Plasmodium falciparum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA597922 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Plasmodium falciparum genome sequencing of imidazolopiperazine resistant strains
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Project description:Transcriptomic Analysis of Cultured Sporozoites of P. falciparum RNA-seq reads from each of three developmental stages (2 replicates per sample) were mapped to the reference Plasmodium falciparum genome, and gene expression levels were calculated for each sample.
2013-12-03 | E-GEOD-52867 | biostudies-arrayexpress
Project description:Fosmidomycin-resistant Plasmodium falciparum whole genome sequencing
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Project description:Epigenetic mechanisms have been poorly understood in Plasmodium falciparum, the causative agent of malaria. To elucidate stage specific epigenetic regulations in P. falciparum, we performed genome-wide mapping of various histone modifications, nucleosomes and RNA Polymerase II. Our comprehensive analysis suggest that transcription initiation and elongation are distinct in Plasmodium. In this study, by analyzing histone modifications, nucleosome occupancy and RNA Polymerase II (Pol II) at three different IEC developmental stages of Plasmodium; ring, trophozoite and schizont, we tried to unravel the epigenetic mechanism associated with gene regulation. Examination of H3K27me3, H3K4me3, H3K9me3, H3K14ac, H3K4me1, H3K79me3, H3K27ac, H3K4me2, H3K9ac, H4ac, RNA Pol II and Histone H3 at three different stages of Plasmodium falciparum
2015-09-23 | E-GEOD-63369 | biostudies-arrayexpress
Project description:To help malaria parasites survive unpredictable host immune responses, it is known that genes for surface proteins express stochastically in Plasmodium falciparum. Here, we demonstrate that gene expression for intracellular metabolic functions may be preordained and insensitive to specific metabolic perturbations. In a tightly-controlled, large microarray study involving over 100 hybridizations to isogenic drug-sensitive and drug-resistant parasites, the lethal antifolate WR99210 failed to over-produce RNA for the biochemically and genetically proven target dihydrofolate reductase-thymidylate synthase (DHFR-TS). Beyond the target, this transcriptional obstinacy carried over to the rest of the parasite genome, including genes for target pathways of folate and pyrimidine metabolism. Even 12 hours after commitment to death, the transcriptome remained faithful to evolutionarily entrained paths. A system-wide transcriptional disregard for metabolic perturbations in malaria parasites may contribute to selective vulnerabilities of the parasite to lethal antimetabolites. While large protective metabolic responses were not detected, DNA microarrays helped capture small, but reproducible drug-dependent perturbations within hours of drug exposure. In addition, in Plasmodium cells that had adapted to long-term drug exposure, DNA microarrays revealed new, large genome-wide transcriptional adjustments in the hard-wired transcriptional program itself. Keywords: Plasmodium falciparum treated with WR99210 RNA from P. falciparum Dd2 and B1G9 (WR99210 resistant cell-line) trophozoites that had been treated with 10 nM WR99210 for varying durations (3, 6, 9, 15, 18, 21 and 24h) was hybridized against a common pool of trophozoite RNA from a cognate clone, a culture containing 0.1% (v/v) DMSO lacking drug was used as untreated control, microarray data were obtained from at least four hybridizations using RNA from two independent parasite cultures
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Project description:Global Profiling of Histone Modifications in Plasmodium falciparum using CUT&RUN.
2022-08-01 | GSE210062 | GEO
Project description:Plasmodium falciparum SJ25081 resistant mutant Genome sequencing
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