Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316438 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3295010.fastq.gz | Fastqsanger.gz | |||
| SRR3295011.fastq.gz | Fastqsanger.gz | |||
| SRR3295012.fastq.gz | Fastqsanger.gz | |||
| SRR3295013.fastq.gz | Fastqsanger.gz | |||
| SRR3295004.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Toxoplasma gondii remodels the cis-regulatory landscape of infected human host cells
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Project description:Toxoplasma gondii remodels the cis-regulatory landscape of infected human host cells
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Project description:Toxoplasma gondii remodels the cis-regulatory landscape of infected human host cells [ATAC-seq]
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Project description:Toxoplasma gondii remodels the cis-regulatory landscape of infected human host cells [HELP-tagging]
| PRJNA316436 | ENA
Project description:Toxoplasma gondii remodels the cis-regulatory landscape of infected human host cells [HELP-GT]
| PRJNA316439 | ENA
Project description:Toxoplasma gondii, the causative agent of toxoplasmosis, is an obligate intracellular protozoan parasite that resides inside a parasitophorous vacuole. During infection, Toxoplasma actively remodels the transcriptome of its hosting cells with profound and coupled impact on the host immune response. We report that Toxoplasma secretes GRA24, a novel dense granule protein which traffics from the vacuole to the host cell nucleus. Once released into the host cell, GRA24 has the unique ability to trigger prolonged autophosphorylation and nuclear translocation of the host cell p38M-NM-1 MAP kinase. This noncanonical kinetics of p38M-NM-1 activation correlates with the up-regulation of the transcription factors Egr-1 and c-Fos and the correlated synthesis of key proinflammatory cytokines, including interleukin-12 and the chemokine MCP-1, both known to control early parasite replication in vivo. Remarkably, the GRA24-p38M-NM-1 complex is defined by peculiar structural features and uncovers a new regulatory signaling path distinct from the MAPK signaling cascade and otherwise commonly activated by stress-related stimuli or various intracellular microbes. GRA24 = PSP7 Mouse bone marrow-derived macrophages (BMDM) were infected with the following Toxoplasma gondii strains: - RHku80 WT versus RHku80(deltaPSP7) mutant - Pruku80 WT versus Pruku80(deltaPSP7) mutant
2013-09-01 | E-GEOD-38782 | biostudies-arrayexpress
Project description:To identify accessible chromatin regions in the human host cells during Toxoplasma parasite infection (uninfected, RH-infected and Pru-infected human foreskin fibroblasts) and in the obligate intracellular parasite Toxoplasma gondii (Type 1 RH strain and Type 2 Pru strain), ATAC-seq was performed.
2022-09-30 | GSE209866 | GEO
Project description:The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (γ) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (α/β) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits type I interferon responses when targeted to the host endo-lysosomal system. While live Toxoplasma fails to induce type I interferon, heat-killed parasites do trigger this response, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that some parasite species, like Toxoplasma gondii, have evolved mechanisms to suppress this response. Human foreskin fibroblasts (HFF; line BJ-5ta) were cultured to confluency in T25 flasks, infected with one representative of each of the three architypial strains of Toxoplasma gondii: GT1 (type I), Prugniaud (type II) and VEG (type III), or the closely related parasite species, Neospora caninum (strain Nc-Liv). RNA was collected from biological replicates for expression profiling by microarray. Uninfected HFF cells were used as a reference.
2013-03-29 | E-GEOD-45633 | biostudies-arrayexpress
Project description:The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (?) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (?/?) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits type I interferon responses when targeted to the host endo-lysosomal system. While live Toxoplasma fails to induce type I interferon, heat-killed parasites do trigger this response, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that some parasite species, like Toxoplasma gondii, have evolved mechanisms to suppress this response. In vitro cultures of bone marrow-derived macrophages from WT or IFNAR2-/- mice were infected with either Toxoplasma gondii (VEG strain) or Neospora caninum (Nc2 strain) for 17 hours. RNA was collected from biological replicates for expression profiling by microarray. Uninfected controls for both WT and IFNAR2-/- were used as a reference.
2013-03-29 | E-GEOD-45632 | biostudies-arrayexpress
Project description:Toxoplasma gondii is an obligate intracellular Apicomplexan parasite capable of invading and surviving within nucleated cells in most warm-blooded animals. This remarkable task is achieved through the delivery of effector proteins from the parasite into the parasitophorous vacuole and host cell cytosol that rewire host cellular pathways, facilitating parasite evasion of the immune system. Here, we have identified a novel export pathway in Toxoplasma that involves cleavage of effector proteins by the Golgi-resident aspartyl protease 5 (ASP5) prior to translocation into the host cell. We demonstrate that ASP5 cleaves a highly constrained amino acid motif that has some similarity to the PEXEL motif of Plasmodium parasites. We show that ASP5 can mature effectors at both the N- and C-terminal ends of proteins and is also required for the trafficking of proteins without this motif. Furthermore, we show that ASP5 controls establishment of the nanotubular network and is required for the efficient recruitment of host mitochondria to the parasitophorous vacuole membrane. Global assessment of host gene expression following infection reveals that ASP5-dependent pathways influence thousands of the transcriptional changes that Toxoplasma imparts on its host cell. This work characterizes the first identified machinery required for export of Toxoplasma effectors into the infected host cell. Three groups of human foreskin fibroblasts are compared. Each group has 3 replicates giving a total of 9 samples. The first group of samples are infected with wild type (GRA16HA) Toxoplasma gondii, the second group with Asp5 knock-out Toxoplasma gondii, and the final group remain uninfected. All fibroblasts are generated from one donor sample.
2015-11-19 | E-GEOD-73986 | biostudies-arrayexpress