Yersinia pestis
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PROVIDER: PRJNA150625 | ENA |
REPOSITORIES: ENA
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Project description:Yersinia pestis is the causative agent of plague, which is transmitted primarily between fleas and mammals and is spread to humans through the bite of an infected flea or contact with afflicted animals. Hfq is proposed to be a global post-transcriptional regulator that acts by mediating interactions between many regulatory small RNAs (sRNAs) and their mRNA targets. Sequence comparisons revealed that Y. pestis appears to produce a functional homologue of E. coli Hfq. Phenotype comparisons using in vitro assays demonstrated that Y. pestis Hfq was involved in resistance to H2O2, heat and polymyxin B and contributed to growth under nutrient-limiting conditions. The role of Hfq in Y. pestis virulence was also assessed using macrophage and mouse infection models, and the gene expression affected by Hfq was determined using microarray-based transcriptome and real time PCR analysis. The macrophage infection assay showed that the Y. pestis hfq deletion strain did not have any significant difference in its ability to associate with J774A.1 macrophage cells. However, hfq deletion appeared to significantly impair the ability of Y. pestis to resist phagocytosis and survive within macrophages at the initial stage of infection. Furthermore, the hfq deletion strain was highly attenuated in mice after subcutaneous or intravenous injection. Transcriptome analysis supported the results concerning the attenuated phenotype of the hfq mutant and showed that the deletion of the hfq gene resulted in significant alterations in mRNA abundance of 243 genes in more than 13 functional classes, about 23% of which are known or hypothesized to be involved in stress resistance and virulence. Our results indicate that Hfq is a key regulator involved in Y. pestis stress resistance, intracellular survival and pathogenesis. It appears that Hfq acts by controlling the expression of many virulence- and stress-associated genes, probably in conjunction with small noncoding RNAs.
2009-09-01 | GSE15579 | GEO
Project description:A microarray was developed to screen rodent samples for pathogens of zoonotic importance In the work described here, a homologue to Yersinia pestis was found in rodent samples after screening with the microarray
2016-02-11 | GSE77765 | GEO
Project description:The transposon site hybridization (TraSH) technique (Sassetti, CM et al. 2001. PNAS 98:12712-7) was utilized to identify genes important for the survival of Y. pestis within murine macrophages. A transposon library was created with ~31,500 Y. pestis KIM6+ insertion mutants. A portion of the Y. pestis transposon insertion mutant library was used to infect BMMs and the surviving bacteria (output pool) were recovered. TraSH was used to compare the output pool to a portion of the library that was not subjected to selection (input pool) in order to identify Y. pestis genes important for survival in macrophages. Each end of the transposon used for mutagenesis contains an outward-reading T7 RNA polymerase promoter. RNAs transcribed from the T7 promoters are complementary to the chromosomal DNA flanking each transposon in the library, so the RNAs can be used as “targets” to identify the approximate position of each transposon insertion in the mutant pool. Differentially labeled targets generated from the output and input pools are competitively hybridized to the 70-mer oligonucleotide microarrays obtained from Pathogen Functional Genomics Resource Center/J. Craig Venter Institute. Genes important for survival of Y. pestis in macrophages are identified by determining the ratio of the signal intensities for the output and input targets hybridizing to a given probe.
2011-11-30 | GSE33982 | GEO
Project description:Yersinia pestis (Y. pestis) is the etiologic agent of the plague, an endemic zoonotic disease of critical clinical and historic importance. The species belongs to a genus comprising eleven members, three of which are human pathogens. Y. pestis and its closest extant relative, Yersinia pseudotuberculosis, are very similar in many respects, yet there is a distinct dichotomy between these species in terms of pathogenicity. Y. pseudotuberculosis produces a relatively benign food- or water-borne gastroenteritis with rare cases of potentially fatal bacteremia. In contrast, the characteristics of high infectivity and high mortality have made Y. pestis a pathogen of historic importance with devastating effects on the human populace over the course of three major pandemics. These qualities coupled with the emergence of multi-drug resistant variants make Y. pestis an ideal candidate for use as a bioterrorism agent. Consequentially, evolutionary biology of this organism has become a priority in the counter-terrorism research effort. The flow of genetic information within the Y. pseudotuberculosis/Y. pestis group motivated us to identify novel genes for the purpose of creating a pan-genome species DNA microarray to better understand the phylogenomic relationships among its members. Based on the sequence information be generated from the novel gene discovery project conducted at the PFGRC as well as other publicly available sources regarding Yersinia spp. genome sequences, we designed a species microarray which represents the hitherto known genetic repertoire of this taxonomic group. In order to create a species microarray that represents novel genes or genes with significant sequence variation, the ArrayOligoSelector software (http://arrayoligosel.sourceforge.net/) was used to design a 70-mer oligonucleotide for each of the annotated ORFs or partial ORFs. A detailed description of the 70-mer oligo design process and filters developed by the PFGRC can be found on the PFGRC web site at (http://pfgrc.tigr.org/presentations/seminars/oligo_design_final.pdf).
2010-09-02 | GSE23797 | GEO
Project description:Temperature is a key environmental factor for facultative pathogens during the host adaptation response. To assess the functional role of temperature in Yersinia pestis, a microarray study was conducted comparing the Δpgm (pigmentation-negative) R88 strain grown at 37°C or 30°C.
2016-01-01 | GSE30333 | GEO
Project description:Yersinia pestis causes bubonic plague in humans and rats. The disease is characterized by an enlarged, painful lymph node, termed a bubo, that develops following bacterial dissemination from an intradermal flea bite injection site. In susceptible animals, the bacteria quickly overcome host innate immune defenses in the lymph node, spread systemically through the blood, and produce fatal sepsis 1,2. At the terminal stage of disease, the bubo contains massive numbers of extracellular bacteria, necrotic lymphoid tissue, hemorrhage, and fibrin 2. The extreme virulence of Y. pestis has been largely ascribed to its ability to avoid innate immunity by preventing phagocytosis, selectively killing immune cells, and down regulating the proinflammatory response 3. Here we report that two innate immune effector mechanisms are generated during bubonic plague in the rat: iron limitation and nitrosative stress. The expression of nitric oxide synthase (iNOS) by rat polymorphonuclear neutrophils (PMNs) was induced in the bubo, and mutation of the Y. pestis hmp gene, which encodes a flavohemoglobin important for resistance to nitric oxide (NO), attenuated virulence. Thus, although Y. pestis avoids uptake and intracellular killing by phagocytes, it still encounters innate immune effector molecules, particularly phagocyte-derived reactive nitrogen species, in the extracellular environment of the bubo. Keywords: repeat
2006-07-28 | GSE3793 | GEO
Project description:The plague agent, Yersinia pestis, employs a type III secretion system (T3SS) to selectively destroy human immune cells, thereby enabling its replication in the bloodstream and transmission to new hosts via fleabite. The host factors responsible for the selective destruction of immune cells by plague bacteria were not known. Here we show that LcrV, the needle cap protein of the Y. pestis T3SS, binds N-formylpeptide receptor (FPR1) on human immune cells to promote the translocation of bacterial effectors.
2019-07-04 | GSE133826 | GEO
Project description:The transposon site hybridization (TraSH) technique (Sassetti, CM et al. 2001. PNAS 98:12712-7) was utilized to identify genes important for the survival of Y. pestis within murine macrophages. A transposon library was created with ~31,500 Y. pestis KIM6+ insertion mutants. A portion of the Y. pestis transposon insertion mutant library was used to infect BMMs and the surviving bacteria (output pool) were recovered. TraSH was used to compare the output pool to a portion of the library that was not subjected to selection (input pool) in order to identify Y. pestis genes important for survival in macrophages. Each end of the transposon used for mutagenesis contains an outward-reading T7 RNA polymerase promoter. RNAs transcribed from the T7 promoters are complementary to the chromosomal DNA flanking each transposon in the library, so the RNAs can be used as “targets” to identify the approximate position of each transposon insertion in the mutant pool. Differentially labeled targets generated from the output and input pools are competitively hybridized to the 70-mer oligonucleotide microarrays obtained from Pathogen Functional Genomics Resource Center/J. Craig Venter Institute. Genes important for survival of Y. pestis in macrophages are identified by determining the ratio of the signal intensities for the output and input targets hybridizing to a given probe. A transposon library was created with ~31,500 Y. pestis KIM6+ insertion mutants. A portion of the Y. pestis transposon insertion mutant library was used to infect BMMs and the surviving bacteria (output pool) were recovered. TraSH was used to compare the output pool to a portion of the library that was not subjected to selection (input pool). Each end of the transposon used for mutagenesis contains an outward-reading T7 RNA polymerase promoter. RNAs transcribed from the T7 promoters are complementary to the chromosomal DNA flanking each transposon in the library, so the RNAs was used as “targets” to identify the approximate position of each transposon insertion in the mutant pool. Differentially labeled targets generated from the output and input pools are competitively hybridized to the 70-mer oligonucleotide microarrays obtained from Pathogen Functional Genomics Resource Center/J. Craig Venter Institute. Genes important for survival of Y. pestis in macrophages are identified by determining the ratio of the signal intensities for the output and input targets hybridizing to a given probe.
2011-11-30 | E-GEOD-33982 | biostudies-arrayexpress
Project description:Background The osmotic regulator OmpR in Escherichia coli regulates differentially the expression of major porin proteins OmpF and OmpC. In Yersinia enterocolitica and Y. pseudotuberculosis, OmpR is required for both virulence and survival within macrophages. However, the phenotypic and regulatory roles of OmpR in Y. pestis are not yet fully understood. Results Y. pestis OmpR is involved in building resistance against phagocytosis and controls the adaptation to various stressful conditions met in macrophages. The ompR mutation likely did not affect the virulence of Y. pestis strain 201 that was a human-avirulent enzootic strain. The microarray-based comparative transcriptome analysis disclosed a set of 224 genes whose expressions were affected by the ompR mutation, indicating the global regulatory role of OmpR in Y. pestis. Real-time RT-PCR or lacZ fusion reporter assay further validated 16 OmpR-dependent genes, for which OmpR consensus-like sequences were found within their upstream DNA regions. ompC, F, X, and R were up-regulated dramatically with the increase of medium osmolarity, which was mediated by OmpR occupying the target promoter regions in a tandem manner. Conclusion OmpR contributes to the resistance against phagocytosis or survival within macrophages, which is conserved in the pathogenic yersiniae. Y. pestis OmpR regulates ompC, F, X, and R directly through OmpR-promoter DNA association. There is an inducible expressions of the pore-forming proteins OmpF, C, and X at high osmolarity in Y. pestis, in contrast to the reciprocal regulation of them in E. coli. The main difference is that ompF expression is not repressed at high osmolarity in Y. pestis, which is likely due to the absence of a promoter-distal OmpR-binding site for ompF.
2011-10-24 | GSE26601 | GEO
Project description:The zinc uptake regulator Zur is a Zn2+-sensing metalloregulatory protein involved in the maintenance of bacterial zinc homeostasis. Up to now, regulation of zinc homeostasis by Zur is poorly understood in Y. pestis. We constructed a zur null mutant of Y. pestis biovar microtus strain 201. Microarray expression analysis disclosed a set of 154 Zur-dependent genes of Y. pestis under zinc rich condition. Real-time reverse transcription (RT)-PCR was subsequently used to validate the microarray data. Based on the 154 Zur-dependent genes, predicted regulatory Zur motifs were used to screen for potential direct Zur targets including three putative operons znuA, znuCB and ykgM-RpmJ2. The LacZ reporter fusion analysis verified that Zur greatly repressed the promoter activity of the above three operons. The subsequent electrophoretic mobility shift assay (EMSA) demonstrated that a purified Zur protein was able to bind to the promoter regions of the above three operons. The DNase I footprinting was used to identify the Zur binding sites for the above three operons, verifying the Zur box sequence as predicted previously in γ-Proteobacteria. The primer extension assay was further used to determine the transcription start sites for the above three operons and to localize the -10 and -35 elements. Zur binding sites overlapped the -10 sequence of its target promoters, which was consistent with the previous observation that Zur binding would block the entry of the RNA polymerase to repress the transcription of its target genes. Zur as a repressor directly controls the transcription of znuA, znuCB and ykgM-RpmJ2 in Y. pestis by employing a conserved mechanism of Zur-promoter DNA association as observed in γ-Proteobacteria. Zur contributes to zinc homeostasis in Y. pestis likely through transcriptional repression of the high-affinity zinc uptake system ZnuACB and two alternative ribosomal proteins YkgM and RpmJ2.
2009-06-01 | GSE15183 | GEO