Yersinia
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ABSTRACT:
PROVIDER: PRJNA1249055 | ENA |
REPOSITORIES: ENA
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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: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:Following a pacemaker implantation, a 75-years-old patient suffered from five successive bacteremia episodes between in 1999 and 2013, during which five bacterial strains were isolated. Phenotypic and whole-genome sequencing analysis of four isolates identified the strains as Yersinia enterocolitica bioserotype 4/O:3. Phylogenetic reconstruction showed that the patient was chronically infected by the same strain, which evolved within the host during 14 years. Single-nucleotide polymorphhism (SNP) analysis indicates that the last two isolates which displayed severe growth defects in vitro and acquired resistance to quinolones, evolved in parallel and formed two independent lineages within the host. Pan-genome analysis and genome comparison showed that their common evolution was characterized by 41 small insertion/deletion events and loss of three large DNA fragments. These mutations, which may account for the observed growth defect and also for the appearance of vegetations on the pacemaker, support antibiotics tolerance. Quinolone resistance was acquired through a so far undescribed deletion in the gyrA gene. 140 genes containing mutations vertically acquired from a common ancestor were also identified in the two lineages. A phylogenetic analysis by maximum likelihood identified two genes presenting a positive selection signal, suggesting that these mutations provided a survival advantage to bacteria during chronic infection. This is the first report allowing identification of genetic changes associated to within-host adaptation of a pathogenic Yersinia species.
2025-05-26 | PXD043567 | Pride
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) at 30°C.
2016-01-01 | GSE30332 | 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: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 Ysp AHL quorum sensing has on gene expression, we conducted microarray studies comparing Yersinia pestis CO92 (∆pgm) to a single AHL mutant strain (∆pgm ΔyspI) at 37°C.
2016-01-01 | GSE30328 | 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 Ysp AHL quorum sensing has on gene expression, we conducted microarray studies comparing Yersinia pestis CO92 (∆pgm) to a single AHL mutant strain (∆pgm ΔyspI) at 30°C.
2016-01-01 | GSE30329 | GEO
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of autoinducer-2 (AI-2) quorum sensing was investigated by comparing transcript profiles when AI-2 quorum-sensing signal is added in to control. The strain Δpgm (pigmentation-negative) mutant was used as wild type.The control consisted of cells grown and treated under the same conditions without added signals.
2016-01-01 | GSE30237 | GEO
Project description:Yersinia pestis is the etiology of plague that is able to sense cell density by quorum sensing. The function of quorum sensing in Y.pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum sensing synthase genes are knocked out. Two strains, ∆pgm (pigmentation-negative) mutant R88 as treatment and 3XQS mutant with mutation (∆pgm, ∆ypeIR, ∆yspIR, and ∆luxS) R115 as control are used in this analysis.
2016-01-01 | GSE20217 | GEO