Ancient Y. pestis genomes (First Pandemic)
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB29991 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3341120_1.fastq.gz | Fastqsanger.gz | |||
| ERR3341120_2.fastq.gz | Fastqsanger.gz | |||
| ERR3341130_1.fastq.gz | Fastqsanger.gz | |||
| ERR3341130_2.fastq.gz | Fastqsanger.gz | |||
| ERR3341140_1.fastq.gz | Fastqsanger.gz |
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Project description:Phylogeography of the second plague pandemic revealed through analysis of historical Y. pestis genomes
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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 first historically documented pandemic caused by Yersinia pestis began as the Justinianic Plague in 541 within the Roman Empire and continued as the so-called First Pandemic until 750. Although paleogenomic studies have previously identified the causative agent as Y. pestis, little is known about the bacterium's spread, diversity, and genetic history over the course of the pandemic. To elucidate the microevolution of the bacterium during this time period, we screened human remains from 21 sites in Austria, Britain, Germany, France, and Spain for Y. pestis DNA and reconstructed eight genomes. We present a methodological approach assessing single-nucleotide polymorphisms (SNPs) in ancient bacterial genomes, facilitating qualitative analyses of low coverage genomes from a metagenomic background. Phylogenetic analysis on the eight reconstructed genomes reveals the existence of previously undocumented Y. pestis diversity during the sixth to eighth centuries, and provides evidence for the presence of multiple distinct Y. pestis strains in Europe. We offer genetic evidence for the presence of the Justinianic Plague in the British Isles, previously only hypothesized from ambiguous documentary accounts, as well as the parallel occurrence of multiple derived strains in central and southern France, Spain, and southern Germany. Four of the reported strains form a polytomy similar to others seen across the Y. pestis phylogeny, associated with the Second and Third Pandemics. We identified a deletion of a 45-kb genomic region in the most recent First Pandemic strains affecting two virulence factors, intriguingly overlapping with a deletion found in 17th- to 18th-century genomes of the Second Pandemic.
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Project description:14th century Yersinia pestis genomes support the emergence of pestis secunda within Europe
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Project description:Although pneumonic plague is the deadliest manifestation of disease caused by the bacterium Yersinia pestis, there is surprisingly little information on the cellular and molecular mechanisms responsible for Y. pestis-triggered pathology in the lung. Therefore, to understand the progression of this unique disease, we developed an intranasal mouse model of primary pneumonic plague. Mice succumbed to a purulent multifocal severe exudative bronchopneumonia that closely resembles the disease observed in humans. In order to assess the adaptation of Y. pestis to a mammalian environment, we employed DNA microarray technology to analyze the transcriptional responses of the bacteria during interaction with the mouse lung as compared to bacteria cultured in vitro. Keywords: Infectious expression analysis
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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.
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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.
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