Theileria orientalis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA49583 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| DRR118936.fastq.gz | Fastqsanger.gz | |||
| DRR118937.fastq.gz | Fastqsanger.gz | |||
| DRR118938.fastq.gz | Fastqsanger.gz | |||
| DRR118939.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 22 |
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Project description:Theileria orientalis Genome sequencing and assembly
| PRJNA835969 | ENA
Project description:Tropical theileriosis in a cattle disease of global economic importance, caused by the tick-borne protozoan parasite Theileria annulata. Conventional control strategies are failing to contain the disease and an attractive alternative is the use of pre-existing genetic resistance or tolerance. However, tropical theileriosis tolerant cattle are less productive than some susceptible breeds. To combine resistance and production traits requires an understanding of the mechanisms involved in resistance. Therefore, we have compared the response of monocytes derived from tolerant (Sahiwals, Bos indicus) and susceptible (Holstein-Friesians, B. taurus) cattle to in vitro infection with T. annulata. Over 150 genes exhibited breed-specific differential expression during the course of infection and nearly one third were differentially expressed in resting cells, implying that there are inherent differences between monocytes from the breeds. Fifty sequences currently only match ESTs or are unique to the library used to generate the microarray. The differential expression of a selection of genes was validated by quantitative RT-PCR, e.g. CD9, prion protein and signal-regulatory protein alpha. A large proportion of the differentially expressed genes encode proteins expressed on the plasma membrane or in the extracellular space and cell adhesion was one of the major Gene Ontology biological processes identified. We therefore hypothesise that the breed-specific tolerance of Sahiwal cattle compared to Holstein-Friesians is due to the interaction of infected cells with other immune cells, which influences the immune response generated against T. annulata infection. The BoMP microarray is available from the ARK-Genomics facility (www.ark-genomics.org).
2007-04-26 | E-MAXD-25 | biostudies-arrayexpress
Project description:Theileria annulata is a tick-transmitted apicomplexan parasite that infects and transforms bovine leukocytes into disseminating tumors that cause a disease called tropical theileriosis. Using comparative transcriptomics we identified genes transcriptionally perturbed during Theileria-induced transformation and highlighted a small set of genes associated with leukocyte dissemination. CRISPR/Cas9-mediated knock-down of GZMA and RASGRP1 in macrophages attenuated for dissemination led to a regain in their dissemination in Rag2/gC mice confirming their suppressor roles in vivo. Comparing the transcriptomes of 934 human cancer cell lines to that of Theileria-transformed bovine B cells again highlighted GZMA and RASGRP1 and CRISPR-mediated overexpression of GZMA and RASGRP1 dampened the dissemination potential of human B-lymphomas. The ensemble provide evidence for a novel suppressor function in the dissemination of both T. annulata-transformed bovine leukocytes and human B-lymphomas.
2020-08-18 | GSE135377 | GEO
Project description:Intracellular pathogens develop elaborate mechanisms to survive within the hostile environments of host cells. Theileria parasites infect bovine leukocytes and cause devastating diseases in cattle in developing countries. Theileria spp. have evolved sophisticated strategies to hijack host leukocytes, inducing proliferative and invasive phenotypes characteristic of cell transformation. Intracellular Theileria parasites secrete proteins into the host cell and recruit host proteins to induce oncogenic signaling for parasite survival. It is unknown how Theileria parasites evade host cell defense mechanisms, such as autophagy, to survive within host cells. Here, we show that Theileria annulata parasites sequester the host eIF5A protein to their surface to escape elimination by autophagic processes. We identified a small-molecule compound that reduces parasite load by inducing autophagic flux in host leukocytes, thereby uncoupling Theileria parasite survival from host cell survival. We took a chemical genetics approach to show that this compound induced host autophagy mechanisms and the formation of autophagic structures via AMPK activation and the release of the host protein eIF5A which is sequestered at the parasite surface. The sequestration of host eIF5A to the parasite surface offers a strategy to escape elimination by autophagic mechanisms. These results show how intracellular pathogens can avoid host defense mechanisms and identify a new anti-Theileria drug that induces autophagy to target parasite removal.
2023-12-19 | GSE250088 | GEO
Project description:Lysine methylation on histone tails impacts genome regulation and cell fate determination in many developmental processes. Apicomplexa intracellular parasites cause major diseases and they have developed complex life cycles with fine-tuned differentiation events. Yet, apicomplexa genomes have few transcription factors and little is known about their epigenetic control systems. Tick-borne Theileria apicomplexa species have relatively small, compact genomes and a remarkable ability to transform leukocytes in their bovine hosts. Here we report enriched H3 lysine 18 monomethylation (H3K18me1) on the gene bodies of repressed genes in Theileria macroschizonts. Differentiation to merozoites (merogony) led to decreased H3K18me1 in parasite nuclei. Pharmacological manipulation of H3K18 acetylation or methylation impacted parasite differentiation and expression of stage-specific genes. Finally, we identified a parasite SET-domain methyltransferase (TaSETup1) that can methylate H3K18 and represses gene expression. Thus, H3K18me1 emerges as an important epigenetic mark which controls gene expression and stage differentiation in Theileria parasites.
2021-03-25 | PXD024599 | Pride
Project description:To understand the immune response of cows to the apicomplexan parasite Theileria annulata, we used ex vivo isolate cells derived from two infected calve : Holstein 12886 (Bos taurus), which is known to be susceptible to the disease, and Sahiwal 82H (Bos indicus), which is known to be resistant. The infected bovine macrophages of the two species with Theileria were collected and performed multiome 10X Chromium genomics scRNA-Seq.
2024-10-09 | E-MTAB-14450 | biostudies-arrayexpress
Project description:Theileria orientalis Shintoku genome sequencing project
| PRJDA49463 | ENA
Project description:Transcriptome of Theileria orientalis
| PRJDB6554 | ENA
Project description:Theileria orientalis strain:Robertson Genome sequencing and assembly
| PRJNA325069 | ENA
Project description:Intracellular pathogens develop elaborate mechanisms to survive within the hostile environments of host cells. Theileria parasites infect bovine leukocytes and cause devastating diseases in cattle in developing countries. Theileria spp. have evolved sophisticated strategies to hijack host leukocytes, inducing proliferative and invasive phenotypes characteristic of cell transformation. Intracellular Theileria parasites secrete proteins into the host cell and recruit host proteins to induce oncogenic signaling for parasite survival. It is unknown how Theileria parasites evade host cell defense mechanisms, such as autophagy, to survive within host cells. Here, we show that Theileria annulata parasites sequester the host eIF5a protein to their surface to escape elimination by autophagic processes. We identified a small-molecule compound that reduces parasite load by inducing autophagic flux in host leukocytes, thereby uncoupling Theileria parasite survival from host cell survival. We took a chemical genetics approach to show that this compound induced host autophagy mechanisms and the formation of autophagic structures via AMPK activation and the release of the host protein eIF5A which is sequestered at the parasite surface. The sequestration of host eIF5a to the parasite surface offers a strategy to escape elimination by autophagic mechanisms. These results show how intracellular pathogens can avoid host defense mechanisms and identify a new anti-Theileria drug that induces autophagy to target parasite removal.
2024-05-24 | PXD047937 | Pride