Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606986 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11094274_1.fastq.gz | Fastqsanger.gz | |||
| SRR11094275_1.fastq.gz | Fastqsanger.gz |
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Project description:This resource comprises a single-cell multi-lineage map of first trimester infected placental cells. We have included data from both uninfected cells and cells infected with three pathogens known to cause maternal and fetal disorders: Plasmodium falciparum, Listeria monocytogenes, and Toxoplasma gondii. We also generated single-nuclei map of infected trophoblasts and their corresponding controls. Furthermore, we created a single-nuclei reference dataset containing information from uninfected primary placental organoids as well as organoids infected with P. falciparum. Additionally, we conducted sequencing at a single-cell level for P. falciparum parasites that were bound to the placenta (pf_b), parasites unbound to the placenta (pf_nb), and parasites that were cultured in vitro (pf_iv).
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Project description:We spiked a small number of placental tissue samples with different combinations of Candida albicans, Plasmodium falciparum, Toxoplasma gondii, Human Cytolomega virus and Salmonella bongori (various combination of the equivalents of 1, 10, 100, 1000 and 10000 genome copies). A DNA isolation was performed on these spiked samples and the resulting DNA was subsequently sequenced by MiSeq (18S). These same samples were also analysed by X Ten to allow for a sensitivity comparison of the two methods of the eukaryotic spiked signals (Candida albicans, Plasmodium falciparum and Toxoplasma gondii). In addition, non-spiked placental samples from 50 cases of Fetal Growth Restriction (FGR) (+ matched healthy controls) and 49 cases of Preeclampsia (+ matched healthy controls) and 100 preterm cases were analyzed for their non-human eukaryotic content.
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Project description:A striking unusual genome architecture characterizes the two related human parasitic pathogens Plasmodium falciparum and Toxoplasma gondii. A major fraction of the bulk parasite genome is packaged as transcriptionally permissive euchromatin with few loci embedded in silenced heterochromatin. Primary chromatin shapers include histone modifications at the nucleosome lateral surface close to the DNA but their mode of action remains unclear. We identify versatile modifications at Lys31 within the globular domain of histone H4 as key determinants of genome organization and expression in Apicomplexa. H4K31 acetylation promotes a relaxed chromatin state at the promoter of active genes through nucleosome disassembly in both parasites. In contrast, monomethylated H4K31 is enriched in the core body of Toxoplasma active genes but inversely correlates with transcription while being astonishingly enriched at transcriptionally inactive pericentromeric heterochromatin in Plasmodium. This is the first evidence for a methylated residue of H4 associating with transcriptional regulation likely by reducing histone turnover hence slowing RNA polymerase progression across transcribed loci.
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Project description:The lytic cycle of the protozoan parasite Toxoplasma gondii, which involves a brief sojourn in the extracellular space, is characterized by defined transcriptional profiles. For an obligate intracellular parasite that is shielded from the cytosolic host immune factors by a parasitophorous vacuole, the brief entry into the extracellular space is likely to exert enormous stress. Due to its role in cellular stress response, we hypothesize that translational control plays an important role in regulating gene expression in Toxoplasma during the lytic cycle. Unlike transcriptional profiles, insights into genome-wide translational profiles of Toxoplasma gondii are lacking. We have performed genome-wide ribosome profiling, coupled with high throughput RNA sequencing, in intracellular and extracellular Toxoplasma gondii parasites to investigate translational control during the lytic cycle. Results: Although differences in transcript abundance were mostly mirrored at the translational level, we observed significant differences in the abundance of ribosome footprints between the two parasite stages. Furthermore, our data suggest that mRNA translation in the parasite is potentially regulated by mRNA secondary structure and upstream open reading frames.
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