Letteratura scientifica selezionata sul tema "Virulence determinant"
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Articoli di riviste sul tema "Virulence determinant":
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Allen, Jonathan P., Egon A. Ozer, George Minasov, Ludmilla Shuvalova, Olga Kiryukhina, Wayne F. Anderson, Karla J. F. Satchell e Alan R. Hauser. "A comparative genomics approach identifies contact-dependent growth inhibition as a virulence determinant". Proceedings of the National Academy of Sciences 117, n. 12 (10 marzo 2020): 6811–21. http://dx.doi.org/10.1073/pnas.1919198117.
Abstract (sommario):
Emerging evidence suggests thePseudomonas aeruginosaaccessory genome is enriched with uncharacterized virulence genes. Identification and characterization of such genes may reveal novel pathogenic mechanisms used by particularly virulent isolates. Here, we utilized a mouse bacteremia model to quantify the virulence of 100 individualP. aeruginosabloodstream isolates and performed whole-genome sequencing to identify accessory genomic elements correlated with increased bacterial virulence. From this work, we identified a specific contact-dependent growth inhibition (CDI) system enriched among highly virulentP. aeruginosaisolates. CDI systems contain a large exoprotein (CdiA) with a C-terminal toxin (CT) domain that can vary between different isolates within a species. Prior work has revealed that delivery of a CdiA-CT domain upon direct cell-to-cell contact can inhibit replication of a susceptible target bacterium. Aside from mediating interbacterial competition, we observed our virulence-associated CdiA-CT domain to promote toxicity against mammalian cells in culture and lethality during mouse bacteremia. Structural and functional studies revealed this CdiA-CT domain to have in vitro tRNase activity, and mutations that abrogated this tRNAse activity in vitro also attenuated virulence. Furthermore, CdiA contributed to virulence in mice even in the absence of contact-dependent signaling. Overall, our findings indicate that thisP. aeruginosaCDI system functions as both an interbacterial inhibition system and a bacterial virulence factor against a mammalian host. These findings provide an impetus for continued studies into the complex role of CDI systems inP. aeruginosapathogenesis.
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Cooper, T. F., e J. A. Heinemann. "Selection for plasmid post–segregational killing depends on multiple infection: evidence for the selection of more virulent parasites through parasite–level competition". Proceedings of the Royal Society B: Biological Sciences 272, n. 1561 (22 febbraio 2005): 403–10. http://dx.doi.org/10.1098/rspb.2004.2921.
Abstract (sommario):
Is the virulence of parasites an outcome of optimized infection? Virulence has often been considered an inevitable consequence of parasite reproduction when the cost incurred by the parasite in reducing the fitness of its current host is offset by increased infection of new hosts. More recent models have focused on how competition occurring between parasites during co–infection might effect selection of virulence. For example, if co–infection was common, parasites with higher intrinsic growth rates might be selected, even at the expense of being optimally adapted to infect new hosts. If growth rate is positively correlated with virulence, then competition would select increased virulence. We tested these models using a plasmid–encoded virulence determinant. The virulence determinant did not contribute to the plasmid's reproduction within or between hosts. Despite this, virulent plasmids were more successful than avirulent derivatives during selection in an environment allowing within–host competition. To explain these findings we propose and test a model in which virulent parasites are selected by reducing the reproduction of competitors.
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Enkerli, Jürg, Garima Bhatt e Sarah F. Covert. "Maackiain Detoxification Contributes to the Virulence of Nectria haematococca MP VI on Chickpea". Molecular Plant-Microbe Interactions® 11, n. 4 (aprile 1998): 317–26. http://dx.doi.org/10.1094/mpmi.1998.11.4.317.
Abstract (sommario):
Nectria haematococca mating population (MP) VI isolates that contain the MAK1 gene are able to degrade maackiain, a chickpea (Cicer arietinum) phytoalexin, to a less toxic compound. To test the contribution of MAK1 to the virulence of N. haematococca MP VI on chickpea, the MAK1 gene was disrupted in a highly virulent Mak+ isolate or added to a weakly virulent Mak- isolate via transformation. The disruption of MAK1 decreased virulence to a moderate level, while addition of multiple copies of MAK1 increased virulence to either a moderate or a high level. These data demonstrate that maackiain detoxification is a determinant, but not the only determinant, of virulence in N. haematococca MP VI isolates capable of causing disease on chickpea. MAK1 is located on a 1.6-Mb conditionally dispensable chromosome. To ascertain if there are additional genes influencing virulence toward chickpea stems on the MAK1 chromosome, the loss of this chromosome was chemically induced in an isolate containing the disrupted MAK1 gene. Loss of the MAK1 chromosome did not reduce virulence toward chickpea stems further, thus indicating that no additional genes for virulence on this part of the host plant are located on the MAK1 chromosome.
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Sanz-Ramos, Marta, Fayna Díaz-San Segundo, Cristina Escarmís, Esteban Domingo e Noemí Sevilla. "Hidden Virulence Determinants in a Viral Quasispecies In Vivo". Journal of Virology 82, n. 21 (20 agosto 2008): 10465–76. http://dx.doi.org/10.1128/jvi.00825-08.
Abstract (sommario):
ABSTRACT The characterization of virulence determinants of pathogenic agents is of utmost relevance for the design of disease control strategies. So far, two classes of virulence determinants have been characterized for viral populations: those imprinted in the nucleotide sequence of some specific genomic regions and those that depend on the complexity of the viral population as such. Here we provide evidence of a virulence determinant that depends neither on a genomic sequence nor on detectable differences in population complexity. Foot-and-mouth disease virus is lethal for C57BL/6 mice showing the highest viral load in pancreas. Virus isolated from pancreas after one passage in mice showed an attenuated phenotype, with no lethality even at the highest dose tested. By contrast, virus from sera of the same mice displayed a virulence similar to that of the parental wild-type clone and virus isolated from spleen displayed an intermediate phenotype. However, viral populations from pancreas, spleen, and serum showed indistinguishable consensus genomic nucleotide sequences and mutant spectrum complexities, as quantified according to the mutation frequencies of both entire genomic nucleotide sequences of biological clones. The results show that the populations with differing virulences cannot be distinguished either by the consensus sequence or by the average complexity of the mutant spectrum. Differential harvesting of virus generated by cell transfection of RNA from serum and pancreas failed to reveal genetic differences between subpopulations endowed with differing virulences. In addition to providing evidence of hidden virulence determinants, this study underlines the capacity of a clone of an RNA virus to rapidly diversify phenotypically in vivo.
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Montes, Nuria, Alberto Cobos, Miriam Gil-Valle, Elena Caro e Israel Pagán. "Arabidopsis thaliana Genes Associated with Cucumber mosaic virus Virulence and Their Link to Virus Seed Transmission". Microorganisms 9, n. 4 (27 marzo 2021): 692. http://dx.doi.org/10.3390/microorganisms9040692.
Abstract (sommario):
Virulence, the effect of pathogen infection on progeny production, is a major determinant of host and pathogen fitness as it affects host fecundity and pathogen transmission. In plant–virus interactions, ample evidence indicates that virulence is genetically controlled by both partners. However, the host genetic determinants are poorly understood. Through a genome-wide association study (GWAS) of 154 Arabidopsis thaliana genotypes infected by Cucumber mosaic virus (CMV), we identified eight host genes associated with virulence, most of them involved in response to biotic stresses and in cell wall biogenesis in plant reproductive structures. Given that virulence is a main determinant of the efficiency of plant virus seed transmission, we explored the link between this trait and the genetic regulation of virulence. Our results suggest that the same functions that control virulence are also important for CMV transmission through seeds. In sum, this work provides evidence of a novel role for some previously known plant defense genes and for the cell wall metabolism in plant virus interactions.
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MIKI, Tsuyoshi. "Virulence determinant of Chromobacterium violaceum". Nippon Saikingaku Zasshi 69, n. 4 (2014): 577–88. http://dx.doi.org/10.3412/jsb.69.577.
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Zhu, Yefei, Renu Nandakumar, Marat R. Sadykov, Nandakumar Madayiputhiya, Thanh T. Luong, Rosmarie Gaupp, Chia Y. Lee e Greg A. Somerville. "RpiR Homologues May Link Staphylococcus aureus RNAIII Synthesis and Pentose Phosphate Pathway Regulation". Journal of Bacteriology 193, n. 22 (16 settembre 2011): 6187–96. http://dx.doi.org/10.1128/jb.05930-11.
Abstract (sommario):
Staphylococcus aureusis a medically important pathogen that synthesizes a wide range of virulence determinants. The synthesis of many staphylococcal virulence determinants is regulated in part by stress-induced changes in the activity of the tricarboxylic acid (TCA) cycle. One metabolic change associated with TCA cycle stress is an increased concentration of ribose, leading us to hypothesize that a pentose phosphate pathway (PPP)-responsive regulator mediates some of the TCA cycle-dependent regulatory effects. Using bioinformatics, we identified three potential ribose-responsive regulators that belong to the RpiR family of transcriptional regulators. To determine whether these RpiR homologues affect PPP activity and virulence determinant synthesis, therpiRhomologues were inactivated, and the effects on PPP activity and virulence factor synthesis were assessed. Two of the three homologues (RpiRB and RpiRC) positively influence the transcription of the PPP genesrpiAandzwf, while the third homologue (RpiRA) is slightly antagonistic to the other homologues. In addition, inactivation of RpiRC altered the temporal transcription of RNAIII, the effector molecule of theagrquorum-sensing system. These data confirm the close linkage of central metabolism and virulence determinant synthesis, and they establish a metabolic override for quorum-sensing-dependent regulation of RNAIII transcription.
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Neilan, J. G., L. Zsak, Z. Lu, G. F. Kutish, C. L. Afonso e D. L. Rock. "Novel Swine Virulence Determinant in the Left Variable Region of the African Swine Fever Virus Genome". Journal of Virology 76, n. 7 (1 aprile 2002): 3095–104. http://dx.doi.org/10.1128/jvi.76.7.3095-3104.2002.
Abstract (sommario):
ABSTRACT Previously we have shown that the African swine fever virus (ASFV) NL gene deletion mutant E70ΔNL is attenuated in pigs. Our recent observations that NL gene deletion mutants of two additional pathogenic ASFV isolates, Malawi Lil-20/1 and Pr4, remained highly virulent in swine (100% mortality) suggested that these isolates encoded an additional virulence determinant(s) that was absent from E70. To map this putative virulence determinant, in vivo marker rescue experiments were performed by inoculating swine with infection-transfection lysates containing E70 NL deletion mutant virus (E70ΔNL) and cosmid DNA clones from the Malawi NL gene deletion mutant (MalΔNL). A cosmid clone representing the left-hand 38-kb region (map units 0.05 to 0.26) of the MalΔNL genome was capable of restoring full virulence to E70ΔNL. Southern blot analysis of recovered virulent viruses confirmed that they were recombinant E70ΔNL genomes containing a 23- to 28-kb DNA fragment of the Malawi genome. These recombinants exhibited an unaltered MalΔNL disease and virulence phenotype when inoculated into swine. Additional in vivo marker rescue experiments identified a 20-kb fragment, encoding members of multigene families (MGF) 360 and 530, as being capable of fully restoring virulence to E70ΔNL. Comparative nucleotide sequence analysis of the left variable region of the E70ΔNL and Malawi Lil-20/1 genomes identified an 8-kb deletion in the E70ΔNL isolate which resulted in the deletion and/or truncation of three MGF 360 genes and four MGF 530 genes. A recombinant MalΔNL deletion mutant lacking three members of each MGF gene family was constructed and evaluated for virulence in swine. The mutant virus replicated normally in macrophage cell culture but was avirulent in swine. Together, these results indicate that a region within the left variable region of the ASFV genome containing the MGF 360 and 530 genes represents a previously unrecognized virulence determinant for domestic swine.
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Gaupp, Rosmarie, Jessica Wirf, B. Wonnenberg, Tanja Biegel, J. Eisenbeis, J. Graham, M. Herrmann et al. "RpiRc Is a Pleiotropic Effector of Virulence Determinant Synthesis and Attenuates Pathogenicity in Staphylococcus aureus". Infection and Immunity 84, n. 7 (25 aprile 2016): 2031–41. http://dx.doi.org/10.1128/iai.00285-16.
Abstract (sommario):
InStaphylococcus aureus, metabolism is intimately linked with virulence determinant biosynthesis, and several metabolite-responsive regulators have been reported to mediate this linkage.S. aureuspossesses at least three members of the RpiR family of transcriptional regulators. Of the three RpiR homologs, RpiRc is a potential regulator of the pentose phosphate pathway, which also regulates RNAIII levels. RNAIII is the regulatory RNA of theagrquorum-sensing system that controls virulence determinant synthesis. The effect of RpiRc on RNAIII likely involves other regulators, as the regulators that bind the RNAIII promoter have been intensely studied. To determine which regulators might bridge the gap between RpiRc and RNAIII,sarA,sigB,mgrA, andacnAmutations were introduced into anrpiRcmutant background, and the effects on RNAIII were determined. Additionally, phenotypic and genotypic differences were examined in the single and double mutant strains, and the virulence of select strains was examined using two different murine infection models. The data suggest that RpiRc affects RNAIII transcription and the synthesis of virulence determinants in concert with σB, SarA, and the bacterial metabolic status to negatively affect virulence.
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Kielian, Tammy, Ambrose Cheung e William F. Hickey. "Diminished Virulence of an Alpha-Toxin Mutant ofStaphylococcus aureus in Experimental Brain Abscesses". Infection and Immunity 69, n. 11 (1 novembre 2001): 6902–11. http://dx.doi.org/10.1128/iai.69.11.6902-6911.2001.
Abstract (sommario):
ABSTRACT Staphylococcus aureus is one of the major etiologic agents of brain abscesses in humans, occasionally leading to focal neurological deficits and even death. The objective of the present study was to identify key virulence determinants contributing to the pathogenesis of S. aureus in the brain using a murine brain abscess model. The importance of virulence factor production in disease development was demonstrated by the inability of heat-inactivated S. aureus to induce proinflammatory cytokine or chemokine expression or brain abscess formation in vivo. To directly address the contribution of virulence determinants in brain abscess development, the abilities of S. aureus strains with mutations in the global regulatory loci sarA andagr were examined. An S. aureus sarA agr double mutant exhibited reduced virulence in vivo, as demonstrated by attenuated proinflammatory cytokine and chemokine expression and bacterial replication. Subsequent studies focused on the expression of factors that are altered in thesarA agr double mutant. Evaluation of an alpha-toxin mutant revealed a phenotype similar to that of the sarA agr mutant in vivo, as evidenced by lower bacterial burdens and attenuation of cytokine and chemokine expression in the brain. This suggested that alpha-toxin is a central virulence determinant in brain abscess development. Another virulence mechanism utilized by staphylococci is intracellular survival. Cells recovered from brain abscesses were shown to harbor S. aureusintracellularly, providing a means by which the organism may establish chronic infections in the brain. Together, these data identify alpha-toxin as a key virulence determinant for the survival ofS. aureus in the brain.
Tesi sul tema "Virulence determinant":
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Aish, Joanne Louise. "Environmental regulation of virulence determinant expression in Staphylococcus aureus". Thesis, University of Sheffield, 2003. http://etheses.whiterose.ac.uk/3030/.
Abstract (sommario):
Staphylococcus aureus is a highly versatile pathogen that causes a wide range of diseases. Appropriate gene expression in various niches within the human body and abiotic environments requires the sensing of environmental conditions. An important environmental parameter affecting S. aureus is NaC1 concentration. This study investigated S. aureus virulence determinant regulation in the presence and absence of NaCl stress. In the absence of NaCl stress, aB was found to repress hla transcription and protease activity, possibly via the repression of agr transcription. The effect of aB on agr probably occurs indirectly, although sarA, sarHi and rot are unlikely to function as intermediates in this pathway. Tn551 mutagenesis identified numerous genes, including lysC, ykuQ, lysA, brnQ and telA, which repress hla transcription and protease activity by upregulating aB activity. These genes are clustered in the SVS (S. aureus virulence and survival) region of the S. aureus genome, in which transposon insertion affected the virulence and survival of mutants isolated in numerous published screens. Other SVS region genes, including asd, dapA, hipO, ac1P and norQ were also found to repress hla transcription and protease activity by upregulating aB activity. In the presence of NaCl stress, virulence determinants (which are normally regulated by agr) come under the control of a novel regulatory system involving an-dependent and aB-independent pathways. Tn917 mutagenesis identified several genes, including citG, opuD, yugT, oppF, ykrP, eprH, yubA, unkl and unk2, which have putative roles in the aB-independent pathway. The SVS region genes analysed may function in the aB- dependent pathway. The sensor saeS was found to upregulate hla transcription in the absence of NaCI stress and may be involved in sensing NaCI stress. The NaCI stress signal may act in concert with other parameters to allow stringent virulence determinant regulation in response to the prevailing environmental conditions.
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Horsburgh, Samantha. "Identification of novel regulators of virulence determinant production in Staphylcoccus aureus". Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274960.
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Dade, Jessica E. "HcZrt2, a Zinc Transporter and Nutritional Virulence Determinant in Histoplasma Capsulatum". University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1470753451.
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Apagyi, Katinka. "Characterization of a novel virulence determinant in Erwinia carotovora subspecies atroseptica SCRI1043". Thesis, University of Cambridge, 2012. https://www.repository.cam.ac.uk/handle/1810/265545.
Abstract (sommario):
This study focused on the characterization of the gene rsmS in Erwinia carotovora subsp. atroseptica (Eca). Eca is a phytopathogenic Gram-negative bacteria, producing virulence factors, such as plant cell wall degrading enzymes {PCWDEs), which enable the initiation and maintenance of host plant invasion. rsmS was shown to encode a short polypeptide, and it has orthologues in many Gramnegative agriculturally and medically relevant bacteria. Plate and spectrophotometry-based assays and microarray studies showed that RsmS suppressed the transcription and activity of several PCWDEs, the transcription of type one, two and six secretion systems and of some of their substrates. RsmS also suppressed general virulence exhibited by Eca in potato tubers, and on the quorum sensing signaling molecule N-{3-oxohexanoylh-homoserine lactone. In many ways, RsmS acted in a similar fashion to RsmA, r a well characterized suppressor of virulence determinants (such as PCWDEs) and quorum sensing found in a wide variety of Gram-negative bacteria. RsmA activated rsmS transcription, and the transcription of both rsmS and rsmA was shown to be upregulated with increasing temperature. Thus, it is possible that RsmA exerts some of its inhibitory effects on virulence determinants through the positive regulation of RsmS. rsmS was shown to be transcribed from a promoter shared with its upstream neighbour, priC. It may also be transcribed from a promoter located within the priC open reading frame, but this result remains to be confirmed with future experiments. Although the genomic arrangement of priC and rsmS is conserved in almost all bacteria with an rsmS orthologue, no further regulatory connection was shown between their protein products. Interestingly, when rsmS was overexpressed without a 225 bp region located within priC, PCWDE activity was increased, in all mutant strains of Eca tested. The reason behind this dominant negative phenotype remains to be fully elucidated by future experiments. Both microarray and plasposon mutagenesis studies identified several genes coding for factors that are regulated by, or regulate, RsmS. It will require further analysis and experiments to unveil which one of these actually interacts with RsmS (directly or indirectly). Such genes include CRISPR-like genes, members of nitrogen metabolism pathways and membrane transport.
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Mateo, Montalcini Solange A. "AGC kinase Sta1 is a virulence determinant in the rice blast fungus". Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531838.
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Stapleton, Melanie. "Studies with SlyA, a transcription regulator and virulence determinant of Salmonella typhimurium". Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274957.
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Marroquin, Stephanie Michelle. "A Novel Abi-domain Protein Controls Virulence Determinant Production in Staphylococcus aureus". Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6725.
Abstract (sommario):
A major factor in the success of Staphylococcus aureus as a pathogen is its vast arsenal of virulence determinants and, more importantly, the tight and precisely- timed regulation of these factors. Here we investigate the product of the S. aureus gene, SAUSA300_1984, encoding a putative transmembrane protein. This as yet uncharacterized protein belongs to the Abi (abortive infection) family, which are commonly annotated as CAAX-proteases, and are significantly understudied in prokaryotes. In S. aureus the disruption of SAUSA300_1984 results in a drastic reduction of proteolytic and hemolytic activity, as well as diminished pigmentation. This phenotype appears to be mediated through reduced agr expression, as determined by qPCR analysis. Importantly, known regulators of agr, such as CodY, MgrA, and ArlR, demonstrate no significant changes in transcription upon 1984 disruption, whilst major alterations were observed for downstream effectors of agr, such as sarS, RNAIII, rot and hla. Complementation and site-directed mutagenesis of 1984 demonstrated that proteolytic activity (via conserved EE residues) was not required for this phenotype, suggesting a potential protein-protein interaction mechanism of interaction. Proteome analysis of the 1984 mutant confirmed a number of our transcriptional observations, such as an increased abundance of Rot and surface associated proteins, as well as a marked decrease in Agr-system proteins levels, with the most striking being AgrB. Virulence profiling revealed a decreased ability of the 1984 mutant to evade constituents of the innate immune response, and impaired survival during murine models of infection. Given that SAUSA300_1984 is encoded 3 genes downstream of RNAIII, our current working hypothesis is that this Abi protein functions to control agr activity through communication with membrane components of this system, potentially via interaction with AgrB. Confirming this, and determining the upstream effectors of this regulatory system are studies currently ongoing in our laboratory.
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Price, Maeve. "SSWl encodes a glycolipid-anchored surface protein and is a virulence determinant in M oryzae". Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526103.
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Sodeinde, Olanrewaju A. "Identification and Characterization of the Virulence Determinant of the 9.5 Kilobase Plasmid of Yersinia Pestis: a Thesis". eScholarship@UMMS, 1990. http://escholarship.umassmed.edu/gsbs_diss/310.
Abstract (sommario):
The pathogenicity of Yersinia pestis, the causative agent of plague, is specified by chromosomal and plasmid encoded genes. At least two plasmids, with sizes of 9.5 and 75 kilobases, are indispensable to the full expression of virulence. Loss of the 75 kb plasmid results in outright avirulence. Strains lacking the 9.5 kb plasmid exhibit LD50s at least six orders of magnitude greater than wild-type following subcutaneous or intraperitoneal infection of mice or guinea-pigs but have LD50s as low as wild-type when injected intravenously. Four biochemical properties are associated with the 9.5 kb plasmid. These include plasminogen activator and coagulase activities in addition to the bacteriocin pesticin, and its immunity determinant. A genetic analysis of this plasmid was undertaken as a first step towards the identification and characterization of its virulence determinant(s). This led to the construction of a physical and genetic map of the plasmid. Four loci were mapped to the plasmid: pst and pim, which encode pesticin and its immunity determinant respectively; pla, which encodes both plasminogen activator and coagulase activities; and ori/inc, the locus containing both the origin of replication and the region responsible for the control of plasmid incompatibility. pst was shown to encode a 45 kD protein but the pim gene product was not identified. pla encodes two outer membrane proteins, α- and β-Pla of 37 and 35 kD, respectively, the latter being derived from the former most probably by a proteolytic processing event. At least one of these proteins is responsible for the highly specific degradation of the YOPs, a set of virulence-associated outer membrane proteins encoded by the 75 kb plasmid. The nucleotide sequence of pla revealed that it possessed significant homology to both prtA (geneE) of Salmonella typhimurium and ompT of Escherichia coli. Subcutaneous infection of mice with isogenic strains of Y. pestis harboring well defined mutations in the genes that reside on the 9.5 kb plasmid revealed that pla is a virulence determinant of Y. pestis, and also that of the genes harbored by the plasmid, pla is both necessary and sufficient to account for the high degree of virulence of Y. pestis for mice from subcutaneous sites of infection. pla encodes an activator of human, rat, and mouse plasminogen but does not induce coagulation of plasma obtained from these species. Treatment of mice with the antifibrinolytic agent, trans-4(aminomethyl)-cyclohexanecarboxylic acid did not affect the outcome of plague infection, indicating that fibrinolysis per se does not play a role in plague pathogenesis.
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Kleij, Lena. "Identification and validation of the virulence determinants of circulating equine influenza viruses". Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL136.
Abstract (sommario):
Les virus influenza sont des virus enveloppés, à ARN négatif segmenté en 8 segments génomiques. Ils sont classés dans la famille des Orthomyxoviridae. Ce sont les agents étiologiques de la grippe, une maladie respiratoire qui touche de nombreuses espèces mammifères et aviaires. La grippe équine est causée par les sous-types H3N8 et H7N7 du virus influenza de type A, ce dernier s'étant éteint depuis les années 1970. Malgré l'existence d'un vaccin, la France a connu plusieurs épidémies de H3N8 depuis les années 2000. Pour réduire l'impact économique important de ces épidémies pour l'industrie équine, il est nécessaire d'établir des tests de diagnostic rapides, robustes et applicables sur le terrain pour limiter au plus la circulation du virus et en identifier les déterminants de virulence et caractériser la dérive antigénique.Nous avons étudié les potentialités de la technique de séquençage dite « long read » développée par Oxford Nanopore Technologies. Nous avons réalisé une caractérisation du génome complet de deux virus H3N8 équins ayant circulé en France en 2009 et 2018 (A/équine/Paris/1/2018 et A/équine/Beuvron-en-Auge/2/2009, deux virus de la clade 1 Florida) ainsi que des deux souches du vaccin couramment utilisé en France.Nos résultats ont démontré la fiabilité de cette technique de séquençage à partir d'amplicons des huit segments génomiques des quatre virus analysés ainsi que la capacité à réaliser des lectures fiables à partir du séquençage direct des ARN viraux (résultats présentés dans une première partie). L'analyse de la séquence en acides aminés de l'hémagglutinine HA des souches circulantes ont mis en évidence une très légère dérive antigénique par rapport aux souches vaccinales avec des substitutions spécifiques comme T161I dans A/equine/Paris/1/2018 and N188T dans les souches post-2015, deux substitutions localisées dans le site antigénique B. Le site antigénique E montre également des modifications dans les souches post-2018, avec la substitution N63D.Le segment génomique 2 code pour une des trois sous-unités de l'ARN-polymérase virale, PB1 ainsi que pour une protéine accessoire, PB1-F2, d'un cadre de lecture alternatif. PB1-F2 est reconnu comme un déterminant de virulence. Alors que la souche A/équine/Paris/1/2018 code pour un variant de 90 acides aminés de long, de nombreuses souches, dont A/équine/Beuvron-en-Auge/2/2009, code pour un variant de seulement 81 résidus. Des essais biologiques et de biochimie ont été réalisés pour caractériser les propriétés de chacune de ces deux formes de PB1-F2. Dans un essai où la forme longue de PB1-F2 est exprimée en cellules eucaryotes sans autre constituant viraux, elle abolit le potentiel membranaire de la mitochondrie cellulaire. Mise en présence de vésicules synthétiques mimant la membrane externe de la mitochondrie, la forme longue de PB1-F2 les perméabilise plus efficacement que la forme courte. Les analyses de séquence en acides aminés des protéines virales (de HA et PB1-F2 essentiellement) sont présentées dans une deuxième partie.Afin de valider l'impact de PB1-F2 sur la virulence en contexte infection, nous avons cherché à établir un système de génétique inverse pour le virus A/équine/Paris/1/2018 (troisième partie). Pour se faire, les 8 segments génomiques ont été clonés dans le plasmide pRF483 permettant d'assurer la synthèse des brins d'ARN génomiques et l'expression des protéines virales. La séquence des inserts de chacun des plasmides a été validée. Pour valider le fonctionnement du complexe réplicatif codé par 4 des 8 segments viraux clonés dans pRF483 (PA, PB1, PB2 et NP), ces plasmides ont été transfectés avec un plasmide codant pour le segment génomique NA dans lequel son cadre de lecture a été substitué par un gène reporter, la luciférase. Dans ces conditions expérimentales, une activité du complexe ARN-polymérase a été détectée. Ces essais seront prolongés pour la production de virus recombinants par transfection des 8 plasmides construitsInfluenza viruses are enveloped, their genome being segmented into 8 negative RNA segments. They are classified in the Orthomyxoviridae family. They are the etiological agents of the flu, a respiratory disease that affects many mammalian and avian species. Equine influenza is caused by the H3N8 and H7N7 subtypes of the type A influenza virus, the latter being extinct since the 1970s. Despite the existence of a vaccine, France has experienced several H3N8 epidemics since the 2000s. To reduce the significant economic impact of these epidemics for the equine industry, it is necessary to establish rapid, robust, and on-terrain applicable diagnostic tests to limit the circulation of the virus as much as possible and identify its virulence determinants as well as characterize antigenic drift.We studied the potential of the so-called “long read” sequencing technique developed by Oxford Nanopore Technologies. We carried out a characterization of the complete genome of two equine H3N8 viruses that circulated in France in 2009 and 2018 (A/equine/Paris/1/2018 and A/equine/Beuvron-en-Auge/2/2009, two viruses of clade 1 Florida) as well as the two strains of the vaccine commonly used in France.Our results demonstrated the reliability of this sequencing technique using amplicons of the eight genomic segments of the four viruses analyzed as well as the ability to produce reliable readings from direct sequencing of viral RNA (results presented in the first part). Analysis of the amino acid sequence of hemagglutinin HA of circulating strains demonstrated a very slight antigenic drift compared to vaccine strains with specific substitutions such as T161I in A/equine/Paris/1/2018 and N188T in the post-2015 strains, two substitutions located in the antigenic site B. The antigenic site E also shows modifications in the post-2018 strains, with the N63D substitution.Genomic segment 2 encodes one of the three subunits of the viral RNA polymerase, PB1, as well as an accessory protein, PB1-F2, of an alternative reading frame. PB1-F2 is recognized as a virulence determinant. While the A/equine/Paris/1/2018 strain encodes a variant 90 amino acids long, many strains, including A/equine/Beuvron-en-Auge/2/2009, encode a variant only 81 residues. Biological and biochemical tests were carried out to characterize the properties of each of these two forms of PB1-F2. In an assay where the long form of PB1-F2 is expressed in eukaryotic cells without other viral constituents, it abolishes the membrane potential of the cellular mitochondria. Placed in the presence of synthetic vesicles mimicking the mitochondrial outer membrane, the long form of PB1-F2 permeabilizes them more effectively than the short form. Amino acid sequence analyzes of the viral proteins (mainly HA and PB1-F2) are presented in a second part.In order to validate the impact of PB1-F2 on virulence in an infectious context, we sought to establish a reverse genetics system for the A/equine/Paris/1/2018 virus (third part). To do this, the 8 genomic segments were cloned into the pRF483 plasmid to ensure the synthesis of genomic RNA strands and the expression of viral proteins. The sequence of the inserts of each of the plasmids was validated. To validate the functioning of the replicative complex encoded by 4 of the 8 viral segments cloned in pRF483 (PA, PB1, PB2 and NP), these plasmids were transfected with a plasmid coding for the NA genomic segment in which its reading frame was substituted. by a reporter gene, luciferase. Under these experimental conditions, activity of the RNA-polymerase complex was detected. These tests will be extended for the production of recombinant viruses by transfection of the 8 constructed plasmids
Libri sul tema "Virulence determinant":
1
Kapoor, Sanjay. Molecular determinants of rotavirus virulence. [s.l.]: typescript, 1995.
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Mack, Kerri Anne. Virulence determinants of Francisella Tularensis. Manchester: University of Manchester, 1994.
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M, Ayoub Elia, Cassell Gail H e American Society for Microbiology, a cura di. Microbial determinants of virulence and host response. Washington, D.C: American Society for Microbiology, 1990.
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McKenney, David. The cell surface and extracellular virulence determinants of Burkholderia Cepacia. Manchester: University of Manchester, 1994.
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Heikinheimo, Riikka. Regulation and characterization of the virulence determinants of the plant pathogen Erwinia carotovora subsp. carotovora. Uppsala: Dept. of Molecular Genetics, Uppsala Genetic Center, Swedish University of Agricultural Sciences, 1995.
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Characterization of a virulence determinant from group A Streptococcus: Identification of a novel chromosomal region responsible for streptolysin S production in Streptococcus pyogenes. Ottawa: National Library of Canada, 1997.
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Moss, Eric Geoffrey. Structural determinants of virulence in poliovirus. 1990.
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Odds, Frank C. Pathogenesis of fungal disease. A cura di Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum e Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0008.
Abstract (sommario):
The pathogenesis of fungal disease involves an interplay between fungal virulence factors and host immune responses. Most fungal pathogens are opportunists that preferentially invade hosts with immune defects, but the fact that relative pathogenicity varies between fungal species (and even between different strains within a species) is evidence that fungi have evolved multiple, different molecular virulence factors. Experiments in which genes encoding putative virulence attributes are specifically disrupted and the resulting mutants are tested for virulence in a range of vertebrate and invertebrate hosts have identified or confirmed many gene products as significant for the pathogenesis of various types of fungal disease. These include factors determining fungal shape in vivo, biofilm formation, and a plethora of surface components, including adhesins and hydrolytic enzymes. This chapter provides an overview of fungal virulence attributes.
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Fuller, Jeffrey D. Characterization of potential virulence determinants in the fish and human pathogen streptococcus iniae. 2003.
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Smoot, Laura Marie. Molecular and genetic analysis of potential virulence determinants harbored by the Brazilian purpuric fever clone of H. influenzae bigroup aegyptius. 1999.
Capitoli di libri sul tema "Virulence determinant":
1
Mittal, Aruna, e Rajneesh Jha. "Chaperonin 60.1 of the Chlamydiae (cHSP60) as a Major Virulence Determinant". In Heat Shock Proteins, 161–72. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6787-4_10.
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Mäkelä, P. Helena, Marianne Hovi, Harri Saxen, Matti Valtonen e Ville Valtonen. "Ability to Activate the Alternative Complement Pathway as a Virulence Determinant in Salmonellae". In Bacteria, Complement and the Phagocytic Cell, 157–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_12.
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Morrow, K. Adam, Dara W. Frank, Ron Balczon e Troy Stevens. "The Pseudomonas aeruginosa Exoenzyme Y: A Promiscuous Nucleotidyl Cyclase Edema Factor and Virulence Determinant". In Non-canonical Cyclic Nucleotides, 67–85. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/164_2016_5003.
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Wake, Akira, e Herbert R. Morgan. "Localization of Virulence Determinants". In Host-Parasite Relationships and the Yersinia Model, 12–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71344-6_3.
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Quinn, F. D., G. W. Newman e C. H. King. "Virulence Determinants of Mycobacterium tuberculosis". In Current Topics in Microbiology and Immunology, 131–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80166-2_6.
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Rico-Hesse, R. "Dengue Virus Virulence and Transmission Determinants". In Current Topics in Microbiology and Immunology, 45–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02215-9_4.
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Clark-Curtiss, J. E. "Identification of Virulence Determinants in Pathogenic Mycobacteria". In Current Topics in Microbiology and Immunology, 57–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80451-9_4.
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Arndt, Annette, e Mary Ellen Davey. "Porphyromonas gingivalis: surface polysaccharides as virulence determinants". In Interface Oral Health Science 2009, 382–87. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_111.
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Rhodes, Judith C., e Axel A. Brakhage. "Molecular Determinants of Virulence in Aspergillus fumigatus". In Molecular Principles of Fungal Pathogenesis, 333–45. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815776.ch24.
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Cheung, Ambrose L. "Global Regulation of Virulence Determinants in Staphylococcus aureus". In Infectious Agents and Pathogenesis, 295–322. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/0-306-46848-4_14.
Atti di convegni sul tema "Virulence determinant":
1
Morea, M., D. Cattivelli, A. Matarante, F. Baruzzi e P. S. Cocconcelli. "eoagulase nega tive-sta phylococci and enterococci in fermented meat products: presence of virulence and antibiotic resistance determinants". In Fourth International Symposium on the Epidemiology and Control of Salmonella and Other Food Borne Pathogens in Pork. Iowa State University, Digital Press, 2001. http://dx.doi.org/10.31274/safepork-180809-1155.
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Li, Jianjun, Adele Martin, Valerie Bouchet, Elke K. H. Schweda, Derek W. Hood, Stephen Pelton, Richard Goldstein, Derek E. Richard Moxon e James C. Richards. "SIALYLATED LIPOPOLYSACCHARIDE GLUCOFORMS ARE CRITICAL VIRULENCE DETERMINANTS IN HAEMOPHILUS INFLUENZAE OTITIS MEDIA: ANALYSIS OF MIDDLE EAR WASHINGS FROM INFECTED CHINCHILLAS BY CAPILLARY ELECTROPHORESIS MASS SPECTROMETRY". In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.402.
Rapporti di organizzazioni sul tema "Virulence determinant":
1
Prusky, Dov, e Jeffrey Rollins. Modulation of pathogenicity of postharvest pathogens by environmental pH. United States Department of Agriculture, dicembre 2006. http://dx.doi.org/10.32747/2006.7587237.bard.
Abstract (sommario):
Until recently, environmental pH was not considered a factor in determining pathogen compatibility. Our hypothesis was that the environmental pH at the infection site, which is dynamically controlled by activities of both the host and the pathogen, regulates the expression of genes necessary for disease development in Colletotrichum gloeosporioides and Sclerotinia sclerotiorum. This form of regulation ensures that genes are expressed at optimal conditions for their encoded activities.Pectate lyase encoded by pelB, has been demonstrated to play a key role in virulence of C. gloeosporioides in avocado fruit. Polyglacturonase synergism with oxalic acid production is considered to be an essential pathogenicity determinant in the interactions of S. sclerotiorum with its numerous hosts. A common regulatory feature of these virulence and pathogenicity factors is their dependence upon environmental pH conditions within the host niche to create optimal conditions for expression and secretion. In this proposal we have examined, 1) the mechanisms employed by these fungi to establish a suitable pH environment, 2) the molecular levels at which genes and gene products are regulated in response to environmental pH, and 3) the molecular basis and functional importance of pH-responsive gene regulation during pathogenicity. The specific objectives of the proposal were: 1. Characterize the mechanism of local pH modulation and the effect of ambient pH on the expression and secretion of virulence factors. 2. Provide evidence that a conserved molecular pathway for pH-responsive gene expression exists in C. gloeosporioides by cloning a pacC gene homologue. 3. Determine the role of pacC in pathogenicity by gene disruption and activating mutations. Major conclusions 1. We determined the importance of nitrogen source and external pH in the secretion of the virulence factor pectate lyase with respect to the ambient pH transcriptional regulator pacC. It was concluded that nitrogen source availability and ambient pH are two independent signals for the transcriptional regulation of genes required for the disease process of C. gloeosporioides and possibly of other pathogens. 2. We also determined that availability of ammonia regulate independently the alkalinization process and pelB expression, pecate lyase secretion and virulence of C. gloeosporioides. 3. Gene disruption of pacC reduced virulence of C. gloeosporioides however did not reduced fully pelB expression. It was concluded that pelB expression is regulated by several factors including pH, nitrogen and carbon sources. 4. Gene disruption of pacC reduced virulence of S. slcerotiourum Creation of a dominant activating
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Coplin, David L., Shulamit Manulis e 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, giugno 2005. http://dx.doi.org/10.32747/2005.7587216.bard.
Abstract (sommario):
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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Sharon, Amir, e Maor Bar-Peled. Identification of new glycan metabolic pathways in the fungal pathogen Botrytis cinerea and their role in fungus-plant interactions. United States Department of Agriculture, 2012. http://dx.doi.org/10.32747/2012.7597916.bard.
Abstract (sommario):
The involvement of glycans in microbial adherence, recognition and signaling is often a critical determinant of pathogenesis. Although the major glycan components of fungal cell walls have been identified there is limited information available on its ‘minor sugar components’ and how these change during different stages of fungal development. Our aim was to define the role of Rhacontaining-glycans in the gray mold disease caused by the necrotrophic fungus B. cinerea. The research was built on the discovery of two genes, Bcdhand bcer, that are involved in formation of UDP-KDG and UDP-Rha, two UDP- sugars that may serve as donors for the synthesis of cell surface glycans. Objectives of the proposed research included: 1) To determine the function of B. cinereaBcDh and BcEr in glycan biosynthesis and in pathogenesis, 2) To determine the expression pattern of BcDH and BcERand cellular localization of their encoded proteins, 3) Characterize the structure and distribution of Rha- containing glycans, 4) Characterization of the UDP-sugar enzymes and potential of GTs involved in glycanrhamnosylation. To address these objectives we generated a series of B. cinereamutants with modifications in the bchdhand bcergenes and the phenotype and sugar metabolism in the resulting strains were characterized. Analysis of sugar metabolites showed that changes in the genes caused changes in primary and secondary sugars, including abolishment of rhamnose, however abolishment of rhamnose synthesis did not cause changes in the fungal phenotype. In contrast, we found that deletion of the second gene, bcer, leads to accumulation of the intermediate sugar – UDP- KDG, and that such mutants suffer from a range of defects including reduced virulence. Further analyses confirmed that UDP-KDG is toxic to the fungus. Studies on mode of action suggested that UDP-KDG might affect integrity of the fungal cell wall, possibly by inhibiting UDP-sugars metabolic enzymes. Our results confirm that bcdhand bcerrepresent a single pathway of rhamnose synthesis in B. cinerea, that rhamnose does not affect in vitro development or virulence of the fungus. We also concluded that UDP-KDG is toxic to B. cinereaand hence UDP-KDG or compounds that inhibit Er enzymes and lead to accumulation of UDP-KDG might have antifungal activity. This toxicity is likely the case with other fungi, this became apparent in a collaborative work with Prof. Bart Thomma of Wageningen University, NETHERLANDS . We have shown the deletion of ER mutant in Verticillium dahlia gave plants resistance to the fungal infection.
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Zhao, Bingyu, Saul Burdman, Ronald Walcott, Tal Pupko e Gregory Welbaum. Identifying pathogenic determinants of Acidovorax citrulli toward the control of bacterial fruit blotch of cucurbits. United States Department of Agriculture, gennaio 2014. http://dx.doi.org/10.32747/2014.7598168.bard.
Abstract (sommario):
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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Chejanovsky, Nor, e Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, gennaio 2010. http://dx.doi.org/10.32747/2010.7592113.bard.
Abstract (sommario):
The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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Gómez Valderrama, Juliana, Lorena García Riaño, Diana Marcela Monroy, Gustavo Adolfo Araque, Carlos Espinel e Laura Villamizar. Enhancement of beauveria bassiana virulence and efficacy to control diatraea saccharalis in sugarcan. Corporación Colombiana de Investigación Agropecuaria - AGROSAVIA, 2016. http://dx.doi.org/10.21930/agrosavia.poster.2016.27.
Abstract (sommario):
El cultivo de caña de azúcar para la producción de panela es de gran importancia en América Latina, América Central y la India. El rendimiento de Panela depende sobre el contenido de sacarosa en la caña de azúcar, característica seriamente afectada por la presencia del complejo de barrenadores del tallo del género Diatraea sp. En Colombia, los estudios en el Valle del río Cauca indican una reducción en el peso de la caña de 0.83% por cada unidad porcentual de entrenudos aburridos, y una pérdida adicional de 0.26% del rendimiento de azúcar en la molienda. El uso de insecticidas no ha sido eficiente debido a la naturaleza crítica de esta plaga que desarrolla su ciclo larval dentro de los tallos de la caña de azúcar. En un trabajo previo, un aislado colombiano de Beauveria bassiana (Bv062) demostró un alto potencial para desarrollar un bioinsecticida para el control de Diatraea sp. El presente trabajo tuvo como objetivo evaluar potenciadores de la virulencia potenciales para conidios fúngicos y determinar la eficacia de los conidios formulados en el laboratorio y condiciones de campo
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Sordillo, Lorraine, Don Wojchowski, Gary Perdew, Arthur Saran e Gabriel Leitner. Identification of Staphylococcus aureaus Virulence Factors Associated with Bovine Mastitis. United States Department of Agriculture, febbraio 2001. http://dx.doi.org/10.32747/2001.7574340.bard.
Abstract (sommario):
Staphylococcus aureus is a major cause of mastitis in dairy cattle. The organism is able to adhere to and penetrate mammary epithelium, forming deep seated abscesses that result in chronic infections. This study was based on the observation that certain genotypes of S. aureus are isolated more frequently from field cases of bovine mastitis than others and the most prevalent genotypes of S. aureus have an increased ability to resist neutrophil phagocytosis and killing compared to the rare variants. It was hypothesized that these predominating genotypes differentially express virulence factors that allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. The overall objective of this study was to determine the mechanisms by which predominating S. aureus genotypes were able to resist mammary gland defense mechanisms. The following specific aims were accomplished to address the overall objectives of this project: 1. Analyze and compare cell surface and secreted protein profiles of common and rare S. aureus genotypes isolated from field cases of bovine mastitis. 2. Purify and sequence selectively synthesized proteins unique to the most prevalent genotypes of S. aureus . 3. Determine the in vitro effects of isolated proteins on essential host defense mechanisms. Results from each specific aim showed that these redominating genotypes differentially express factors that may allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. Using complementary approaches, both the US and Israeli teams identified differentially expressed S. aureus factors that were positively correlated with virulence as determined by the ability to modify host immune cell responses and increase disease pathogenesis. Several candidate virulence factors have ben identified at both the molecular (US team) and protein (Israeli team) levels. Components of the phosphotransferase system were shown to be differentially expressed in prevalent strains of S. aureus and to modify the growth potential of these strains in a milk microenvironment. Evidence provided by both the Israeli and US teams also demonstrated a potential role of Staphylococcal enterotoxins in the pathogenesis of mastitis. Certain enterotoxins were shown to directly affect neutrophil bactericidal activities which can profoundly affect the establishment of new intramammary infections. Other evidence suggests that S. aureus superantigens can suppress mammary defenses by enhancing lymphoid suppressor cell activity. Collectively, these data suggest that unique factors are associated with predominating S. aureus genotypes that can affect in vitro and in vivo virulence as related to the pathogenesis of bovine mastitis. The potential development of a subunit mastitis vaccine which incorporates only relevant antigenic determinants has not been investigated in depth. Experiments outlined in this proposal has identified putative virulence factors which contribute to the pathogenesis of S. aureus mastitis and which may be used to formulate an efficacious subunit mastitis vaccine. Results from these studies may lead to the development of new methods to prevent this costly disease, providing a viable alternative to less effective mastitis control procedures based on chemotherapy.
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Yedidia, I., H. Senderowitz e A. O. Charkowski. Small molecule cocktails designed to impair virulence targets in soft rot Erwinias. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134165.bard.
Abstract (sommario):
Chemical signaling between beneficial or pathogenic bacteria and plants is a central factor in determining the outcome of plant-microbe interactions. Pectobacterium and Dickeya (soft rot Erwinias) are the major cause of soft rot, stem rot, and blackleg formed on potato and ornamentals, currently with no effective control. Our major aim was to establish and study specific bacterial genes/proteins as targets for anti-virulence compounds, by combining drug design tools and bioinformatics with experimental work. The approach allowed us to identify and test compounds (small molecules) that specifically interfere with the activities of these targets, by this impairing bacterial virulence. Two main targets were selected within the frame of the BARD project. The first is the ATP-binding cassette (ABC) transporters and methyl-accepting chemotaxis proteins (MCP) that have been characterized here for the first time in Pectobacteriaceae, and the second is the quorum sensing (QS) machinery of Pectobacterium with its major proteins and in particular, the AHL synthase ExpI that was identified as the preferred target for inhibition. Both systems are strongly associated with bacterial virulence and survival in planta. We found that Pectobacteriaceae, namely Dickeya and Pectobacterium, encode more ABC transporters and MCP in their genomes, compared to other bacteria in the order. For MCP, soft rot Pectobacteriaceae not only contain more than 30 MCP genes per strain, but also have more diverse ligand binding domains than other species in the Enterobacteriales. These findings suggest that both ABC transporters and MCP are important for soft rot Pectobacteriaceae pathogenicity. We now have a selection of mutants in these proteins that may be further explored to understand their direct involvement in virulence. In parallel, we studied the QS central proteins in pectobacteria, the signaling molecule N-acyl-homoserine lactone synthase, ExpI, and the response regulator ExpR, and established their phylogenetic relations within plant pathogenic Gram negative bacteria. Next, these proteins were used for virtual screening of millions of compounds in order to discover new compounds with potential to interfere with the QS machinery. Several natural compounds were tested for their interference with virulence related traits in Pectobacterium and their capability to minimize soft rot infections. Our findings using microcalorimetric binding studies have established for the first time direct interaction between the protein ExpI and two natural ligands, the plant hormone salicylic acid and the volatile compound carvacrol. These results supported a model by which plants interfere with bacterial communication through interkingdom signaling. The collaborative project yielded two research papers and a comprehensive review, which included new computational and bioinformatics data, in Annu. Rev. Phytopathol., the highest ranked journal in phytopathology. Additional two papers are in preparation. In order to transform the fundamental knowledge that have been gained during this collaborative BARD project into agricultural practice, to control soft rot bacteria, we have submitted a continual project.
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Samish, Michael, K. M. Kocan e Itamar Glazer. Entomopathogenic Nematodes as Biological Control Agents of Ticks. United States Department of Agriculture, settembre 1992. http://dx.doi.org/10.32747/1992.7568104.bard.
Abstract (sommario):
This research project was aimed to create a basis for the use of entomopathogenic nematodes (Steinernematidae an Heterorhabditidae) for biological control of ticks. The specific objectives were to determinate: 1) Nematode virulence to various. 2) Host-parasite interactions of nametodes and ticks. 3) Effect of environmental factors of tick habitats on nematode activity. 4) To test nematodes (anti tick activity) in defined field trials. Throughout the project 12 nematode strains from five species were tested in laboratory assays against all developmental stages of eight tick species. All tick species were found susceptible to nematode infection. The nematode strains the IS-5 and IS-12 of Heterorhabditis bacteriophora were found to be the most virulent. Engorged adults, particularly females, were the most susceptible stages. Despite the high susceptibility, ticks are not suitable hosts for nematode development and propagation. Entomopathogenic namatodes enter ticks and kill them by releasing the symbiotic bacteria from their foregut. Under favorable conditions, i.e. moist soil, moderate temperature (22-27oC) and sandy soil, nematode efficacy against B. annulatus engorged females was very high (>5% w/w) and high animal manure concentration in soil adversely effect nematode efficacy. In field trails, nematodes were effective when soil moisture was maintained at high levels. The results indicate that under favorable conditions the nematodes show promise as a biological control method for ticks. However, we still face several potential obstacles to the use of nematodes under less favorable conditions.
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Burdman, S., E. Welbaum, R. Walcott e B. Zhao. erial fruit blotch, elucidating the mechanisms of fruit infection by Acidovorax citrulli. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134162.bard.
Abstract (sommario):
Bacterial fruit blotch (BFB) of cucurbits is caused by the Gram-negative bacterium Acidovorax citrulli. BFB affects cucurbit production worldwide, and mainly watermelon and melon. Most A. citrulli strains are divided into two genetically differentiated groups: while group I strains have been mainly associated with melon and other non-watermelon cucurbits, group II strains are more aggressive on watermelon. Like many Gram-negative plant-pathogenic bacteria, A. citrulli relies on a functional type III secretion system (T3SS) for pathogenicity. The T3SS is responsible for direct secretion of bacterial protein effectors to the host cell. Type III-secreted effectors (T3Es) contribute to virulence through manipulation of the host cell metabolism and suppression of plant defense. Our previous collaboration showed that group I and II strains significantly differ in their T3E arsenal (Eckshtain-Levi et al., Phytopathology 2014, 104:1152-1162). Using comparative genomics, we also showed that group I and II strains of A. citrulli have substantial differences in their genome content (Eckshtain-Levi et al., Front. Microbiol. 2016, 7:430). Our long-term goals are to identify the genetic determinants that contribute to virulence and host preferential association of the two major groups of A. citrulli, and to exploit these insights to develop effective BFB management strategies. We hypothesize that differences in the arsenal of T3Es, are greatly responsible for the differences in host preferential association between strains belonging to the two groups. The specific objectives of this project were: (1) to investigate the susceptibility of cucurbit species to group I and II strains under field conditions; (2) to assess the contribution of T3Es and other virulence factors to A. citrulli virulence and host preference; and (3) to characterize the mechanisms of action of selected T3Es of A. citrulli. In the frame of objective 1, we carried out three field experiments involving inoculation of several cucurbit crops (watermelon, melon, pumpkin and squash) with group I and II strains. Findings from these experiments confirmed that A. citrulli strains exhibit a preference for watermelon and melon. Moreover, we demonstrated, for the first time under field conditions, host-preferential association of group I and II strains to melon and watermelon, respectively. While host-preferential association was observed in leaves and in fruit tissues, it was more pronounced in the latter. In this part of the project we also developed a duplex PCR assay to differentiate between group I and II strains. In the frame of objective 2, we employed a multifaceted approach combining bioinformatics and experimental methods to elucidate the T3E arsenal of A. citrulli. These experiments led to discovery that A. citrulli strains possess large arsenals with more than 60 T3E genes. Remarkably, we found that ~15% of the T3E genes are group-specific. Advances were achieved on the contribution of selected T3E genes and other virulence determinants to the ability of A. citrulli to colonize the fruit and other tissues of melon and watermelon. Last, in the frame of objective 3, we advanced our understanding on the mode of action of few key T3Es of A. citrulli. We also optimized a virus-induced gene silencing (VIGS) system for functional genomics in melon and watermelon. This system will allow us to test melon and watermelon genes that may have defense or susceptibility roles related to BFB disease. Overall, this collaboration substantially enriched our knowledge on basic aspects of BFB disease. We believe that the fruits of this collaboration will greatly contribute to our ultimate goal, which is generation of durable resistance of melon and watermelon to A. citrulli.