Detection of a Yersinia pestis homologue in rodent samples
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PROVIDER: PRJNA311512 | ENA |
REPOSITORIES: ENA
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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 A number of rodent samples from the UK and Canada were identified as carrying a homologue to a Yersinia pestis gene
2016-02-11 | E-GEOD-77765 | biostudies-arrayexpress
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:Yunnan Province, China is thought to be the original source of biovar Orientalis of Yersinia pestis, the causative agent of the third plague pandemic that has spread globally since the end of the 19th century. Although encompassing a large area of natural plague foci, Y. pestis strains have rarely been found in live rodents during surveillance in Yunnan, and most isolates are from rodent corpses and their fleas. In 2017, 10 Y. pestis strains were isolated from seven live rodents and three fleas in Heqing County (HQ) of Yunnan. These strains were supposed to have low virulence to local rodents Eothenomys miletus and Apodemus chevrieri because the rodents were healthy and no dead animals were found in surrounding areas, as had occurred in previous epizootic disease. We performed microscopic and biochemical examinations of the isolates,and compared their whole-genome sequences and transcriptome with those of 10 high virulence Y. pestis strains that were isolated from the adjacent city (Lijiang). We analyzed the phenotypic, genomic, and transcriptomic characteristics of live rodent isolates. The isolates formed a previously undefined monophyletic branch of Y. pestis that was named 1.IN5. Six SNPs, two indels, and one copy number variation were detected between live rodent isolates and the high virulence neighbors. No obvious functional consequence of these variations was found according to the known annotation information. Among the genes that were differentially expressed between the live rodent isolates and their high virulence neighbors, we detected five iron transfer-related genes that were significantly up-regulated in live rodent isolates compared with high virulence isolates (|log2 (FC) | >1, p.adjust <0.05), indicating these genes may be related to the low-virulence phenotype. The novel genotype of Y. pestis reported here provides further insights into the evolution and spread of plague as well as clues that may help to decipher the virulence mechanism of this notorious pathogen.
2021-04-20 | GSE161888 | 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:We looked at H-NS bound sites in wild type Yersinia pestis and in a mutant strain in which the psaE gene was deleted.
2021-06-01 | E-MTAB-10694 | biostudies-arrayexpress
Project description:The etiologic agent of bubonic plague, Yersinia pestis, senses cell density-dependent chemical signals to synchronize transcription between cells of the population in a process named quorum sensing. Though the closely related enteric pathogen Y. pseudotuberculosis uses quorum sensing system to regulate motility, the role of YpeIR quorum sensing in Y. pestis has been unclear. YpeIR is one of the AHL quorum sensing system in Y. pestis. In this study we performed transcriptional profiling experiments to identify Y. pestis YpeIR quorum sensing regulated functions at 37°C.
2016-01-01 | GSE30341 | GEO
Project description:Quorum sensing is a cell to cell communication process that involves chemical signaling. Yersinia pestis, the agent of plague, has two functional AHL quorum sensing systems Ysp and Ype. For several reasons, it was not clear what effect AHL pathways have on virulence gene expression and survival in the two different hosts, flea and human. To investigate to what effect AHL quorum sensing has on gene expression, we conducted microarray studies comparing Yersinia pestis CO92 (∆pgm) to a double AHL mutant strain (∆pgm ΔypeIR ΔyspIR) at 37°C.
2016-01-01 | GSE30331 | GEO
Project description:288 strains from a worldwide collection of Yersinia pestis were genotyped. The SNP positions tested were from a comparison of 15 genomes plus low resolution SNP discovery in up to 186 kb with dHPLC.
2010-05-01 | E-MTAB-213 | biostudies-arrayexpress
Project description:We looked at binding sites in wild type Yersinia pestis using a strain with psaE either FLAG-tagged or His-tagged.
2019-10-04 | E-MTAB-8370 | biostudies-arrayexpress
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