Trypanosoma cruzi
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136343 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR094782.fastq.gz | Fastqsanger.gz | |||
| SRR094783.fastq.gz | Fastqsanger.gz | |||
| SRR094784.fastq.gz | Fastqsanger.gz | |||
| SRR094785.fastq.gz | Fastqsanger.gz | |||
| SRR094786.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic regulation of transcription and virulence of Trypanosoma cruzi
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Project description:Comparative genomic analysis of Trypanosoma cruzi G with Trypanosoma cruzi D11.
2022-03-06 | GSE197870 | GEO
Project description:Comparative genomic analysis of T. cruzi CLB vs Trypanosoma rangeli (strains SC, Choachí, C23, H14, R1625 and PIT10) and Trypanosoma conorhini
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Project description:Unlike other eukaryotes, the protein coding genes of Trypanosoma cruzi are arranged into large polycistronic gene clusters transcribed by polymerase II (Pol II). Thus, trypanosomes rely on post-transcriptional processes to regulate gene expression. Here, we show that the glucosylated thymine DNA base (-D-glucosyl hydroxymethyluracil or base J) is present within sequences flanking the polycistronic units (PTU) in T. cruzi. loss of base J at sites of transcription initiation, via deletion of the two enzymes that regulate J synthesis (JBP1 and JBP2), correlates with an increased rate of Pol II transcription and subsequent genome-wide increase in gene expression. genes include virulence genes and the resulting parasites are defective in host cell invasion and egress. These studies indicate that base J represents an epigenetic factor regulating Pol II transcription initiation in kinetoplastids, and provides the first biological role of the only hyper-modified DNA base in eukaryotes. This entry contains the results using SLT, digital gene expression profiling of tags read off the spliced leader sequence of all mature trypanosomatid messages, for the life-cycle of T. cruzi, four stages, in wild-type as well as JBP1 KO cells.
2011-01-21 | GSE26754 | GEO
Project description:Trypanosoma cruzi, a flagellated protozoan, is the causative agent of Chagas’ disease, a chronic and potentially fatal disease that causes irreversible damage to heart and digestive tract in humans. Like all trypanosomes, the protein coding genes of T. cruzi are arranged into large polycistronic gene clusters transcribed by polymerase II (Pol II). Therefore, trypanosomes presumably rely on post-transcriptional process to regulate gene expression. Pol II promoters have not been identified and there is no evidence for regulated gene expression at the transcriptional level. However, the presence of the hyper-modified DNA base J, Beta-D-glucosyl hydroxymethyluracil, at regions flanking the polycistronic units (PTU) in T. brucei suggested its involvement in regulating Pol II transcription. We now demonstrate that base J is localized at PTU flanking regions in T. cruzi and levels are differentially regulated by the thymidine hydroxylases, JBP1 and JBP2, involved in J biosynthesis. Microarray analysis of the JBP1dKO and JBP2dKO indicate the up and down regulation of several hundred genes distributed throughout the genome. We show a large increase in Pol II transcription rate following the decrease in base J at the PTU flanks. Changes in gene expression include virulence genes and parasites are defective in host cell invasion and egress. There is a direct correlation between the reduction in base J levels, number of genes affected and strength of the virulence phenotype. These studies indicate that base J represents an epigenetic factor regulating Pol II transcription initiation in kinetoplastids and provides a biological role of the only hyper-modified DNA base in eukaryotes.
2011-01-01 | GSE23855 | GEO
Project description:Antibody recognition of Trypanosoma cruzi conserved proteins was assessed by evaluating pools of patient IgG samples on microarrays of 400,000 peptides covering these proteins as 15-mers with an overlap of 13 amino acids.
2024-02-28 | GSE235074 | GEO
Project description:Trypanosoma cruzi, a flagellated protozoan, is the causative agent of Chagas’ disease, a chronic and potentially fatal disease that causes irreversible damage to heart and digestive tract in humans. Like all trypanosomes, the protein coding genes of T. cruzi are arranged into large polycistronic gene clusters transcribed by polymerase II (Pol II). Therefore, trypanosomes presumably rely on post-transcriptional process to regulate gene expression. Pol II promoters have not been identified and there is no evidence for regulated gene expression at the transcriptional level. However, the presence of the hyper-modified DNA base J, Beta-D-glucosyl hydroxymethyluracil, at regions flanking the polycistronic units (PTU) in T. brucei suggested its involvement in regulating Pol II transcription. We now demonstrate that base J is localized at PTU flanking regions in T. cruzi and levels are differentially regulated by the thymidine hydroxylases, JBP1 and JBP2, involved in J biosynthesis. Microarray analysis of the JBP1dKO and JBP2dKO indicate the up and down regulation of several hundred genes distributed throughout the genome. We show a large increase in Pol II transcription rate following the decrease in base J at the PTU flanks. Changes in gene expression include virulence genes and parasites are defective in host cell invasion and egress. There is a direct correlation between the reduction in base J levels, number of genes affected and strength of the virulence phenotype. These studies indicate that base J represents an epigenetic factor regulating Pol II transcription initiation in kinetoplastids and provides a biological role of the only hyper-modified DNA base in eukaryotes. J1 and J2 null mutant trypomastigotes were each compared to wild type trypomastigotes. There were 3 biological replicates for each comparison.
2011-01-01 | E-GEOD-23855 | biostudies-arrayexpress
Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Keywords: infection response
2008-02-06 | GSE7047 | GEO