Academic literature on the topic 'Host-bacterial interaction'
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Journal articles on the topic "Host-bacterial interaction"
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Mosher, Deane. "Targeting the bacterial-host interaction." Virulence 3, no. 4 (July 2012): 349–50. http://dx.doi.org/10.4161/viru.21269.
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Wu, Yao-Wen, and Fu Li. "Bacterial interaction with host autophagy." Virulence 10, no. 1 (January 1, 2019): 352–62. http://dx.doi.org/10.1080/21505594.2019.1602020.
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Barnett, Timothy C., Jin Yan Lim, Amelia T. Soderholm, Tania Rivera-Hernandez, Nicholas P. West, and Mark J. Walker. "Host–pathogen interaction during bacterial vaccination." Current Opinion in Immunology 36 (October 2015): 1–7. http://dx.doi.org/10.1016/j.coi.2015.04.002.
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Libbing, Cassandra L., Adam R. McDevitt, Rea-Mae P. Azcueta, Ahila Ahila, and Minal Mulye. "Lipid Droplets: A Significant but Understudied Contributor of Host–Bacterial Interactions." Cells 8, no. 4 (April 15, 2019): 354. http://dx.doi.org/10.3390/cells8040354.
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Lipid droplets (LDs) are cytosolic lipid storage organelles that are important for cellular lipid metabolism, energy homeostasis, cell signaling, and inflammation. Several bacterial, viral and protozoal pathogens exploit host LDs to promote infection, thus emphasizing the importance of LDs at the host–pathogen interface. In this review, we discuss the thus far reported relation between host LDs and bacterial pathogens including obligate and facultative intracellular bacteria, and extracellular bacteria. Although there is less evidence for a LD–extracellular bacterial interaction compared to interactions with intracellular bacteria, in this review, we attempt to compare the bacterial mechanisms that target LDs, the host signaling pathways involved and the utilization of LDs by these bacteria. Many intracellular bacteria employ unique mechanisms to target host LDs and potentially obtain nutrients and lipids for vacuolar biogenesis and/or immune evasion. However, extracellular bacteria utilize LDs to either promote host tissue damage or induce host death. We also identify several areas that require further investigation. Along with identifying LD interactions with bacteria besides the ones reported, the precise mechanisms of LD targeting and how LDs benefit pathogens should be explored for the bacteria discussed in the review. Elucidating LD–bacterial interactions promises critical insight into a novel host–pathogen interaction.
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Yang, Huiying, Yuehua Ke, Jian Wang, Yafang Tan, Sebenzile K. Myeni, Dong Li, Qinghai Shi, et al. "Insight into Bacterial Virulence Mechanisms against Host Immune Response via the Yersinia pestis-Human Protein-Protein Interaction Network." Infection and Immunity 79, no. 11 (September 12, 2011): 4413–24. http://dx.doi.org/10.1128/iai.05622-11.
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ABSTRACTAYersinia pestis-human protein interaction network is reported here to improve our understanding of its pathogenesis. Up to 204 interactions between 66Y. pestisbait proteins and 109 human proteins were identified by yeast two-hybrid assay and then combined with 23 previously published interactions to construct a protein-protein interaction network. Topological analysis of the interaction network revealed that human proteins targeted byY. pestiswere significantly enriched in the proteins that are central in the human protein-protein interaction network. Analysis of this network showed that signaling pathways important for host immune responses were preferentially targeted byY. pestis, including the pathways involved in focal adhesion, regulation of cytoskeleton, leukocyte transendoepithelial migration, and Toll-like receptor (TLR) and mitogen-activated protein kinase (MAPK) signaling. Cellular pathways targeted byY. pestisare highly relevant to its pathogenesis. Interactions with host proteins involved in focal adhesion and cytoskeketon regulation pathways could account for resistance ofY. pestisto phagocytosis. Interference with TLR and MAPK signaling pathways byY. pestisreflects common characteristics of pathogen-host interaction that bacterial pathogens have evolved to evade host innate immune response by interacting with proteins in those signaling pathways. Interestingly, a large portion of human proteins interacting withY. pestis(16/109) also interacted with viral proteins (Epstein-Barr virus [EBV] and hepatitis C virus [HCV]), suggesting that viral and bacterial pathogens attack common cellular functions to facilitate infections. In addition, we identified vasodilator-stimulated phosphoprotein (VASP) as a novel interaction partner of YpkA and showed that YpkA could inhibitin vitroactin assembly mediated by VASP.
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Sun, Hongmin. "The Interaction Between Pathogens and the Host Coagulation System." Physiology 21, no. 4 (August 2006): 281–88. http://dx.doi.org/10.1152/physiol.00059.2005.
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There is mounting evidence that the hemostatic system is critical in host responses to bacterial infection. Invasive bacteria have evolved virulence strategies to interact with host hemostatic factors such as plasminogen and fibrinogen for infection. Furthermore, genetic variations in host hemostatic factors also influence host response to bacterial infection.
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Ceri, Howard, and Yolande Westra. "Host binding proteins and bacterial adhesion: ecology and binding model." Biochemistry and Cell Biology 66, no. 6 (June 1, 1988): 541–48. http://dx.doi.org/10.1139/o88-064.
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Defining the involvement of specific recognition and (or) adhesion molecules in the precise association formed between cells of an organism during development or between bacteria and specific host tissues has become a focus of extensive research. The possibility that the same molecules responsible for cellular adhesion in the host may also play a major role in determining host–bacterial interactions is now becoming more evident. The following review looks at the interaction of a group of host binding proteins, including lectins, fibronectin, and laminin, with respect to their specific association with bacteria. This information is dealt with both from the perspective of the ecology of the host and its autochthonous and pathogenic bacterial populations, as well as in terms of the difficulties in defining the nature of ligand associations even in the more simplified bacterial–host interaction.
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Khan, M. A., H. Satoh, T. Mino, H. Katayama, F. Kurisu, and T. Matsuo. "Bacteriophage-host interaction in the enhanced biological phosphate removing activated sludge system." Water Science and Technology 46, no. 1-2 (July 1, 2002): 39–43. http://dx.doi.org/10.2166/wst.2002.0453.
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Bacteriophages were isolated from a laboratory scale enhanced biological phosphate removing (EBPR) activated sludge process, and their host range was examined. Bacterial isolates to host the bacteriophages were isolated from the EBPR activated sludge process. Bacteriophages were eluted from the EBPR activated sludge, enriched by incubation with the bacterial isolates, and then tested for plaque formation on each of the bacterial isolates. Out of 12 bacterial isolates isolated, 4 supported plaque formation. Four bacteriophages were obtained from the plaques. The host range test was conducted with the combination of the bacteriophage isolates and the bacterial isolates. Three of the bacteriophages were found to form plaques on more than one host, and one of them formed plaques on both Gram +ve and Gram −ve bacterial isolates. Two of the four bacteriophages failed to form plaques on their original bacterial host, indicating the existence of mutation on either both or one of the host and the bacteriophage. This study strongly suggests that bacteriophages are an active part of the activated sludge microbial ecosystem, having very complex interaction with their host bacteria.
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Lin, Borong, Xue Qing, Jinling Liao, and Kan Zhuo. "Role of Protein Glycosylation in Host-Pathogen Interaction." Cells 9, no. 4 (April 20, 2020): 1022. http://dx.doi.org/10.3390/cells9041022.
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Host-pathogen interactions are fundamental to our understanding of infectious diseases. Protein glycosylation is one kind of common post-translational modification, forming glycoproteins and modulating numerous important biological processes. It also occurs in host-pathogen interaction, affecting host resistance or pathogen virulence often because glycans regulate protein conformation, activity, and stability, etc. This review summarizes various roles of different glycoproteins during the interaction, which include: host glycoproteins prevent pathogens as barriers; pathogen glycoproteins promote pathogens to attack host proteins as weapons; pathogens glycosylate proteins of the host to enhance virulence; and hosts sense pathogen glycoproteins to induce resistance. In addition, this review also intends to summarize the roles of lectin (a class of protein entangled with glycoprotein) in host-pathogen interactions, including bacterial adhesins, viral lectins or host lectins. Although these studies show the importance of protein glycosylation in host-pathogen interaction, much remains to be discovered about the interaction mechanism.
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Ling, Jessmi M. L., and Anthony B. Schryvers. "Perspectives on interactions between lactoferrin and bacteriaThis paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 3 (June 2006): 275–81. http://dx.doi.org/10.1139/o06-044.
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Lactoferrin has long been recognized for its antimicrobial properties, initially attributed primarily to iron sequestration. It has since become apparent that interaction between the host and bacteria is modulated by a complex series of interactions between lactoferrin and bacteria, lactoferrin and bacterial products, and lactoferrin and host cells. The primary focus of this review is the interaction between lactoferrin and bacteria, but interactions with the lactoferrin-derived cationic peptide lactoferricin will also be discussed. We will summarize what is currently known about the interaction between lactoferrin (or lactoferricin) and surface or secreted bacterial components, comment on the potential physiological relevance of the findings, and identify key questions that remain unanswered.
Dissertations / Theses on the topic "Host-bacterial interaction"
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de, Klerk Nele. "Host-bacteria interactions : Host cell responses and bacterial pathogenesis." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-126425.
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Helicobacter pylori colonizes the human stomach, where it causes gastritis that may develop into peptic ulcer disease or cancer when left untreated. Neisseria gonorrhoeae colonizes the urogenital tract and causes the sexually transmitted disease gonorrhea. In contrast, Lactobacillus species are part of the human microbiota, which is the resident microbial community, and are considered to be beneficial for health. The first host cell types that bacteria encounter when they enter the body are epithelial cells, which form the border between the inside and the outside, and macrophages, which are immune cells that engulf unwanted material. The focus of this thesis has been the interaction between the host and bacteria, aiming to increase our knowledge of the molecular mechanisms that underlie the host responses and their effects on bacterial pathogenicity. Understanding the interactions between bacteria and the host will hopefully enable the development of new strategies for the treatment of infectious disease. In paper I, we investigated the effect of N. gonorrhoeae on the growth factor amphiregulin in cervical epithelial cells and found that the processing and release of amphiregulin changes upon infection. In paper II, we examined the expression of the transcription factor early growth response-1 (EGR1) in epithelial cells during bacterial colonization. We demonstrated that EGR1 is rapidly upregulated by many different bacteria. This upregulation is independent of the pathogenicity, Gram-staining type and level of adherence of the bacteria, but generally requires viable bacteria and contact with the host cell. The induction of EGR1 is mediated primarily by signaling through EGFR, ERK1/2 and β1-integrins. In paper III, we described the interactions of the uncharacterized protein JHP0290, which is secreted by H. pylori, with host cells. JHP0290 is able to bind to several cell types and induces apoptosis and TNF release in macrophages. For both of these responses, signaling through Src family kinases and ERK is essential. Apoptosis is partially mediated by TNF release. Finally, in paper IV, we showed that certain Lactobacillus strains can reduce the colonization of H. pylori on gastric epithelial cells. Lactobacilli decrease the gene expression of SabA and thereby inhibit the binding mediated by this adhesin.At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 4: Manuscript.
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Shah, Samir Ashok. "The Effect of Smoking on Host-Bacterial Interaction." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338316888.
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Akpa, Abubakar Dominic. "Host-parasite interaction in bacterial blight of pea caused by Pseudomonas syringae pv. pisi." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47328.
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Aljannat, Mahab. "Bacterial moonlighting proteins of N. meningitidis : interaction with the host and role in pathogenesis." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/41073/.
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Neisseria meningitidis is a human-restricted pathogen that colonizes the nasopharynx, mostly without causing any disease. However, bacteria can invade into the bloodstream and cross the blood brain barrier resulting in life threatening sepsis and meningitis. Protein moonlighting is a concept established to describe the additional task(s) that a protein exhibits alongside its canonical function. After translocation to the cell surface by an unknown mechanism, moonlighting proteins may interact with various host proteins, and exhibit virulence-associated functions. Enolase (Eno), peroxiredoxin (Prx) and DnaK are meningococcal housekeeping proteins that are functionally described as a glycolytic enzyme, an anti-oxidant protein and a molecular chaperon, respectively. They have been identified on the surface of meningococci achieving non-housekeeping (moonlighting) functions related to interactions with the human protein plasminogen. This study sheds light on the moonlighting properties of these three proteins in the pathogenesis of meningococcal disease. Meningococcal Eno, Prx and DnaK were cloned, overexpressed in E. coli cells, and the corresponding wild type recombinant proteins were affinity purified under non-denaturing conditions. The oligomerization status of each recombinant protein was determined by analytical gel filtration, in which rEno was identified as an octamer, rPrx as a hexamer and rDnaK was either in a dimeric or monomeric state. Polyclonal antiserum targeted against each recombinant protein was raised in rabbits. A markerless pxn-knockout was generated in N. meningitidis MC58 rpsL-. The streptomycin resistance phenotype that the rpsL- allele confers was the basis behind the adopted mutation strategy. To delete NMB0946 (encoding meningococcal Prx), two mutagenic plasmids (pGUD2 and pGUD3) were constructed to allow two homologous recombination events. N. meningitidis rpsL- ∆pxn KanR rpsL+ was the resultant strain from the first event. The second homologous recombination event, facilitated by pGUD3, involved removing the selectable marker (KanR plus rpsL+ allele) to generate the markerless N. meningitidis rpsL- ∆pxn. Given that NMB0946 is part of a two-gene operon necessitated the construction of a complementation strain, in which a wild type copy of NMB0946 was reintroduced at an ectopic site of N. meningitidis rpsL- ∆pxn genome to complement that deletion. Using equimolar amounts of the recombinant proteins in EIA assays, it was found that meningococcal rEno binds plasminogen (Plg) more strongly than rDnaK and rPrx. Plg binding was inhibited when the lysine analogue ϵ-aminocapronic acid was added suggesting the potential involvement of lysine residues. Substitution of the C-terminal lysine residues of rEno, rPrx and rDnaK with alanine residues, significantly yet not completely, reduced binding to Plg. For rEno, lysine residues at positions 297 and 355 were identified for the first time as additional sites for Plg. rPrx with mutation in the active cysteine site (rPrx185CA), which is known to inactivate the protein, was able to bind Plg to the same level as the wild type strain. Unlike the C-terminal lysine residues, substituting the sub-terminal lysines of rPrx and rDnaK (at positions 230 and 641, respectively) did not alter binding to Plg. Employing whole-cell EIA, Prx and DnaK could be detected on the surface of wild-type encapsulated N. meningitidis MC58, while surface localisation of Eno was not detected under these conditions. Under hydrogen peroxide-mediated oxidative stress, the N. meningitidis ∆pxn-mutant survived remarkably better than the parental strain. Using human whole blood as a model of meningococcal bacteraemia, it was found that N. meningitidis ∆pxn-mutant has a survival defect compared with the wild-type strain. Preliminary data suggest that the survival of the ∆pxn-mutant cells in the presence of polymorphonuclear leukocytes (PMNs) isolated from peripheral blood was similar to controls containing no PMNs. Moreover, the absence of Prx could not significantly reduce the ability of whole meningococcal cells to bind Plg. In summary, the data suggest that Eno, Prx and DnaK bind plasminogen mainly via the C-terminal lysine residues. Lysine 297 and 355 of rEno are required for optimal Plg binding. The canonical and the moonlighting functions of meningococcal Prx are independent. This study also proposes that the absence of Prx does not impair overall Plg binding, has a positive impact on the ability of meningococci to tolerate exogenous hydrogen peroxide, and finally, has a very significant effect on the survival of meningococcal cells in human whole blood.
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Maldonado-Arocho, Francisco J. "Characterization of host-pathogen interaction of two bacterial toxins anthrax edema toxin and Escherichia coli cytolethal distending toxin /." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1973060671&sid=4&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Lopez, Fernandez Juan Sebastian [Verfasser], and Michael [Akademischer Betreuer] Steinert. "Molecular ecological interaction of bacterial endophytes with their host Vitis vinifera (L) / Juan Sebastian Lopez Fernandez ; Betreuer: Michael Steinert." Braunschweig : Technische Universität Braunschweig, 2017. http://d-nb.info/1175817228/34.
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Lopez, Fernandez Juan Sebastian Verfasser], and Michael [Akademischer Betreuer] [Steinert. "Molecular ecological interaction of bacterial endophytes with their host Vitis vinifera (L) / Juan Sebastian Lopez Fernandez ; Betreuer: Michael Steinert." Braunschweig : Technische Universität Braunschweig, 2017. http://nbn-resolving.de/urn:nbn:de:gbv:084-2017072708547.
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Shekhar, Sudhanshu. "A study on the role of lung dendritic cells and their interaction with innate lymphocytes in host defense against a bacterial lung infection." Karger, 2015. http://hdl.handle.net/1993/30622.
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Chlamydia is an obligate intracellular bacterial pathogen that causes a wide spectrum of diseases worldwide. At present, there are no vaccines to prevent chlamydial infections due to poor understanding of how anti-chlamydial immunity ensues. In this study, we employed a variety of in vitro and in vivo systems, including knockout (KO) mice and adoptive transfer, to investigate the role of lung dendritic cells (LDCs) and their relationship with innate lymphocytes, natural killer (NK) and invariant NKT (iNKT) cells, in host defense against chlamydial lung infections in mice. We found that iNKT cells altered the phenotype and cytokine production pattern of LDCs following C. pneumoniae infection. Adoptive transfer of LDCs from infected Jα18-KO mice, which lack iNKT cells, into naïve wild-type (WT) mice promoted Th2 (IL-4) immunity following infection challenge, whereas the transfer of LDCs from the infected WT mice induced protective Th1/Tc1 (IFN-γ) immunity. On the other hand, upon adoptive transfer, LDCs from C. muridarum-infected NK-cell-depleted mice (NK-LDCs) conferred reduced protection after chlamydial challenge than the recipients of LDCs from infected sham-treated mice (NK+LDCs). NK+LDC recipients exhibited an enhanced Th1/Th17, in contrast to Th2, response compared to the NK-LDC recipients. In coculture experiments, NK cells isolated from the infected mice promoted IL-12p70, IL-6, and IL-23 production by LDCs through NKG2D receptor signaling. These findings indicate that iNKT and NK cells condition LDCs to confer protective Th1/Tc1/Th17 immunity against chlamydial lung infection.
We also analyzed the contribution of major LDC subsets, CD103+ and CD11bhi LDCs, in host defense against C. muridarum infection. We found that CD103+ and CD11bhi LDC subsets expanded following chlamydial infection. CD103+ LDCs showed higher expression of costimulatory molecules and greater production of Th1- and Th17-inducing cytokines (IL-12, IL-6 and IL-23) than CD11bhi LDCs. Coculture of Chlamydia-specific CD4+ T cells with LDC subsets revealed that the T cells cultured with CD103+ LDCs produced larger amounts of IFN-γ and IL-17 compared to those with CD11bhi LDCs. To test their function in vivo, we isolated CD103+ and CD11bhi LDC subsets from infected mice and transferred them into naïve syngeneic mice that received chlamydial challenge. CD103+ LDC-recipients showed better protection, as evidenced by their reduced body weight loss, bacterial burden and lung pathology, than CD11bhi LDC recipients. Mice that received CD103+, compared to CD11bhi, LDCs produced enhanced Th1/Th17 cytokines (IFN-γ and IL-17) in the lung and the MLNs. In conclusion, these findings demonstrate that CD103+ LDCs are more efficient in inducing Th1/Th17 immunity to chlamydial infection than CD11bhi LDCs.
Taken together, our findings have provided direct in vivo evidence on the role of LDCs and their conditioning by iNKT and NK cells in generating mucosal T-cell immunity against a bacterial lung infection. The findings have added new knowledge to the field of lung immunology, which have implications for developing prophylactic and/or therapeutic strategies against respiratory diseases.October 2015
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Yan, Shuangchun. "Using the Bacterial Plant Pathogen Pseudomonas syringae pv. tomato as a Model to Study the Evolution and Mechanisms of Host Range and Virulence." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/77293.
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Most plant pathogens are specialists where only few plant species are susceptible, while all other plants are resistant. Unraveling the mechanisms behind this can thus provide valuable information for breeding or engineering crops with durable disease resistance. A group of Pseudomonas syringae strains with different host ranges while still closely related were thus chosen for comparative study. We confirmed their close phylogenetic relationship. We found evidence supporting that these strains recombined during evolution. The Arabidopsis thaliana and tomato pathogen P. syringae pv. tomato (Pto) DC3000 was found to be an atypical tomato strain, distinct from the typical Pto strains commonly isolated in the field that do not cause disease in A. thaliana, such as Pto T1. Comparing A. thaliana defense responses to DC3000 and T1, we found that T1 is eliciting stronger responses than DC3000. T1 is likely lacking Type III effector genes necessary to suppress plant defense. To test this, we sequenced the genomes of strains that cause and do not cause disease in A. thaliana. Comparative genomics revealed candidate effector genes responsible for this host range difference. Effector genes conserved in strains pathogenic in A. thaliana were expressed in T1 to test whether they would allow T1 to growth better in A. thaliana. Surprisingly, most of them reduced T1 growth. One of the effectors, HopM1, was of particular interest because it is disrupted in typical Pto strains. Although HopM1 has known virulence function in A. thaliana, HopM1 reduced T1 growth in both A. thaliana and tomato. HopM1 also increased the number of bacterial specks but reduced their average size in tomato. Our data suggest that HopM1 can trigger defenses in these plants. Additionally, transgenic detritivore Pseudomonas fluorescens that can secrete HopM1 shows dramatically increased growth in planta. The importance of genetic background of the pathogen for the functions of individual effectors is discussed. T1 cannot be manipulated to become an A. thaliana pathogen by deleting or adding individual genes. We now have a list of genes that can be studied in the future for the molecular basis of host range determination.Ph. D.
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Dorling, Jack. "Peptidoglycan recycling in the Gram-positive bacterium Staphylococcus aureus and its role in host-pathogen interaction." Thesis, University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:3fc4f926-296d-43a1-bb45-af9f37a87d8d.
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Bacteria are enclosed by a peptidoglycan sacculus, an exoskeleton-like polymer composed of glycan strands cross-linked by short peptides. The sacculus surrounds the cell in a closed bag-like structure and forms the main structural component of the bacterial cell wall. As bacteria grow and divide, cell wall remodelling by peptidoglycan hydrolases results in the release of peptidoglycan fragments from the sacculus. In Gram-negative bacteria, these fragments are efficiently trapped and recycled. Gram-positive bacteria however shed large quantities of peptidoglycan fragments into the environment. For nearly five decades, Gram-positive bacteria were thus assumed not to recycle peptidoglycan and this process has remained enigmatic until recently. In this thesis, the occurrence and physiological role of peptidoglycan recycling in the Gram-positive pathogen Staphylococcus aureus was investigated. S. aureus is an important pathogen, and is becoming increasingly resistant to many antibiotics. Through bioinformatic and experimental means it was determined that S. aureus may potentially recycle components of peptidoglycan and novel peptidoglycan recycling components were identified and characterised. Though disruption of putative peptidoglycan recycling in S. aureus appears not affect growth or gross morphology of this bacterium, potential roles for peptidoglycan recycling in cell wall homeostasis and in virulence were identified. This is to my knowledge the first demonstration of a potential role of peptidoglycan recycling in either of these aspects of bacterial physiology in any Gram-positive bacterium. This is an important step forward in understanding the basic biology of Gram-positive bacteria, and in understanding the mechanisms of virulence in S. aureus. Future study of this process in S. aureus and other Gram-positive bacteria promises to reveal yet further facets of this process and its functions, potentially leading to the identification of novel therapeutic approaches to combat infections.
Books on the topic "Host-bacterial interaction"
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Knirel, Yuriy A., and Miguel A. Valvano. Bacterial lipopolysaccharides: Structure, chemical synthesis, biogenesis, and interaction with host cells. Wien: Springer, 2011.
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David, O'Callaghan, and Annette C. Vergunst. Host-bacteria interactions: Methods and protocols. New York: Humana Press, 2014.
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Workshop Conference Hoechst (18th 1987 Schloss Ringberg). Surface structures of microorganisms and their interactions with the mammalian host: Proceedings of the Eighteenth Workshop Conference Hoechst, Schloss Ringberg, October 20-23, 1987. Weinheim, F.R.G: VCH, 1988.
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Jean-Pierre, Gorvel, ed. Intracellular pathogens in membrane interactions and vacuole biogenesis. Georgetown, Tex: Landes Bioscience, 2004.
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Miller, Robert V. The importance of the dynamics of bacteriophage-host interactions to bacterial abundance and genetic diversity in aquatic environments. Ada, OK: U.S. Environmental Protection Agency, National Risk Management Research Laboratory, 1998.
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A, Salyers Abigail, ed. Bacterial pathogenesis: A molecular approach. 3rd ed. Washington, DC: ASM Press, 2011.
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PhD, Henderson Brian, ed. Cellular microbiology: Bacteria-host interactions in health and disease. Chichester: J. Wiley, 1999.
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International Symposium on Pyelonephritis (4th 1986 Göteborg, Sweden). Host-parasite interactions in urinary tract infections: Proceedings of the Fourth International Symposium on Pyelonephritis held in Göteborg, Sweden, 23-25 June 1986. Chicago: University of Chicago Press, 1989.
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D, O'Connor C., Smith D. G. E, and Society for General Microbiology, eds. Microbial subversion of host cells. Cambridge, U.K: Cambridge University Press, 2003.
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Schaible, Ulrich E., and Haas Albert. Intracellular niches of microbes: A pathogens guide through the host cell. Weinheim: Wiley-VCH, 2009.
Find full textBook chapters on the topic "Host-bacterial interaction"
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Kim, Cheorl-Ho. "Bacterial Toxin Protein Interaction with Host Cells GSL." In Glycosphingolipids Signaling, 93–118. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5807-8_5.
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King, Jane E., and Ian S. Roberts. "Bacterial Surfaces: Front Lines in Host–Pathogen Interaction." In Biophysics of Infection, 129–56. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32189-9_10.
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Spier, Anna, Fabrizia Stavru, and Pascale Cossart. "Interaction between Intracellular Bacterial Pathogens and Host Cell Mitochondria." In Bacteria and Intracellularity, 1–13. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2020. http://dx.doi.org/10.1128/9781683670261.ch1.
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Aguilar, Carmen, Miguel Mano, and Ana Eulalio. "Multifaceted Roles of MicroRNAs in Host-Bacterial Pathogen Interaction." In Bacteria and Intracellularity, 247–66. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2020. http://dx.doi.org/10.1128/9781683670261.ch17.
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Kolattukudy, P. E., Joseph Sebastian, William F. Ettinger, and Mark S. Crawford. "Cutinase and Pectinase in Host-Pathogen and Plant-Bacterial Interaction." In Molecular genetics of plant-microbe interactions, 43–50. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-4482-4_9.
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Barel, Monique, and Alain Charbit. "Detection of the Interaction Between Host and Bacterial Proteins: Eukaryotic Nucleolin Interacts with Francisella Elongation Factor Tu." In Host-Bacteria Interactions, 123–39. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1261-2_7.
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Yadav, Sudheer K., Jai S. Patel, Gagan Kumar, Arpan Mukherjee, Anupam Maharshi, Surendra Singh, Harikesh B. Singh, and Birinchi K. Sarma. "Host-Parasite Interaction during Development of Major Seed-Borne Bacterial Diseases." In Seed-Borne Diseases of Agricultural Crops: Detection, Diagnosis & Management, 245–64. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-32-9046-4_10.
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Sharma, Sahil, and Cynthia M. Sharma. "Identification of RNA Binding Partners of CRISPR-Cas Proteins in Prokaryotes Using RIP-Seq." In Methods in Molecular Biology, 111–33. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1851-6_6.
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AbstractCRISPR-Cas systems consist of a complex ribonucleoprotein (RNP) machinery encoded in prokaryotic genomes to confer adaptive immunity against foreign mobile genetic elements. Of these, especially the class 2, Type II CRISPR-Cas9 RNA-guided systems with single protein effector modules have recently received much attention for their application as programmable DNA scissors that can be used for genome editing in eukaryotes. While many studies have concentrated their efforts on improving RNA-mediated DNA targeting with these Type II systems, little is known about the factors that modulate processing or binding of the CRISPR RNA (crRNA) guides and the trans-activating tracrRNA to the nuclease protein Cas9, and whether Cas9 can also potentially interact with other endogenous RNAs encoded within the host genome. Here, we describe RIP-seq as a method to globally identify the direct RNA binding partners of CRISPR-Cas RNPs using the Cas9 nuclease as an example. RIP-seq combines co-immunoprecipitation (coIP) of an epitope-tagged Cas9 followed by isolation and deep sequencing analysis of its co-purified bound RNAs. This method can not only be used to study interactions of Cas9 with its known interaction partners, crRNAs and tracrRNA in native systems, but also to reveal potential additional RNA substrates of Cas9. For example, in RIP-seq analysis of Cas9 from the foodborne pathogen Campylobacter jejuni (CjeCas9), we recently identified several endogenous RNAs bound to CjeCas9 RNP in a crRNA-dependent manner, leading to the discovery of PAM-independent RNA cleavage activity of CjeCas9 as well as non-canonical crRNAs. RIP-seq can be easily adapted to any other effector RNP of choice from other CRISPR-Cas systems, allowing for the identification of target RNAs. Deciphering novel RNA-protein interactions for CRISPR-Cas proteins within host bacterial genomes will lead to a better understanding of the molecular mechanisms and functions of these systems and enable us to use the in vivo identified interaction rules as design principles for nucleic acid-targeting applications, fitted to each nuclease of interest.
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Bock, Klaus, Karl-Anders Karlsson, Nicklas Strömberg, and Susann Teneberg. "Interaction of Viruses, Bacteria and Bacterial Toxins with Host Cell Surface Glycolipids. Aspects on Receptor Identification and Dissection of Binding Epitopes." In The Molecular Immunology of Complex Carbohydrates, 153–86. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_7.
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Kuespert, Katharina, and Christof R. Hauck. "Characterizing Host Receptor Recognition by Individual Bacterial Pathogens." In Host-Pathogen Interactions, 57–65. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-204-5_5.
Full textConference papers on the topic "Host-bacterial interaction"
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Claude, Jocelyn A., Amy Grimm, and Kent E. Pinkerton. "Host-Pathogen Interaction Of Viral Infection Complicated By An Opportunistic Bacterial Challenge." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1025.
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Petrova, O. E., O. I. Parfirova, J. P. Sergeeva, and V. Yu Gorshkov. "Stringent response is key player in plant-microbe interaction." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.195.
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Bacterial SpoT-dependent SR was activated in Pectobacterium atrosepticum when pathogen infected potato as well as tobacco plants. Pba induced plastid stringent response in tobacco plants, but not in potato plants. Jasmonic acid defense pathway was activated in tobacco plants, provoking rapid maceration of plant tissues. Salicylic acid defense pathway was induced in potato plants, probably ensuring a more prolonged coexistence of the phytopathogen with its host.
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Neubert, P., M. Haderer, H. Gschwendtner, K. Gülow, C. Kunst, and M. Müller-Schilling. "Investigating spontaneous bacterial peritonitis – a novel role of the p53 family in bacteria-host-interaction." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722001.
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Neubert, P., M. Haderer, H. Gschwendtner, K. Gülow, C. Kunst, and M. Müller-Schilling. "A novel role of the p53 family in bacteria-host-interaction - analyzing the pathomechanism of spontaneous bacterial peritonitis." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716194.
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Al-Asmar, Jawaher, Sara Rashwan, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Bacterial Infection on Host Survival and Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0186.
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Enterobacteriaceae, a large family of facultative anaerobic bacteria, encloses a broad spectrum of bacterial species including Escherichia coli, Salmonella enterica, and Shigella sonnei, that produce enterotoxins and cause gastrointestinal tract diseases. While much is known about the regulation and function of enterotoxins within the intestine of the host; the lack of cheap, practical, and genetically tractable model organisms has restricted the investigation of others facets of this host-pathogen interaction. Our group, among others, has employed Drosophila melanogaster, as a model organism to shed more light on some aspects of host-pathogen interplays. In this project, we addressed the effect of Escherichia coli, Salmonella enterica, and Shigella sonnei infection on altering the metabolic homeostasis of the host. Drosophila melanogaster flies were orally infected with Escherichia coli, Salmonella enterica, or Shigella sonnei, a method that mimics the natural route used by enteric pathogens to gain access to the gastrointestinal tract in humans. The results of our study revealed that both Escherichia coli and Shigella sonnei pathogens were capable of colonizing the host gut, resulting in a reduction in the life span of the infected host. Escherichia coli and Shigella sonnei infected flies also exhibited altered metabolic profiles including lipid droplets deprivation from their fat body (normal lipid storage organ in flies), irregular accumulation of lipid droplets in their gut, and significant elevation of systemic glucose and triglyceride levels. These metabolic alterations could be mechanistically attributed to the differential down-regulation in the expression of metabolic peptide hormones (Allatostatin A, Diuretic hormone 31, and Tachykinin) detected in the gut of Escherichia coli and Shigella sonnei infected flies. Salmonella enterica; however, was unable to colonize the gut of the host; and therefore, Salmonella enterica infected flies exhibited a relatively normal metabolic status as that of non infected flies. Gaining a proper mechanistic understanding of infection-induced metabolic alterations helps in modulating the pathogenesis of gastrointestinal tract diseases in a host and opens up for promising therapeutic approaches for infection induced metabolic disorders
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Wouters, Katinka, Hugo Moors, and Natalie Leys. "Boom Clay Borehole Water, Home of a Diverse Bacterial Community." In ASME 2013 15th International Conference on Environmental Remediation and Radioactive Waste Management. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icem2013-96222.
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For over two decades, Boom Clay has been studied in the framework of geological disposal of nuclear waste thereby mainly addressing its geochemical properties. Today, also the microbiological properties and the possibility of microbes interacting with radionuclides or repository components including the waste form, in a host formation like Boom Clay are considered [2,3]. In the past, a reference composition for synthetic Boom Clay pore water (BCPW) was derived, based on interstitial water sampled from different layers within the Boom clay [1]. Similarly, the primary aim of this microbiological study was to determine the core BCPW bacterial community and identify representative water samples for future microbial directed lab experiments. In this respect, BCPW was sampled from different Boom Clay layers using the Morpheus piezometer (Fig. 1) and subsequently analysed by microscopy and molecular techniques, in search for overall shared and abundant micro-organisms.
Reports on the topic "Host-bacterial interaction"
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Tzfira, Tzvi, Michael Elbaum, and Sharon Wolf. DNA transfer by Agrobacterium: a cooperative interaction of ssDNA, virulence proteins, and plant host factors. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7695881.bard.
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Agrobacteriumtumefaciensmediates genetic transformation of plants. The possibility of exchanging the natural genes for other DNA has led to Agrobacterium’s emergence as the primary vector for genetic modification of plants. The similarity among eukaryotic mechanisms of nuclear import also suggests use of its active elements as media for non-viral genetic therapy in animals. These considerations motivate the present study of the process that carries DNA of bacterial origin into the host nucleus. The infective pathway of Agrobacterium involves excision of a single-stranded DNA molecule (T-strand) from the bacterial tumor-inducing plasmid. This transferred DNA (T-DNA) travels to the host cell cytoplasm along with two virulence proteins, VirD2 and VirE2, through a specific bacteriumplant channel(s). Little is known about the precise structure and composition of the resulting complex within the host cell and even less is known about the mechanism of its nuclear import and integration into the host cell genome. In the present proposal we combined the expertise of the US and Israeli labs and revealed many of the biophysical and biological properties of the genetic transformation process, thus enhancing our understanding of the processes leading to nuclear import and integration of the Agrobacterium T-DNA. Specifically, we sought to: I. Elucidate the interaction of the T-strand with its chaperones. II. Analyzing the three-dimensional structure of the T-complex and its chaperones in vitro. III. Analyze kinetics of T-complex formation and T-complex nuclear import. During the past three years we accomplished our goals and made the following major discoveries: (1) Resolved the VirE2-ssDNA three-dimensional structure. (2) Characterized VirE2-ssDNA assembly and aggregation, along with regulation by VirE1. (3) Studied VirE2-ssDNA nuclear import by electron tomography. (4) Showed that T-DNA integrates via double-stranded (ds) intermediates. (5) Identified that Arabidopsis Ku80 interacts with dsT-DNA intermediates and is essential for T-DNA integration. (6) Found a role of targeted proteolysis in T-DNA uncoating. Our research provide significant physical, molecular, and structural insights into the Tcomplex structure and composition, the effect of host receptors on its nuclear import, the mechanism of T-DNA nuclear import, proteolysis and integration in host cells. Understanding the mechanical and molecular basis for T-DNA nuclear import and integration is an essential key for the development of new strategies for genetic transformation of recalcitrant plant species. Thus, the knowledge gained in this study can potentially be applied to enhance the transformation process by interfering with key steps of the transformation process (i.e. nuclear import, proteolysis and integration). Finally, in addition to the study of Agrobacterium-host interaction, our research also revealed some fundamental insights into basic cellular mechanisms of nuclear import, targeted proteolysis, protein-DNA interactions and DNA repair.
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Gafni, Yedidya, Moshe Lapidot, and Vitaly Citovsky. Dual role of the TYLCV protein V2 in suppressing the host plant defense. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597935.bard.
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TYLCV-Is is a major tomato pathogen, causing extensive crop losses in Israel and the U.S. We have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing. Intriguingly, the counter-defense function of V2 may not be limited to silencing suppression. Our recent data suggest that V2 interacts with the tomato CYP1 protease. CYP1 belongs to the family of papain-like cysteine proteases which participate in programmed cell death (PCD) involved in plant defense against pathogens. Based on these data we proposed a model for dual action of V2 in suppressing the host antiviral defense: V2 targets SGS3 for degradation and V2 inhibits CYP1 activity. To study this we proposed to tackle three specific objectives. I. Characterize the role of V2 in SGS3 proteasomal degradation ubiquitination, II. Study the effects of V2 on CYP1 maturation, enzymatic activity, and accumulation and, III. Analyze the effects of the CYP1-V2 interaction on TYLCV-Is infection. Here we describe results from our study that support our hypothesis: the involvement of the host's innate immune system—in this case, PCD—in plant defense against TYLCV-Is. Also, we use TYLCV-Is to discover the molecular pathway(s) by which this plant virus counters this defense. Towards the end of our study we discovered an interesting involvement of the C2 protein encoded by TYLCV-Is in inducing Hypersensitive Response in N. benthamianaplants which is not the case when the whole viral genome is introduced. This might lead to a better understanding of the multiple processes involved in the way TYLCV is overcoming the defense mechanisms of the host plant cell. In a parallel research supporting the main goal described, we also investigated Agrobacteriumtumefaciens-encoded F-box protein VirF. It has been proposed that VirF targets a host protein for the UPS-mediated degradation, very much the way TYLCV V2 does. In our study, we identified one such interactor, an Arabidopsistrihelix-domain transcription factor VFP3, and further show that its very close homolog VFP5 also interacted with VirF. Interestingly, interactions of VirF with either VFP3 or VFP5 did not activate the host UPS, suggesting that VirF might play other UPS-independent roles in bacterial infection. Another target for VirF is VFP4, a transcription factor that both VirF and its plant functional homolog VBF target to degradation by UPS. Using RNA-seqtranscriptome analysis we showed that VFP4 regulates numerous plant genes involved in disease response, including responses to viral and bacterial infections. Detailed analyses of some of these genes indicated their involvement in plant protection against Agrobacterium infection. Thus, Agrobacterium may facilitate its infection by utilizing the host cell UPS to destabilize transcriptional regulators of the host disease response machinery that limits the infection.
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Manulis, Shulamit, Christine D. Smart, Isaac Barash, Guido Sessa, and Harvey C. Hoch. Molecular Interactions of Clavibacter michiganensis subsp. michiganensis with Tomato. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697113.bard.
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Clavibacter michiganensis subsp. michiganensis (Cmm), the causal agent of bacterial wilt and canker of tomato, is the most destructive bacterial disease of tomato causing substantial economic losses in Israel, the U.S.A. and worldwide. The molecular strategies that allow Cmm, a Gram-positive bacterium, to develop a successful infection in tomato plants are largely unknown. The goal of the project was to elucidate the molecular interactions between Cmmand tomato. The first objective was to analyze gene expression profiles of susceptible tomato plants infected with pathogenic and endophytic Cmmstrains. Microarray analysis identified 122 genes that were differentially expressed during early stages of infection. Cmm activated typical basal defense responses in the host including induction of defense-related genes, production of scavenging of free oxygen radicals, enhanced protein turnover and hormone synthesis. Proteomic investigation of the Cmm-tomato interaction was performed with Multi-Dimensional Protein Identification Technology (MudPIT) and mass spectroscopy. A wide range of enzymes secreted by Cmm382, including cell-wall degrading enzymes and a large group of serine proteases from different families were identified in the xylem sap of infected tomato. Based on proteomic results, the expression pattern of selected bacterial virulence genes and plant defense genes were examined by qRT-PCR. Expression of the plasmid-borne cellulase (celA), serine protease (pat-1) and serine proteases residing on the chp/tomA pathogenicity island (chpCandppaA), were significantly induced within 96 hr after inoculation. Transcription of chromosomal genes involved in cell wall degradation (i.e., pelA1, celB, xysA and xysB) was also induced in early infection stages. The second objective was to identify by VIGS technology host genes affecting Cmm multiplication and appearance of disease symptoms in plant. VIGS screening showed that out of 160 tomato genes, which could be involved in defense-related signaling, suppression of 14 genes led to increase host susceptibility. Noteworthy are the genes Snakin-2 (inhibitor of Cmm growth) and extensin-like protein (ELP) involved in cell wall fortification. To further test the significance of Snakin -2 and ELP in resistance towards Cmm, transgenic tomato plants over-expressing the two genes were generated. These plants showed partial resistance to Cmm resulting in a significant delay of the wilt symptoms and reduction in size of canker lesion compared to control. Furthermore, colonization of the transgenic plants was significantly lower. The third objective was to assess the involvement of ethylene (ET), jasmonate (JA) and salicylic acid (SA) in Cmm infection. Microarray and proteomic studies showed the induction of enzymes involved in ET and JA biosynthesis. Cmm promoted ET production 8 days after inoculation and SIACO, a key enzyme of ET biosynthesis, was upregulated. Inoculation of the tomato mutants Never ripe (Nr) impaired in ET perception and transgenic plants with reduced ET synthesis significantly delayed wilt symptoms as compared to the wild-type plants. The retarded wilting in Nr plants was shown to be a specific effect of ET insensitivity and was not due to altered expression of defense related genes, reduced bacterial population or decrease in ethylene biosynthesis . In contrast, infection of various tomato mutants impaired in JA biosynthesis (e.g., def1, acx1) and JA insensitive mutant (jai1) yielded unequivocal results. The fourth objective was to determine the role of cell wall degrading enzymes produced by Cmm in xylem colonization and symptoms development. A significance increase (2 to 7 fold) in expression of cellulases (CelA, CelB), pectate lyases (PelA1, PelA2), polygalacturonase and xylanases (XylA, XylB) was detected by qRT-PCR and by proteomic analysis of the xylem sap. However, with the exception of CelA, whose inactivation led to reduced wilt symptoms, inactivation of any of the other cell wall degrading enzymes did not lead to reduced virulence. Results achieved emphasized the complexity involved in Cmm-tomato interactions. Nevertheless they provide the basis for additional research which will unravel the mechanism of Cmm pathogenicity and formulating disease control measures.
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Sessa, Guido, and Gregory Martin. A functional genomics approach to dissect resistance of tomato to bacterial spot disease. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695876.bard.
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The research problem. Bacterial spot disease in tomato is of great economic importance worldwide and it is particularly severe in warm and moist areas affecting yield and quality of tomato fruits. Causal agent of spot disease is the Gram-negative bacterium Xanthomonas campestris pv. vesicatoria (Xcv), which can be a contaminant on tomato seeds, or survive in plant debris and in association with certain weeds. Despite the economic significance of spot disease, plant protection against Xcvby cultural practices and chemical control have so far proven unsuccessful. In addition, breeding for resistance to bacterial spot in tomato has been undermined by the genetic complexity of the available sources of resistance and by the multiple races of the pathogen. Genetic resistance to specific Xcvraces have been identified in tomato lines that develop a hypersensitive response and additional defense responses upon bacterial challenge. Central goals of this research were: 1. To identify plant genes involved in signaling and defense responses that result in the onset of resistance. 2. To characterize molecular properties and mode of action of bacterial proteins, which function as avirulence or virulence factors during the interaction between Xcvand resistant or susceptible tomato plants, respectively. Our main achievements during this research program are in three major areas: 1. Identification of differentially expressed genes during the resistance response of tomato to Xcvrace T3. A combination of suppression subtractive hybridization and microarray analysis identified a large set of tomato genes that are induced or repressed during the response of resistant plants to avirulent XcvT3 bacteria. These genes were grouped in clusters based on coordinate expression kinetics, and classified into over 20 functional classes. Among them we identified genes that are directly modulated by expression of the type III effector protein AvrXv3 and genes that are induced also during the tomato resistance response to Pseudomonas syringae pv. tomato. 2. Characterization of molecular and biochemical properties of the tomato LeMPK3MAP kinase. A detailed molecular and biochemical analysis was performed for LeMPK3 MAP kinase, which was among the genes induced by XcvT3 in resistant tomato plants. LeMPK3 was induced at the mRNA level by different pathogens, elicitors, and wounding, but not by defense-related plant hormones. Moreover, an induction of LeMPK3 kinase activity was observed in resistant tomato plants upon Xcvinfection. LeMPK3 was biochemically defined as a dual-specificity MAP kinase, and extensively characterized in vitro in terms of kinase activity, sites and mechanism of autophosphorylation, divalent cation preference, Kₘand Vₘₐₓ values for ATP. 3. Characteriztion of molecular properties of the Xcveffector protein AvrRxv. The avirulence gene avrRxvis involved in the genetic interaction that determines tomato resistance to Xcvrace T1. We found that AvrRxv functions inside the plant cell, localizes to the cytoplasm, and is sufficient to confer avirulence to virulent Xcvstrains. In addition, we showed that the AvrRxv cysteine protease catalytic core is essential for host recognition. Finally, insights into cellular processes activated by AvrRxv expression in resistant plants were obtained by microarray analysis of 8,600 tomato genes. Scientific and agricultural significance: The findings of these activities depict a comprehensive and detailed picture of cellular processes taking place during the onset of tomato resistance to Xcv. In this research, a large pool of genes, which may be involved in the control and execution of plant defense responses, was identified and the stage is set for the dissection of signaling pathways specifically triggered by Xcv.
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Fisher, Charles, and James Childress. Host-Symbiont Interactions between a Marine Mussel and Methanotrophic Bacterial Endosymbionts. Fort Belvoir, VA: Defense Technical Information Center, April 1991. http://dx.doi.org/10.21236/ada235562.
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Fisher, Charles, and James Childress. Host-Symbiont Interactions Between a Marine Mussel and Methanotrophic Bacterial Endosymbionts. Fort Belvoir, VA: Defense Technical Information Center, April 1991. http://dx.doi.org/10.21236/ada244810.
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Zhao, Bingyu, Saul Burdman, Ronald Walcott, Tal Pupko, and Gregory Welbaum. Identifying pathogenic determinants of Acidovorax citrulli toward the control of bacterial fruit blotch of cucurbits. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598168.bard.
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The specific objectives of this BARD proposal were: Use a comparative genomics approach to identify T3Es in group I, II and III strains of A. citrulli. Determine the bacterial genes contributing to host preference. Develop mutant strains that can be used for biological control of BFB. Background to the topic: Bacterial fruit blotch (BFB) of cucurbits, caused by Acidovoraxcitrulli, is a devastating disease that affects watermelon (Citrulluslanatus) and melon (Cucumismelo) production worldwide, including both Israel and USA. Three major groups of A. citrullistrains have been classified based on their virulence on host plants, genetics and biochemical properties. The host selection could be one of the major factors that shape A. citrullivirulence. The differences in the repertoire of type III‐ secreted effectors (T3Es) among the three A. citrulligroups could play a major role in determining host preferential association. Currently, there are only 11 A. citrulliT3Es predicted by the annotation of the genome of the group II strain, AAC00‐1. We expect that new A. citrulliT3Es can be identified by a combination of bioinformatics and experimental approaches, which may help us to further define the relationship of T3Es and host preference of A. citrulli. Implications, both scientific and agricultural: Enriching the information on virulence and avirulence functions of T3Es will contribute to the understanding of basic aspects of A. citrulli‐cucurbit interactions. In the long term, it will contribute to the development of durable BFB resistance in commercial varieties. In the short term, identifying bacterial genes that contribute to virulence and host preference will allow the engineering of A. citrullimutants that can trigger SAR in a given host. If applied as seed treatments, these should significantly improve the effectiveness and efficacy of BFB management in melon and atermelon production.
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Crowley, David E., Dror Minz, and Yitzhak Hadar. Shaping Plant Beneficial Rhizosphere Communities. United States Department of Agriculture, July 2013. http://dx.doi.org/10.32747/2013.7594387.bard.
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PGPR bacteria include taxonomically diverse bacterial species that function for improving plant mineral nutrition, stress tolerance, and disease suppression. A number of PGPR are being developed and commercialized as soil and seed inoculants, but to date, their interactions with resident bacterial populations are still poorly understood, and-almost nothing is known about the effects of soil management practices on their population size and activities. To this end, the original objectives of this research project were: 1) To examine microbial community interactions with plant-growth-promoting rhizobacteria (PGPR) and their plant hosts. 2) To explore the factors that affect PGPR population size and activity on plant root surfaces. In our original proposal, we initially prqposed the use oflow-resolution methods mainly involving the use of PCR-DGGE and PLFA profiles of community structure. However, early in the project we recognized that the methods for studying soil microbial communities were undergoing an exponential leap forward to much more high resolution methods using high-throughput sequencing. The application of these methods for studies on rhizosphere ecology thus became a central theme in these research project. Other related research by the US team focused on identifying PGPR bacterial strains and examining their effective population si~es that are required to enhance plant growth and on developing a simulation model that examines the process of root colonization. As summarized in the following report, we characterized the rhizosphere microbiome of four host plant species to determine the impact of the host (host signature effect) on resident versus active communities. Results of our studies showed a distinct plant host specific signature among wheat, maize, tomato and cucumber, based on the following three parameters: (I) each plant promoted the activity of a unique suite of soil bacterial populations; (2) significant variations were observed in the number and the degree of dominance of active populations; and (3)the level of contribution of active (rRNA-based) populations to the resident (DNA-based) community profiles. In the rhizoplane of all four plants a significant reduction of diversity was observed, relative to the bulk soil. Moreover, an increase in DNA-RNA correspondence indicated higher representation of active bacterial populations in the residing rhizoplane community. This research demonstrates that the host plant determines the bacterial community composition in its immediate vicinity, especially with respect to the active populations. Based on the studies from the US team, we suggest that the effective population size PGPR should be maintained at approximately 105 cells per gram of rhizosphere soil in the zone of elongation to obtain plant growth promotion effects, but emphasize that it is critical to also consider differences in the activity based on DNA-RNA correspondence. The results ofthis research provide fundamental new insight into the composition ofthe bacterial communities associated with plant roots, and the factors that affect their abundance and activity on root surfaces. Virtually all PGPR are multifunctional and may be expected to have diverse levels of activity with respect to production of plant growth hormones (regulation of root growth and architecture), suppression of stress ethylene (increased tolerance to drought and salinity), production of siderophores and antibiotics (disease suppression), and solubilization of phosphorus. The application of transcriptome methods pioneered in our research will ultimately lead to better understanding of how management practices such as use of compost and soil inoculants can be used to improve plant yields, stress tolerance, and disease resistance. As we look to the future, the use of metagenomic techniques combined with quantitative methods including microarrays, and quantitative peR methods that target specific genes should allow us to better classify, monitor, and manage the plant rhizosphere to improve crop yields in agricultural ecosystems. In addition, expression of several genes in rhizospheres of both cucumber and whet roots were identified, including mostly housekeeping genes. Denitrification, chemotaxis and motility genes were preferentially expressed in wheat while in cucumber roots bacterial genes involved in catalase, a large set of polysaccharide degradation and assimilatory sulfate reduction genes were preferentially expressed.
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Gottlieb, Yuval, and Bradley A. Mullens. Might Bacterial Symbionts Influence Vectorial Capacity of Biting Midges for Ruminant Viruses? United States Department of Agriculture, September 2010. http://dx.doi.org/10.32747/2010.7699837.bard.
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- Original objectives and revision: The feasibility study performed in the last year was aimed at determining the symbiotic profiles of eight selected Culicoidesspecies in Israel and the USA by: Comparing bacterial communities among geographic populations of primary bluetongue virus (BTV) vectors. Comparing bacterial communities between adults of field-collected, mammal-feeding BTV vectors and non-vectors. Comparing bacterial communities within and between mammal feeders and bird feeders, with special attention to species with unique immature habitats. We made an effort to collect the eight species during the beginning of the project, however, due to the short available collection season, and the significant changes in habitats available for Israeli Culicoides, we initially determined the symbiotic profile of five species: two BTV vectors (C. sonorensis, C. imicola), one mammal feeders with unknown vectoring ability (C. schultzei), one bird feeder (C. crepuscularis), and one unique habitat species (C. cacticola). In addition, upon preliminary symbiont identification we focused our effort on relevant specific symbionts. Background: Biting midges (Culicoides, Diptera: Ceratopogonidae) are vectors of many major viral diseases affecting farm animals, including BT, which is listed among the most damaging by the World Organization for Animal Health (OIE) and has recently emerged in completely unexpected areas (Northern Europe). One of the strategies to reduce the vectorial capacity of insect vectors is by manipulating their specific symbionts either to affect the vector species or to influence performance of the disease agent within it. Despite significant efforts to elucidate the vectorial capacity of certain Culicoidesspecies, and the critical basis of variability in infection, almost no attention has been given to symbiotic interactions between the vector and its bacterial tenants. It is now established that bacterial symbionts have major influences on their host biology, and may interact with disease agents vectored by their hosts. - Major conclusions, solutions, achievements: During the feasibility project we have found two major bacterial symbionts in Israeli and American Culicoides. In Israel we discovered that C. imicola, a known vector of BT, and C. schultzeigp. a suspected vector of BT, carry the symbiotic bacterium Cardinium, a reproductive manipulator symbiont. In C. imicolathe infection rate was close to 50%, and in C. schultzeiit was lower, and restricted to one of two species within Schultzeigroup. In 3 American species (C. sonorensis, C. crepuscularis, C. cacticola) we found the bacterium Burkholderiasp. In all species tested we have also found other bacterial species in diverse quantities and frequencies. - Implications, both scientific and agricultural: Finding specific symbionts in Culicoidesvector species is the first step in developing symbiont based control (SBC) strategies. Both identified symbionts are known from other insects, and Cardiniumis also known as a reproductive manipulator that can cause cytoplasmic incompatibility, an important phenomenon that can be used for spreading desired traits in infected populations. The role of the symbionts in Culicoideshost can be target for manipulation to reduce the vectorial capacity of the host by either changing its fitness so that it is unable to serve as a vector, or by directly changing the symbiont in a way that will affect the performance of the disease agent in its vector. Since Burkholderiaperhaps can be cultured independently of the host, it is a promising candidate for the later option. Thus, we have now opened the door for studying the specific interactions between symbionts and vector species.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.
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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.