to cause disease in more than 250 plant species. R. solanacearum injects its T3Es through this molecular syringe directly inside the host plant. These T3Es hijack plant defense responses in either the cytoplasm or the nucleus aiming to suppress plant immunity and promote bacterial multiplication. T3E secretion is finely controlled at the post-translational level by helper proteins, called T3SS control proteins, and type III chaperones.To date, the in planta function of these effectors and helper proteins and how R. solanacearum modulates plant genes to its favor remains poorly understood. My thesis project aimed to better understand the role of R. solanacearum pathogenicity determinants by identifying some of the direct or indirect plant targets of A. thaliana, modulated by the bacterium. For this purpose, I used natural populations of A. thaliana on two geographical scales and adopted the approach of challenging mapping populations to R. solanacearum mutants in which major pathogenic determinants are mutated. This approach is new since most of the GWAS (Genome-Wide Association Studies) in plant-pathogen interactions use wild-type strains of phytopathogens. Furthermore, it unveiled a previously undetected diversity of responses. In the first part of my Ph.D. project, I identified QTLs (Quantitative Trait Loci) involved in quantitative disease resistance to R. solanacearum single mutants and I validated these QTLs as susceptibility factors. In the second part of my thesis, we studied a gene encoding for a NLR protein that we called Bacterial Wilt Susceptibility 1 (BWS1). We showed that BWS1 was acting as quantitative susceptibility factor, mediating a negative regulation of an SGT1-dependent immune response
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Bailey, Christopher Michael. "A Bioinformatics Analysis of Bacterial Type-III Secretion System Genes and Proteins." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1300/.

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Type-III secretion systems (T3SSs) are responsible for the biosynthesis of flagella, and the interaction of many animal and plant pathogens with eukaryotic cells. T3SSs consist of multiple proteins which assemble to form an apparatus capable of exporting proteins through both membranes of Gram-negative bacteria in one step. Proteins conserved amongst T3SSS can be used for analysis of these systems using computational homology searching. By using tools including BLAST and HMMER in conjunction phylogenetic analysis this thesis examines the range of T3SSs, both in terms of the proteins they contain, and also the bacteria which contain them. In silico analysis of several of the conserved components of T3SSs shows similarities between them and other secretion systems, as well as components of ATPases. Use of conserved components allows for identification of T3SS loci in diverse bacteria, in order to assess in the different proteins used by different T3SSs, and to see where, in evolutionary space, these differences arose. Analysis of homology data also allows for comprehensive re-annotation of T3SS loci within Desulfovibrio, Lawsonia and Hahella, and subsequent comparison of these T3SSs with related Yersinial T3SSs, and also (in conjunction with in vitro assays) for identification of many novel effectors in E. coli.
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Panina, Ekaterina Mikhailovna. "Identification and characterization of type III secretion effector proteins in gram-negative bacteria." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1481675641&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Muschiol, Sandra. "Small molecule inhibitors of type III secretion and their effect on Chlamydia development." Stockholm, 2009. http://diss.kib.ki.se/2009/978-91-7409-645-3/.

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Smollett, Katherine Louise. "Characterisation of the enteropathogenic E. coli type III secretion system effector proteins ESPG and ESPG2." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439818.

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Haraga, Andrea. "Study of the intracellular function of the Salmonella enterica serovar Typhimurium type III secretion effector SspH1 /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/11486.

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Ohlson, Maikke B. "Characterization of the intracellular activities of SseJ and SifA, two Salmonella enterica serovar typhimurium type III secretion effector proteins /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/11485.

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Wilson, Rebecca Kerry. "Functional analysis of EscF and EscJ : two structural proteins of the type III secretion system of enteropathogenic Escherichia coli." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406326.

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Alzahrani, Ashwag. "Identification of Human Proteins Interacting with the Protein IcsB of Shigella flexneri." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38333.

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Edqvist, Petra J. "Multiple twists in the molecular tales of YopD and LcrH in type III secretion by Yersinia pseudotuberculosis." Doctoral thesis, Umeå : Umeå University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-985.

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Books on the topic "Type III secretion helper proteins"

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Type III secretion chaperones: A molecular toolkit for all occasions. Hauppauge, N.Y: Nova Science Publishers, 2009.

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Book chapters on the topic "Type III secretion helper proteins"

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Condry, Danielle L. Jessen, and Matthew L. Nilles. "Analysis of Type III Secretion System Secreted Proteins." In Methods in Molecular Biology, 93–99. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6649-3_8.

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Alvine, Travis D., Patrick Osei-Owusu, Danielle L. Jessen Condry, and Matthew L. Nilles. "Expression and Purification of N-Terminally His-Tagged Recombinant Type III Secretion Proteins." In Methods in Molecular Biology, 183–91. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6649-3_16.

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Preston, Gail M., and Alan Collmer. "The Type III Secretion Systems of Plant-Associated Pseudomonads: Genes and Proteins on the Move." In Pseudomonas, 181–219. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9084-6_6.

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El Qaidi, Samir, Miaomiao Wu, Congrui Zhu, and Philip R. Hardwidge. "Salmonella, E. coli, and Citrobacter Type III Secretion System Effector Proteins that Alter Host Innate Immunity." In Protein Reviews – Purinergic Receptors, 205–18. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/5584_2018_289.

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Collmer, Alan, B. H. Kvitko, J. E. Morello, K. R. Munkvold, H. S. Oh, and C. F. Wei. "Exploring the Functions of Proteins Secreted by the Hrp Type III Secretion System of Pseudomonas syringae." In Pseudomonas syringae Pathovars and Related Pathogens – Identification, Epidemiology and Genomics, 229–37. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6901-7_24.

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Alvine, Travis D., David S. Bradley, and Matthew L. Nilles. "Mouse Immunization with Purified Needle Proteins from Type III Secretion Systems and the Characterization of the Immune Response to These Proteins." In Methods in Molecular Biology, 193–201. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6649-3_17.

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Larson, Charles L., Jeffrey E. Christensen, Sophia A. Pacheco, Scott A. Minnich, and Michael E. Konkel. "Campylobacter jejuni Secretes Proteins via the Flagellar Type III Secretion System That Contribute to Host Cell Invasion and Gastroenteritis." In Campylobacter, 315–32. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815554.ch18.

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Orth, Kim, Jack E. Dixon, and James B. Bliska. "20 Effector proteins of bacterial type III protein secretion systems: Elucidating their biochemical effects on eukaryotic signaling cascades." In Methods in Microbiology, 361–76. Elsevier, 2002. http://dx.doi.org/10.1016/s0580-9517(02)31021-3.

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Kombade, Sarika, and Navneet Kaur. "Pathogenicity Island in Salmonella." In Salmonella - a Challenge From Farm to Fork [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96443.

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Considering a complex set of interplay with its host, Salmonella needs numerous genes for its full virulence. These genes responsible for invasion, survival, and extra intestinal spread are located on pathogenicity islands known as Salmonella pathogenicity islands (SPIs) that are thought to be acquired by horizontal gene transfer. A total of 17 SPIs (1–17) are recognized so far. The type III secretion system (T3SS) encoded by SPI-1 is considered as the most important virulence factor for Salmonella that delivers effector proteins necessary for invasion and production of enteritis. Among various SPIs, the role in virulence is well proven for SPI1 and SPI2 and further insight into the complex regulatory network of SPIs can contribute to drug investigation and prevention of infection.
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Primrose, Sandy B. "The Three Great Pandemics of Plague." In Microbiology of Infectious Disease, 25–30. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780192863843.003.0003.

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The bacterium Yersinia pestis causes bubonic plague (infection of lymph glands) when transmitted by fleas, and pneumonic plague if transmitted by aerosols from a person with a lung infection. Yersinia pestis was responsible for three great plague pandemics: the Justinian plague (541–750), the Black Death (1347–1700s), and the Third Pandemic (1894–mid-twentieth century). Ancient DNA (aDNA) of Yersinia pestis has been recovered from teeth of victims of each of these plagues. Yersinia pestis diverged from the much less pathogenic Yersinia pseudotuberculosis about 5,700 years ago. Following divergence, Yersinia pestis acquired a number of plasmids that carry key virulence determinants. These included the ymt gene, essential for bacterial growth in the flea gut, the pla gene, necessary for the disease to spread in the body, and a type III secretion system. Key virulence aspects of Yersinia pestis are immune evasion mediated by outer membrane proteins, an absence of pathogen-associated molecular patterns, and an ability to survive in phagosomes.
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Reports on the topic "Type III secretion helper proteins"

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Alfano, James, Isaac Barash, Thomas Clemente, Paul E. Staswick, Guido Sessa, and Shulamit Manulis. Elucidating the Functions of Type III Effectors from Necrogenic and Tumorigenic Bacterial Pathogens. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592638.bard.

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Many phytopathogenic bacteria use a type III protein secretion system (T3SS) to inject type III effectors into plant cells. In the experiments supported by this one-year feasibility study we investigated type III effector function in plants by using two contrasting bacterial pathogens: Pseudomonas syringae pv. tomato, a necrotrophic pathogen and Pantoea agglomerans, a tumorigenic pathogen. The objectives are listed below along with our major conclusions, achievements, and implications for science and agriculture. Objective 1: Compare Pseudomonas syringae and Pantoea agglomerans type III effectors in established assays to test the extent that they can suppress innate immunity and incite tumorigenesis. We tested P. agglomerans type III effectors in several innate immunity suppression assays and in several instances these effectors were capable of suppressing plant immunity, outputs that are suppressed by P. syringae effectors. Interestingly, several P. syringae effectors were able to complement gall production to a P. agglomerans pthGmutant. These results suggest that even though the disease symptoms of these pathogens are dramatically different, their type III effectors may function similarly. Objective 2: Construct P. syringae mutants in different combinations of type III-related DNA clusters to reduce type III effector redundancy. To determine their involvement in pathogenicity we constructed mutants that lack individual and multiple type III-related DNA clusters using a Flprecombinase-mediated mutagenesis strategy. The majority of single effector mutants in DC3000 have weak pathogenicity phenotypes most likely due to functional redundancy of effectors. Supporting this idea, Poly-DNAcluster deletion mutants were more significantly reduced in their ability to cause disease. Because these mutants have less functional redundancy of type III effectors, they should help identify P. syringae and P. agglomerans effectors that contribute more significantly to virulence. Objective 3: Determine the extent that P. syringae and P. agglomerans type III effectors alter hormone levels in plants. Inhibition of auxin polar transport by 2,3,5-triiodobenzoic acid (TIBA) completely prevented gall formation by P. agglomerans pv. gypsophilae in gypsophila cuttings. This result supported the hypothesis that auxin and presumably cytokinins of plant origin, rather than the IAA and cytokinins secreted by the pathogen, are mandatory for gall formation. Transgenic tobacco with pthGshowed various phenotypic traits that suggest manipulation of auxin metabolism. Moreover, the auxin levels in pthGtransgenic tobacco lines was 2-4 times higher than the control plants. External addition of auxin or cytokinins could modify the gall size in gypsophila cuttings inoculated with pthGmutant (PagMx27), but not with other type III effectors. We are currently determining hormone levels in transgenic plants expressing different type III effectors. Objective 4: Determine whether the P. agglomerans effectors HsvG/B act as transcriptional activators in plants. The P. agglomerans type III effectors HsvG and HsvB localize to the nucleus of host and nonhost plants and act as transcription activators in yeast. Three sites of adjacent arginine and lysine in HsvG and HsvB were suspected to act as Nuclear localization signals (NLS) domains. A nuclear import assay indicated two of the three putative NLS domains were functional NLSs in yeast. These were shown to be active in plants by fusing HsvG and HsvB to YFP. localization to the nucleus was dependent on these NLS domains. These achievements indicate that our research plan is feasible and suggest that type III effectors suppress innate immunity and modulate plant hormones. This information has the potential to be exploited to improve disease resistance in agricultural crops.
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Coplin, David, Isaac Barash, and Shulamit Manulis. Role of Proteins Secreted by the Hrp-Pathways of Erwinia stewartii and E. herbicola pv. gypsophilae in Eliciting Water-Soaking Symptoms and Initiating Galls. United States Department of Agriculture, June 2001. http://dx.doi.org/10.32747/2001.7580675.bard.

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Many bacterial pathogens of plants can inject pathogenicity proteins into host cells using a specialized type III secretion system encoded by hrpgenes. This system deliver effector proteins, into plant cells that function in both susceptible and resistant interactions. We have found that the virulence of Erwinia stewartii(Es; syn. Pantoea stewartii) and Erwinia herbicola pv. gypsophilae (Ehg, syn. Pantoea agglomerans), which cause Stewart's wilt of corn and galls on Gypsophila, respectively, depends on hrpgenes. The major objectives of this project were: To increase expression of hrpgenes in order to identify secreted proteins; to identify genes for proteins secreted by the type-III systems and determine if they are required for pathogenicity; and to determine if the secreted proteins can function within eukaryotic cells. We found that transcription of the hrp and effector genes in Es and Ehg is controlled by at least four genes that constitute a regulatory cascade. Environmental and/or physiological signaling appears to be mediated by the HrpX/HrpY two component system, with HrpX functioning as a sensor-kinase and HrpY as a response regulator. HrpYupregulateshrpS, which encodes a transcriptional enhancer. HrpS then activates hrpL, which encodes an alternate sigma factor that recognizes "hrp boxes". All of the regulatory genes are essential for pathogenicity, except HrpX, which appears only to be required for induction of the HR in tobacco by Es. In elucidating this regulatory pathway in both species, we made a number of significant new discoveries. HrpX is unusual for a sensor-kinase because it is cytoplasmic and contains PAS domains, which may sense the redox state of the bacterium. In Es, a novel methyl-accepting protein may function upstream of hrpY and repress hrp gene expression in planta. The esaIR quorum sensing system in Es represses hrp gene expression in Es in response to cell-density. We have discovered six new type III effector proteins in these species, one of which (DspE in Ehg and WtsE in Es) is common to both pathogens. In addition, Es wtsG, which is a homolog of an avrPpiB from P. syringae pv. pisi, and an Ehg ORF, which is a homolog of P. syringae pv. phaseolicola AvrPphD, were both demonstrated to encode virulence proteins. Two plasmidborne, Ehg Hop proteins, HsvG and PthG, are required for infection of gypsophilia, but interestingly, PthG also acts as an Avr elicitor in beets. Using a calmodulin-dependent adenylate cyclase (cyaA) reporter gene, we were successful in demonstrating that an HsvG-CyaA fusion protein can be transferred into human HeLa cells by the type-III system of enteropathogenic E. coli. This is a highly significant accomplishment because it is the first direct demonstration that an effector protein from a plant pathogenic bacterium is capable of being translocated into a eukaryotic cell by a type-III secretion system. Ehg is considered a limiting factor in Gypsophila production in Israel and Stewart’s Wilt is a serious disease in the Eastern and North Central USA, especially on sweet corn in epidemic years. We believe that our basic research on the characterization of type III virulence effectors should enable future identification of their receptors in plant cells. This may lead to novel approaches for genetically engineering resistant plants by modifying their receptors or inactivating effectors and thus blocking the induction of the susceptible response. Alternatively, hrp gene regulation might also provide a target for plant produced compounds that interfere with recognition of the host by the pathogen. Such strategies would be broadly applicable to a wide range of serious bacterial diseases on many crops throughout the USA and Israel.
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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.

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Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.
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