Plasmodium falciparum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA254114 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:New antimalarial drugs are urgently needed to control drug resistant forms of the malaria parasite, Plasmodium falciparum. Although mitochondrial metabolism is the target of both existing drugs and new lead compounds, the role of the mitochondrial tricarboxylic acid (TCA) cycle remains poorly understood. Herein, we describe 11 genetic knockout parasite lines that delete six of the eight TCA cycle enzymes. Although all TCA knockouts grew normally in asexual blood stages, these metabolic deficiencies halted lifecycle progression in later stages. Specifically, aconitase knockout parasites arrested as late gametocytes, whereas α-ketoglutarate dehydrogenase deficient parasites failed to develop oocysts in the mosquitoes. Mass-spectrometry analysis of 13C isotope-labeled TCA mutant parasites showed that P. falciparum has significant flexibility in TCA metabolism. This flexibility manifested itself through changes in pathway fluxes and through altered exchange of substrates between cytosolic and mitochondrial pools. Our findings suggest that mitochondrial metabolic plasticity is essential for parasite development . Two parallel timecourses resulting in a total of 16 samples (8 wildtype, Isocitrate Dehydrogenase/alpha-Ketogluterate Dehydrogenase double knockout) were hybridized against a Cy3-labeled reference pool of 3D7 mixed stage parasites on a two-color array.
2014-08-01 | E-GEOD-59015 | biostudies-arrayexpress
Project description:Role of H4K8ac in P. falciparum life cycle [gene expression]
| PRJNA328408 | ENA
Project description:In order to further our understanding of the metabolic network of the malaria parasite, Plasmodium falciparum, we carried out a concurrent transcriptomic and metabolomic study of the parasite's intraerythrocytic developmental cycle. These microarray data were generated to compare the expression levels of metabolic enzymes to the concentrations of their associated metabolites over the 48-hour life cycle.
2009-01-24 | GSE14524 | GEO
Project description:Dynamics of epigenetic regulation of gene expression during Plasmodium falciparum life cycle
| PRJNA170431 | ENA
Project description:New antimalarial drugs are urgently needed to control drug resistant forms of the malaria parasite, Plasmodium falciparum. Although mitochondrial metabolism is the target of both existing drugs and new lead compounds, the role of the mitochondrial tricarboxylic acid (TCA) cycle remains poorly understood. Herein, we describe 11 genetic knockout parasite lines that delete six of the eight TCA cycle enzymes. Although all TCA knockouts grew normally in asexual blood stages, these metabolic deficiencies halted lifecycle progression in later stages. Specifically, aconitase knockout parasites arrested as late gametocytes, whereas α-ketoglutarate dehydrogenase deficient parasites failed to develop oocysts in the mosquitoes. Mass-spectrometry analysis of 13C isotope-labeled TCA mutant parasites showed that P. falciparum has significant flexibility in TCA metabolism. This flexibility manifested itself through changes in pathway fluxes and through altered exchange of substrates between cytosolic and mitochondrial pools. Our findings suggest that mitochondrial metabolic plasticity is essential for parasite development .
2014-08-01 | GSE59015 | GEO
Project description:Expression data of gene knockout Plasmodium falciparum clones
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Project description:Global transcriptomic changes of either cell cycle arrested parasites or cell cycle re-entered asexual P. falciparum 3D7 parasites.
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Project description:Role of H4K8ac in P. falciparum life cycle [ChIP]
| PRJNA328407 | ENA
Project description:Transcriptomic and metabolomic profiles of the Plasmodium falciparum developmental cycle
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