Genome-wide mapping of transcription initiation in the asexual stages of Toxoplasma gondii
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ABSTRACT:
PROVIDER: PRJNA670025 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12828336_1.fastq.gz | Fastqsanger.gz | |||
| SRR12828336_2.fastq.gz | Fastqsanger.gz | |||
| SRR12828337_1.fastq.gz | Fastqsanger.gz | |||
| SRR12828337_2.fastq.gz | Fastqsanger.gz | |||
| SRR12828338_1.fastq.gz | Fastqsanger.gz |
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Project description:The lack of a comprehensive map of transcription start sites in Toxoplasma gondii has impeded advances in decrypting the molecular mechanisms underlying the regulation of gene expression. Genome-wide approaches for mapping transcription initiation have been instrumental in defining the determinants of transcription initiation in a range of model eukaryotes. We used a protocol for 5′-end RNA sequencing, called RAMPAGE, to sequence the 5′-ends of capped mRNA from ME49 and RH tachyzoites, as well as from ME49 bradyzoites. This allowed us to generate maps of transcription initiation events at single-nucleotide resolution across the asexual stages of the parasite.
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Project description:This SuperSeries is composed of the following subset Series: GSE11437: Expression QTL mapping of Toxoplasma gondii genes, Bradyzoite array GSE11514: Expression QTL mapping of Toxoplasma gondii genes, Tachyzoite array Keywords: SuperSeries Refer to individual Series
2008-05-22 | E-GEOD-11515 | biostudies-arrayexpress
Project description:Toxoplasma gondii is a zoonotic pathogen for which felids serve as definitive hosts. In cats, the parasite undergoes several rounds of asexual replication before entering the sexual cycle which gives rise to oocysts that are shed into the environment. These then sporulate and become infective to humans and live stock. To understand the genes involved in the parasite development in the felid host and identify potential intervention targets, we designed a transcriptomic approach to compare the cat intestinal stages with the well characterised tachyzoites that mediate acute infection and tissue cysts that are responsible for chronic infection. Cats were infected with T. gondii tissue cysts from mouse brain and sampled the intestinal stages at day 3, 5 and 7 post infection. As an input sample, we also collected tissue cysts from mouse brain as well as in vitro cultivated tachyzoites. Total RNA was extracted, enriched for mRNA and used for cDNA synthesis. RNA-Seq was then performed to describe the transcriptomic repertoire of each time point/life cycle stage.
2018-03-30 | GSE108740 | GEO
Project description:Toxoplasma gondii is a common parasite of humans and animals, causing life-threatening disease in the immunocompromized, fetal abnormalities when contracted during gestation, and recurrent ocular lesions in some patients. Central to the prevalence and pathogenicity of this protozoan is its ability to adapt to a broad range of environments, and to differentiate between acute and chronic stages. These processes are underpinned by a major rewiring of gene expression, yet the mechanisms that regulate transcription in this parasite are only partially characterized. Deciphering these mechanisms requires a precise and comprehensive map of transcription start sites (TSSs); however, Toxoplasma TSSs have remained incompletely defined. To address this challenge, we used 5'-end RNA sequencing to genomically assess transcription initiation in both acute and chronic stages of Toxoplasma. Here, we report an in-depth analysis of transcription initiation at promoters, and provide empirically-defined TSSs for 7603 (91%) protein-coding genes, of which only 1840 concur with existing gene models. Comparing data from acute and chronic stages, we identified instances of stage-specific alternative TSSs that putatively generate mRNA isoforms with distinct 5' termini. Analysis of the nucleotide content and nucleosome occupancy around TSSs allowed us to examine the determinants of TSS choice, and outline features of Toxoplasma promoter architecture. We also found pervasive divergent transcription at Toxoplasma promoters, clustered within the nucleosomes of highly-symmetrical phased arrays, underscoring chromatin contributions to transcription initiation. Corroborating previous observations, we asserted that Toxoplasma 5' leaders are among the longest of any eukaryote studied thus far, displaying a median length of approximately 800 nucleotides. Further highlighting the utility of a precise TSS map, we pinpointed motifs associated with transcription initiation, including the binding sites of the master regulator of chronic-stage differentiation, BFD1, and a novel motif with a similar positional arrangement present at 44% of Toxoplasma promoters. This work provides a critical resource for functional genomics in Toxoplasma, and lays down a foundation to study the interactions between genomic sequences and the regulatory factors that control transcription in this parasite.
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Project description:Recent advances in high throughput sequencing methodologies allow the opportunity to probe in depth the transcriptomes of organisms including N. caninum and Toxoplasma gondii. In this project, we are using Illumina sequencing technology to analyze the transcriptome (RNA-Seq) of experimentally accessible stages (e.g. tachyzoites at different times points) of T. gondii VEG strain. The aim is to make comparative transcriptional landscape maps of Neospora and Toxoplasma at different time points at different life cycle stages and compare levels of expression of orthologous genes in these two organisms.
2011-02-08 | E-MTAB-550 | biostudies-arrayexpress
Project description:Toxoplasma gondii is an intracellular parasite with a significant impact on human health, especially in cases where individuals are immunocompromised (e.g., due to HIV/AIDS). In Europe and North America only a few clonal genotypes appear to be responsible for the vast majority of Toxoplasma infections, and these clonotypes have been intensely studied to identify strain-specific phenotypes that may play a role in the manifestation of more severe disease. To identify and genetically map strain-specific differences in gene expression, we have carried out expression quantitative trait locus (eQTL) analysis on Toxoplasma gene expression phenotypes using spotted cDNA microarrays. This led to the identification of 16 Toxoplasma genes that had significant and mappable strain-specific variation in hybridization intensity. While the analysis should identify both cis and trans-mapping hybridization profiles, we only identified loci with strain-specific hybridization differences that are most likely due to differences in the locus itself (i.e., cis-mapping). Interestingly, a larger number of these cis-mapping genes than would be expected by chance encode either confirmed or predicted secreted proteins, many of which are known to localize to the specialized secretory organelles characteristic of members of the phylum Apicomplexa. For 6 of the cis-mapping loci we determined if the strain-specific hybridization differences were due to true transcriptional differences or rather strain-specific differences in hybridization efficiency because of extreme polymorphism and/or deletion, and we found examples of both scenarios. Keywords: eQTL mapping; virulence; Toxoplasma gondii 17 F1 progeny from a cross between a type II parent (PDS) and a type III parent (CTG) were used in RNA hybridizations to identify cis and trans-mapping loci regulating gene expression
2008-05-22 | E-GEOD-11437 | biostudies-arrayexpress
Project description:Toxoplasma gondii is an intracellular parasite with a significant impact on human health, especially in cases where individuals are immunocompromised (e.g., due to HIV/AIDS). In Europe and North America only a few clonal genotypes appear to be responsible for the vast majority of Toxoplasma infections, and these clonotypes have been intensely studied to identify strain-specific phenotypes that may play a role in the manifestation of more severe disease. To identify and genetically map strain-specific differences in gene expression, we have carried out expression quantitative trait locus (eQTL) analysis on Toxoplasma gene expression phenotypes using spotted cDNA microarrays. This led to the identification of 16 Toxoplasma genes that had significant and mappable strain-specific variation in hybridization intensity. While the analysis should identify both cis and trans-mapping hybridization profiles, we only identified loci with strain-specific hybridization differences that are most likely due to differences in the locus itself (i.e., cis-mapping). Interestingly, a larger number of these cis-mapping genes than would be expected by chance encode either confirmed or predicted secreted proteins, many of which are known to localize to the specialized secretory organelles characteristic of members of the phylum Apicomplexa. For 6 of the cis-mapping loci we determined if the strain-specific hybridization differences were due to true transcriptional differences or rather strain-specific differences in hybridization efficiency because of extreme polymorphism and/or deletion, and we found examples of both scenarios. Keywords: eQTL mapping; virulence; Toxoplasma gondii 19 F1 progeny from a cross between a type II parent (PDS) and a type III parent (CTG) were used in RNA hybridizations to identify cis and trans-mapping loci regulating gene expression
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Project description:Toxoplasma gondii persists in humans by converting from actively replicating acute stage tachyzoites to slow-growing chronic stage bradyzoites. The molecular mechanisms that mediate T. gondii differentiation remain poorly understood. Through a chemical mutagenesis screen, we identified translation initiation factor eIF1.2 as being critical for T. gondii differentiation. The presence of an F97L mutation in eIF1.2 identified in the screen or the complete lack eIF1.2 (∆eIF1.2) markedly impeded bradyzoite cyst formation in culture and in the brains of infected mice. ∆eIF1.2 parasites were defective in the upregulation of bradyzoite differentiation regulators BFD1 and BFD2 during stress-induced differentiation. Conditional overexpression of BFD1 or BFD2 rescued differentiation in ∆eIF1.2 parasites. We further show that eiF1.2 interacted with the yeast 40S ribosome and directed the scanning of a model 5’ untranslated region. Together, our findings imply that eIF1.2 functions by regulating the translation of key differentiation factors necessary to establish T. gondii chronic infection.
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