Ontology highlight
ABSTRACT:
PROVIDER: PRJNA661196 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR12581831_1.fastq.gz | Fastqsanger.gz | |||
| SRR12581831_2.fastq.gz | Fastqsanger.gz | |||
| SRR12581832_1.fastq.gz | Fastqsanger.gz | |||
| SRR12581832_2.fastq.gz | Fastqsanger.gz |
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Project description:New genotype of Yersinia pestis found in live rodents in Yunnan Province, China
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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.
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Project description:A spectrum dataset with 329 tree leaf samples and a blank control file from Yunnan Province, Southwest China. Collection and extraction was completed in Yang Jie Group
| MSV000092950 | MassIVE
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:A spectrum dataset with 329 tree leaf samples and a blank control file from Yunnan Province, Southwest China. Collection and extraction was completed in Yang Jie Group
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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.
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Project description:The global transcriptome profile of lung tissue in mice after exposure to aerosolized yersinia pestis strain 201
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Project description:Microarrays were used to determine the transcriptional profile of Y. pestis that is growing inside macrophages. J774A.1 macrophage-like cells were infected with Y. pestis KIM5 and incubated in the presence of gentamicin in tissue culture media. RNA was isolated from intracellular bacteria at various time points post infection. Control bacteria were grown for 4 hours in tissue culture medium under the same conditions without macrophages or gentamicin. The transcriptional profiles of intracellular Y. pestis at different time points were compared to those of control Y. pestis using the 70-mer oligonucleotide microarrays obtained from Pathogen Functional Genomics Resource Center/J. Craig Venter Institute (Y. pestis microarray version 2). RNA from samples of Yersinia pestis KIM5 at 3 time points in were compared to 12 Yersinia pestis in DMEM for 4 hours.
2010-07-07 | E-GEOD-22168 | biostudies-arrayexpress
Project description:Initiation of treatment during the pre-symptomatic phase of infection with Yersinia pestis (Y. pestis) is particularly critical because the rapid proliferation of Y. pestis is coupled with the manifestation of common flu-like early symptoms that often delay the intervention. Our study used African Green Monkeys that didn’t exhibited clear clinical symptoms for nearly two days after intranasal challenge with Y. pestis and succumbed within a day after showing the first signs of clinical discomfort. Colonization of Y. pestis was detected in blood one day post-infection although blood transcripts were found to be altered immediately after the pathogenic assault. The organs of the respiratory tract and those adjacent, such as lungs and submandibular lymph nodes, accumulated significant Y. pestis colonization immediately after pathogenic challenge. Hence organ-specific molecular investigations are deemed to be the key in elucidation of the mechanisms of the initial host response. Based on results from our previous investigation of the blood transcriptomic profile, we explored the early involvement of the ubiquitin-microtubule-mediated host defense mechanism in detail. Genes enriching the ubiquitin network were altered, indicating an early suppression of the network functions in the submandibular lymph nodes. In concert, the upstream toll-like receptor signaling and downstream IκB kinase/NFκB signaling were inhibited at the transcription level. The inflammatory response was suppressed in the lungs, submandibular lymph nodes and mediastinal lymph nodes. By dysregulating both ubiquitin and the microtubule networks, Yersinia pestis was able to impair host-mediated proteolysis activities and evade autophagosome capture. A synchronized suppression of the immune response may render the peripheral organs more vulnerable to the imminent pathogenic assault. Furthermore, a comprehensive early onset of apoptosis was found across these three organ types. This was possibly a parallel mechanism undertaken by Yersinia pestis to further weaken the host response and enable a permissive colonization of the host. Targeting these networks in an organ-specific and time-resolved fashion could be essential for development of the next generation therapeutics for pneumonic plague.
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