Trypanosoma cruzi
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| DRR001109.fastq.gz | Fastqsanger.gz | |||
| SRR058509.fastq.gz | Fastqsanger.gz | |||
| SRR058510.fastq.gz | Fastqsanger.gz | |||
| SRR058511.fastq.gz | Fastqsanger.gz |
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Project description:Trypanosoma cruzi is a protozoan parasite that causes Chagas’ disease in humans and throughout its life cycle faces different environment changes. Protein methylation is an important post-translational modification by which cells respond and adapt to the environment. To understand the importance of protein methylation in T.cruzi biology, we applied mass spectrometry-based proteomics and report the first proteomic analysis of both arginine and lysine methylproteome in T. cruzi.
2023-05-15 | PXD034140 | Pride
Project description:Trypanosoma cruzi is an obligate intracellular protozoan parasite that causes human Chagas’ disease, a leading cause of heart failure in Latin America. Using Affymetrix oligonucleotide arrays we screened phenotypically diverse human cells (foreskin fibroblasts, microvascular endothelial cells and vascular smooth muscle cells) for a common transcriptional response signature to T. cruzi. A common feature was a prominent type I interferon response, indicative of a secondary response to secreted cytokines. Using transwell plates to distinguish cytokine-dependent and -independent gene expression profiles in T. cruzi-infected cells, a core cytokine-independent response was identified in fibroblasts and endothelial cells that featured metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding. Significant downregulation of genes involved in mitotic cell cycle and cell division predicted that T. cruzi infection impedes cell cycle progression in the host cell.
2009-06-04 | GSE13791 | GEO
Project description:Trypanosoma cruzi is a protozoan parasite etiological agent of the vector-borne disease American trypanosomiasis, also known as Chagas disease. During its life cycle, T. cruzi undergoes some fundamental processes: metacyclogenesis (transition from epimastigote to metacyclic trypomastigote form) – occurring in the invertebrate host, amastigogenesis (transition from trypomastigote to amastigote form) and trypomastigogenesis (transition from amastigote to trypomastigote form) – both occurring within nucleated cells of the mammalian host, and finally epimastigogenesis (transition from trypomastigote to epimastigote forms) – which occurs as soon as the invertebrate host ingests trypomastigote forms during the bloodmeal. The precise mechanisms that regulate these processes remain elusive but certainly depend on kinases. The canonical function of the inositol hexakisphosphate kinases (IP6Ks) is to phosphorylate the phosphate groups from inositol hexaphosphate (IP6), leading to the formation of inositol pyrophosphates (PP-IPs). However, recent studies have been describing non-canonical functions for this kinase family. Here, after disrupting a single IP6K allele of T. cruzi and confirming its downregulation, we observed that the life cycle of this parasite was profoundly impaired. Epimastigote forms of T. cruzi IP6K-deficient showed morphological alterations, increased population presenting a dormant-like state (quiescence), and a reduced differentiation capacity during metacyclogenesis. The restricted metacyclic forms of T. cruzi IP6K-deficient that were able to differentiate had reduced infective potential (invasion rate) in human cardiomyocytes. Interestingly, 120 h after infection, the amastigote forms of T. cruzi IP6K-deficient showed an impaired ability to transform into trypomastigotes, with most of the population egressing from human cardiomyocytes without completing trypomastigogenesis. Transcriptomic data show that the levels of surface proteins (mucins and trans-sialidases) were altered in both epimastigote and trypomastigote forms in response to the low levels of IP6K, which helps explain our findings. Finally, we observed that the few trypomastigote forms of T. cruzi IP6K-deficient that egressed from human cardiomyocytes could not complete the epimastigogenesis. Together, our findings strongly suggest that IP6K is critical to sustain the T. cruzi life cycle. Thus, as the disruption of both IP6K alleles did not generate viable parasites and the similarity relative to its human homolog is ~15%, this kinase could be a potential target for drug development against Chagas disease.
2026-02-13 | GSE309901 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-04 | GSE27054 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-17 | GSE27353 | GEO
Project description:Trypanosoma cruzi is a protozoan parasite and the etiologic agent of Chagas disease, an important public health problem in Latin America. T. cruzi is diploid, almost exclusively asexual, and displays an extraordinarily diverse population structure both genetically and phenotypically. Yet, to date the genotypic diversity of T. cruzi and its relationship, if any, to biological diversity have not been studied at the whole genome level. In this study, we used whole genome oligonucleotide tiling arrays to compare gene content in biologically disparate T. cruzi strains by comparative genomic hybridization (CGH). We observed that T. cruzi strains display widespread and focal copy number variations (CNV) and a substantially greater level of diversity than can be adequately defined by the current genetic typing methods. As expected, CNV were particularly frequent in gene family-rich regions containing mucins and trans-sialidases but were also evident in core genes. Gene groups that showed little variation in copy numbers among the strains tested included those encoding protein kinases and ribosomal proteins, suggesting these loci were less permissive to CNV. Moreover, frequent variation in chromosome copy numbers were observed, and chromosome-specific CNV signatures were shared by genetically divergent T. cruzi strains, suggesting a greater degree of chromosome exchange than previously thought.
2011-08-06 | GSE23576 | GEO
Project description:The short non-coding transcriptome of the protozoan parasite Trypanosoma cruzi
| PRJDB2604 | ENA
Project description:Trypanosoma cruzi is the protozoan that causes Chagas disease, an endemic parasitosis in Latin America that has spread around the globe. Recently, a series of studies indicate that the gastrointestinal tract represents an important reservoir for T. cruzi in the chronic phase. It is also known that, during contact between T. cruzi and host cells, there is a release of extracellular vesicles (EVs) that modulates the immune system and enhances the infection, but the dynamics of secretion of host and parasite molecules through these EVs is not understood. In this study, we used two cell lines to simulate the environments found by the parasite in the host: C2C12 cell (myoblast) and Caco-2 cell (intestinal epithelium). We isolated large EVs (LEVs) from the interaction of T. cruzi culture-derived trypomastigotes (TCTs) belonging to two distinct strains (CL Brener, DTU Tc VI and Dm28c DTU Tc I) in contact with C2C12 and Caco-2 cells to 2 hours and after 24 hours of infection. The interaction of the parasite with the host cell induces a switch in the functionality of proteins carried by LEVs and a varied tissue answer. Protein-protein interaction analysis indicates that LEVs carry key proteins for host-pathogen interaction that could participate in the pathogenesis of Chagas Disease.
2024-05-17 | PXD046906 | Pride
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis). We are working with an enzyme able to directly transfer sialyl residues among macromolecules known as the trans-sialidase. It constitutes a virulence factor from Trypanosoma cruzi, the agent of the Chagas' Disease the American trypanosomiasis. We described the ability of this virulence factor to induce thymocyte apoptosis in vivo that happens after silayl residue mobilization. The apoptosis is mediated by the thymic epithelial cells in the nurse cell complex. By employing the microarray approach we wish to analyze the gene expression induced in the thymus after TS treatment. Examination of differential expression in thymocytes between male and female mice of genes related to glycosylation. RNA samples (in triplicate) purified from thymocytes were analyzed by Glyco-gene Chip analysis.
2011-02-04 | E-GEOD-27054 | biostudies-arrayexpress
Project description:Chagas disease is a parasitic infection originally endemic to latinamerican countries but now spreaded worldwide that can be transmitted congenitally. Current specific therapy involves benznidazole, however, other therapies may modify gene expression that can change genetic expression profile, allowing cell programming to provide a more unfavorable environment for intracellular parasite development. Herein, microarray analysis was performed to Human Umbilical Vein Endothelial Cells (HUVEC), treated with benznidazole and the anti-inflammatory drugs aspirin or simvastatin, and infected with T. cruzi, the causative agent of Chagas disease.
2019-03-14 | GSE128270 | GEO