Rickettsia felis str. LSU
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA258182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| JSEM01.dat.gz | Other | |||
| JSEM01.fasta.gz | Fasta.gz | |||
| JSEM01.master.dat | Other | |||
| JSEM01.dat.gz | Other |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Rickettsia felis genome sequencing for assessing host-specific variability (L. bostrychophila)
| PRJNA258188 | ENA
Project description:RNA sequencing of Rickettsia felis str. LSU infecting Ctenocephalides felis and Rickettsia felis str. LSU-Lb infecting Liposcelis bostrychophila
| PRJNA285354 | ENA
Project description:Rickettsia felis isolate:MAG5 Genome sequencing
| PRJNA1168282 | ENA
Project description:Rickettsia spp. can cause mild to severe human disease. These intracellular bacteria are associated with arthropods, nematodes and trematodes, and usually, are efficiently transmitted transovarially to the progeny of the invertebrate host. We recently demonstrated foreign gene acquisition by lateral gene transfer in Rickettsia genomes. The unexpected presence of laterally transferred toxin-antitoxin (TA) genetic elements (including vapBC) in several Rickettsia genomes has not been connected with the pathogenic process or the host-bacteria relationship. We suspect that vapBC are selfish genetic elements that addict eukaryotic hosts to Rickettsia. We identified a statistical link between the transovarial transmission of Rickettsia in invertebrate hosts and the presence of TA operons, specifically vapBC, in the Rickettsia genome. These TA are neighboring to type IV secretion genes. Tunel assays and whole-genome expression of infected cells showed that antibiotic eradication of TA-containing Rickettsia from the host in cell culture initiates a proapoptotic program. Rickettsia VapC toxins inhibit the growth of transformed Escherichia coli and Saccharomyces cerevisiae. Rickettsia toxin presents in vitro RNase activity. Annexin-V staining and time-lapse video showed that intracytoplasmic injections of VapC toxins in cells cause apoptosis. These data demonstrate that host cells may develop a dependence on Rickettsia spp. expressing the vapBC operon. This would constitute a new evolutionary M-bM-^@M-^\mafia strategyM-bM-^@M-^] of intracellular bacteria based on host addiction. Fresh cells from the human microvascular endothelial cell line (HMEC-1) [26] were infected with R. felis California-2 strain in the presence and absence of antibiotics, at a rate of 5 bacteria per eukaryotic cell. Then, we added or not antibiotics (chloramphenicol 50 M-BM-5g/ml or doxycycline to 40 M-BM-5g/ml) in both experimental (R.felis-infected) and control, mock-infected cells for 6 hours. The cells were harvested and RNA was extracted using the RNeasy Mini Kit (Qiagen). DNA contamination was removed using the Turbo DNA-free Kit (Ambion). RNA were labeled using the Quick Amp Labeling Kit One-color (Agilent) and hybridized onto a Whole Human Genome Microarray, 4x44K (Agilent) as recommended by the manufacturer. Arrays were scanned with DNA Microarray Scanner (Agilent), and data were extracted using Feature Extractor (Agilent).
2012-05-23 | E-GEOD-22072 | biostudies-arrayexpress
Project description:Rickettsia spp. can cause mild to severe human disease. These intracellular bacteria are associated with arthropods, nematodes and trematodes, and usually, are efficiently transmitted transovarially to the progeny of the invertebrate host. We recently demonstrated foreign gene acquisition by lateral gene transfer in Rickettsia genomes. The unexpected presence of laterally transferred toxin-antitoxin (TA) genetic elements (including vapBC) in several Rickettsia genomes has not been connected with the pathogenic process or the host-bacteria relationship. We suspect that vapBC are selfish genetic elements that addict eukaryotic hosts to Rickettsia. We identified a statistical link between the transovarial transmission of Rickettsia in invertebrate hosts and the presence of TA operons, specifically vapBC, in the Rickettsia genome. These TA are neighboring to type IV secretion genes. Tunel assays and whole-genome expression of infected cells showed that antibiotic eradication of TA-containing Rickettsia from the host in cell culture initiates a proapoptotic program. Rickettsia VapC toxins inhibit the growth of transformed Escherichia coli and Saccharomyces cerevisiae. Rickettsia toxin presents in vitro RNase activity. Annexin-V staining and time-lapse video showed that intracytoplasmic injections of VapC toxins in cells cause apoptosis. These data demonstrate that host cells may develop a dependence on Rickettsia spp. expressing the vapBC operon. This would constitute a new evolutionary “mafia strategy” of intracellular bacteria based on host addiction.
2012-05-24 | GSE22072 | GEO
Project description:Comparison of gene expression between the virulent Rickettsia rickettsii R strain and avirulent Rickettsia rickettsii Iowa. Keywords: virulent vs avirulent Virulent Rickettsia rickettsii R strain in triplicate was compared to avirulent Rickettsia rickettsii Iowa in triplicate
2010-05-26 | E-GEOD-8041 | biostudies-arrayexpress
Project description:Comparison of gene expression between the virulent Rickettsia rickettsii R strain and avirulent Rickettsia rickettsii Iowa. Keywords: virulent vs avirulent
2008-06-04 | GSE8041 | GEO
Project description:The green rice leafhopper Nephotettix cincticeps have two mutualistic symbiotic bacteria (Candidatus Sulcia muelleri and Candidatus Nasuia deltocephalinicola) in its symbiont special organ bacteriome and are also infected to rickettsia. In order to determine immune challenge is induced or not by rickettsia infection in N. cincticeps, we investigated gene expression between rickettsia-infected and rifampicin treated uninfected N. cincticeps colonies.
2019-08-20 | GSE135973 | GEO
Project description:The molecular details underlying differences in pathogenicity between Rickettsia species remain to be fully understood. Evidence points to macrophage permissiveness as a key mechanism in rickettsial virulence. Different studies have shown that several rickettsial species responsible for mild forms of rickettsioses can also escape macrophage-mediated killing mechanisms and establish a replicative niche within these cells. However, their manipulative capacity with respect to host cellular processes is far from being understood. A deeper understanding of the interplay between mildly pathogenic rickettsiae and macrophages and the commonalities and specificities of host responses to infection would illuminate differences in immune evasion mechanisms and pathogenicity. We have used quantitative proteomics by SWATH-MS/MS to profile alterations resulting from infection of THP-1 macrophages with three mildly pathogenic rickettsiae: R. parkeri, R. africae, and R. massiliae, all successfully proliferating in these cells. We show that all three species trigger different proteome signatures. Our results reveal a significant impact of infection in proteins categorized as type-I interferon responses, here included several components of the RIG-1-like signaling pathway, mRNA splicing, and protein translation. Moreover, significant differences in protein content between infection conditions anticipate species-specific induced alterations. Indeed, we confirm a distinct impact on host inflammatory responses between species during infection, demonstrating that these species trigger different levels of INF-β, differences in the bioavailability of the pro-inflammatory cytokine IL1-β, and in triggering pyroptotic events. This work reveals novel aspects and exciting nuances of macrophage-Rickettsia interactions, adding additional layers of complexity between Rickettsia and host cells constant arms race for survival.
2022-01-11 | PXD026982 | Pride