Stone Age Yersinia pestis genomes shed light on the early evolution, diversity and ecology of plague
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ABSTRACT:
PROVIDER: PRJEB51099 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR8958750_1.fastq.gz | Fastqsanger.gz | |||
| ERR8958750_2.fastq.gz | Fastqsanger.gz | |||
| ERR8958760_1.fastq.gz | Fastqsanger.gz | |||
| ERR8958760_2.fastq.gz | Fastqsanger.gz | |||
| ERR8958770_1.fastq.gz | Fastqsanger.gz |
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Project description:The bacterial pathogen Yersinia pestis gave rise to devastating outbreaks throughout human history, and ancient DNA evidence has shown it afflicted human populations as far back as the Neolithic. Y. pestis genomes recovered from the Eurasian Late Neolithic/Early Bronze Age (LNBA) period have uncovered key evolutionary steps that led to its emergence from a Yersinia pseudotuberculosis-like progenitor; however, the number of reconstructed LNBA genomes are too few to explore its diversity during this critical period of development. Here, we present 17 Y. pestis genomes dating to 5,000 to 2,500 y BP from a wide geographic expanse across Eurasia. This increased dataset enabled us to explore correlations between temporal, geographical, and genetic distance. Our results suggest a nonflea-adapted and potentially extinct single lineage that persisted over millennia without significant parallel diversification, accompanied by rapid dispersal across continents throughout this period, a trend not observed in other pathogens for which ancient genomes are available. A stepwise pattern of gene loss provides further clues on its early evolution and potential adaptation. We also discover the presence of the flea-adapted form of Y. pestis in Bronze Age Iberia, previously only identified in in the Caucasus and the Volga regions, suggesting a much wider geographic spread of this form of Y. pestis. Together, these data reveal the dynamic nature of plague’s formative years in terms of its early evolution and ecology.
| S-EPMC9169917 | biostudies-literature
Project description:Two Neolithic Y. pestis genomes from Warburg
| PRJEB49648 | ENA
Project description:Phylogeography of the second plague pandemic revealed through analysis of historical Y. pestis genomes
| PRJEB29990 | ENA
Project description:A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV– Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF-á and IFN-ã, were not induced at all by pYV– Y. pestis, and appeared only late in infection with WT Y. pestis.
2010-12-07 | GSE22299 | GEO
Project description:A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV– Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF-á and IFN-ã, were not induced at all by pYV– Y. pestis, and appeared only late in infection with WT Y. pestis. Rats treated with PBS and Yersinia pestis at various time points.
2010-12-07 | E-GEOD-22299 | biostudies-arrayexpress
Project description:Extinct lineages of Yersinia pestis, the causative agent of the plague, have been identified in several individuals from Eurasia between 5000 and 2500 years before present (BP). One of these, termed the 'LNBA lineage' (Late Neolithic and Bronze Age), has been suggested to have spread into Europe with human groups expanding from the Eurasian steppe. Here, we show that the LNBA plague was spread to Europe's northwestern periphery by sequencing three Yersinia pestis genomes from Britain, all dating to ~4000 cal BP. Two individuals were from an unusual mass burial context in Charterhouse Warren, Somerset, and one individual was from a single burial under a ring cairn monument in Levens, Cumbria. To our knowledge, this represents the earliest evidence of LNBA plague in Britain documented to date. All three British Yersinia pestis genomes belong to a sublineage previously observed in Bronze Age individuals from Central Europe that had lost the putative virulence factor yapC. This sublineage is later found in Eastern Asia ~3200 cal BP. While the severity of the disease is currently unclear, the wide geographic distribution within a few centuries suggests substantial transmissibility.
| S-EPMC10229654 | biostudies-literature
Project description:Ancient Yersinia pestis and Salmonella enterica genomes from Bronze Age Crete
| PRJEB52494 | ENA
Project description:Yersinia pestis genomes reveal plague in Britain 4,000 years ago
| PRJEB61230 | ENA
Project description:The rapid pace of bacterial evolution enables organisms to adapt to the laboratory environment with repeated passage and thus diverge from naturally-occurring environmental (“wild”) strains. Distinguishing wild and laboratory strains is clearly important for biodefense and bioforensics; however, DNA sequence data alone has thus far not provided a clear signature, perhaps due to lack of understanding of how diverse genome changes lead to convergent phenotypes, difficulty in detecting certain types of mutations, or perhaps because some adaptive modifications are epigenetic. Monitoring protein abundance, a molecular measure of phenotype, can overcome some of these difficulties. We have assembled a collection of Yersinia pestis proteomics datasets from our own published and unpublished work, and from a proteomics data archive, and demonstrated that protein abundance data can clearly distinguish laboratory-adapted from wild. We developed a lasso logistic regression classifier that uses binary (presence/absence) or quantitative protein abundance measures to predict whether a sample is laboratory-adapted or wild that proved to be ~98% accurate, as judged by replicated 10-fold cross-validation. Protein features selected by the classifier accord well with our previous study of laboratory adaptation in Y. pestis. The input data was derived from a variety of unrelated experiments and contained significant confounding variables. We show that the classifier is robust with respect to these variables. The methodology is able to discover signatures for laboratory facility and culture medium that are largely independent of the signature of laboratory adaptation. Going beyond our previous laboratory evolution study, this work suggests that proteomic differences between laboratory-adapted and wild Y. pestis are general, potentially pointing to a process that could apply to other species as well. Additionally, we show that proteomics datasets (even archived data collected for different purposes) contain the information necessary to distinguish wild and laboratory samples. This work has clear applications in biomarker detection as well as biodefense.
2017-09-08 | PXD007254 | Pride
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