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Lysophosphatidylcholine regulates sexual stage differentiation in the human malaria parasite Plasmodium falciparum

ABSTRACT: Lysophosphatidylcholine regulates sexual stage differentiation in the human malaria parasite Plasmodium falciparum

PROVIDER: PRJNA408290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6057510_1.fastq.gz	Fastqsanger.gz
	SRR6057510_2.fastq.gz	Fastqsanger.gz
	SRR6057520_1.fastq.gz	Fastqsanger.gz
	SRR6057520_2.fastq.gz	Fastqsanger.gz
	SRR6057511_1.fastq.gz	Fastqsanger.gz

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Lysophosphatidylcholine regulates sexual stage differentiation in the human malaria parasite Plasmodium falciparum

Project description:Purpose: The goal of this study was to identify genes associated with increased sexual differentiation in P. falciparum. Method: RNAseq analysis of two different P. falciparum strains (NF54 and Pf2004/164tdTom) cultured under sexual differentiation-inducing (-SerM) and non-inducing (-SerM/LysoPC and -SerM/Serum) conditions Results: We found a total of 342 genes significantly induced in response to LysoPC depletion, thereby determining changes associated with sexual differentiation and limiting Kenndedy pathway substrates.

2017-11-16 | GSE104114 | GEO

Replication origin mapping in the malaria parasite P. falciparum

Project description:Replication origin mapping in the malaria parasite Plasmodium falciparum

2022-08-04 | GSE210010 | GEO

Capturing the dynamic RNA landscape of the malaria parasite P. falciparum

Project description:To date, total mRNA analysis throughout intraerythrocytic development of the malaria parasite, Plasmodium falciparum, has only revealed abundance profiles of each gene at a given time. Here, we establish a new methodology in Plasmodium falciparum that enables biosynthetic labeleing and capture of sub-population mRNA. As a proof of principle for this novel method, we examine the mRNA dynamics of early gametocyte commitment.

2015-09-04 | GSE72695 | GEO

Protein phosphatase PfPPM2 signaling and dephosphorylation of Heterochromatin HP1 is critical for asexual division and sexual differentiation of malaria parasite.

Project description:We demonstrate that Protein Phosphatase PfPPM2 regulates both asexual and sexual development of human malaria parasite P. falciparum. It is involved in the division of the parasite during asexual development and promotes its sexual differentiation. Phosphoproteomics studies revealed that PfPPM2 targets in the parasite include key regulators of protein translation and chromatin remodelling. We demonstrate that it regulates dephosphorylation of S33 of Heterochromatin Protein 1 (HP1), a regulator of heritable gene silencing and contributes to both mitotic proliferation as well as sexual differentiation of the parasite into sexual forms. Detailed investigations revealed that PfPPM2 mediated dephosphorylation of HP1 at S33 is a signal for parasite sexual conversion. HP1- S33 dephosphorylation impairs its interaction with trimethylated form of histone 3 (H3) at lysine 9 (H3K9me3), which is known to stabilize the heterochromatin. As a result, the expression of transcription of ap2g-which is repressed by HP1-H3K9me3-was stimulated resulting in sexual conversion of the parasite. Interestingly, the state of HP1-S33 phosphorylation seems to largely reflect the fate of the parasite-its optimal phosphorylation is important for asexual division whereas it is dephosphorylated form favours sexual differentiation. PfPPM2 also regulates protein synthesis in the parasite by repressing a signaling pathway involved in the phosphorylation of initiation factor eIF2α, which are likely to contribute to parasite division and possibly differentiation.

2025-04-08 | GSE275086 | GEO

Characterization of human malaria parasite Plasmodium falciparum eIF4E homologue and mRNA 5â² cap status

Project description:The mRNA 5â² cap is normally essential for eukaryotic mRNA translation, stabilization and transport and both the cap and eIF4E are important elements of post-transcriptional gene regulation. To further our understanding of mRNA translation in the human malaria parasite Plasmodium falciparum, we have investigated the parasite translation initiation factor eIF4E and its interaction with 5â² capped mRNA. We have purified P. falciparum eIF4E as a recombinant protein and demonstrated that it has canonical mRNA 5â² cap binding activity. We used this protein to purify P. falciparum full-length 5â² capped mRNAs from total parasite RNA. Microarray analysis comparing total and eIF4E-purified 5â² capped mRNAs shows that a subset of 34 features were more than two-fold under-represented in the purified RNA sample, including 19 features representative of nuclear transcripts. The uncapped nuclear transcripts may represent a class of mRNAs targeted for storage and cap removal. Keywords: total RNA vs purified capped mRNA The microarray data were obtained from four hybridizations using RNA from two independent GST-PfeIF4E purifications from separate malaria cultures.

2010-06-10 | E-GEOD-6356 | biostudies-arrayexpress

Transcriptional profiling defines histone acetylation as a regulator of gene expression during human-to-mosquito transmission of the malaria parasite Plasmodium falciparum

Project description:Transmission of the malaria parasite Plasmodium falciparum from the human to the mosquito is mediated by the intraerythrocytic gametocytes, which, once taken up during a blood meal, become activated to initiate sexual reproduction. Because gametocytes are the only parasite stages able to establish an infection in the mosquito, they are crucial for spreading the tropical disease. During gametocyte maturation, different repertoires of genes are switched on and off in a well-coordinated sequence, pointing to regulatory mechanisms of gene expression. While epigenetic gene control has been studied during erythrocytic schizogony of P. falciparum, little is known about this process during parasite human-to-mosquito transmission of the parasite. To unveil the potential role of histone acetylation during gene expression in gametocytes, we carried out a microarray-based transcriptome analysis on gametocytes treated with the histone deacetylase inhibitor trichostatin A (TSA).

2017-05-24 | GSE99223 | GEO

Whole genome transcriptome profiling of P. falciparum sexually comitted ring stage parasite from malaria patient's peripheral blood

Project description:Malaria is spread by the transmission of sexual stage parasites, called gametocytes. However, with Plasmodium falciparum, gametocytes can only be detected in peripheral blood when they are mature and transmissible to a mosquito, which complicates control efforts. Here, we identify the set of genes overexpressed in patient blood samples with high levels of gametocyte-committed ring stage parasites. Expression of all 18 genes was regulated by transcription factor AP2-G, which is required for gametocytogenesis. We selected three genes, not expressed in mature gametocytes, to develop as biomarkers. All three biomarkers were validated in vitro using 6 different parasite lines and an algorithm developed that predicted gametocyte production in ex vivo samples and volunteer infection studies. The biomarkers were also sensitive enough to monitor gametocyte production in asymptomatic P. falciparum carriers allowing early detection and treatment of infectious reservoirs, as well as the in vivo analysis of factors that modulate sexual conversion.

2020-09-25 | GSE152536 | GEO

Discovery of Telomere Repeat-binding Zinc finger protein in the malaria parasite Plasmodium falciparum

Project description:ChIP-seq experiments were performed for the putative Telomere Repeat-binding Zinc finger protein (PfTRZ) in the malaria parasite Plasmodium falciparum strain 3D7. The gene encoding this factor (PF3D7_1209300) was endogenously tagged with either a GFP- or a 3xHA-tag and these transgenic parasite lines were used in ChIP-sequencing experiments. Sequencing of the ChIP and input libraries showed enrichment of PfTRZ at all telomere-repeat containing chromosome ends (reference genome Plasmodium falciparum 3D7 from PlasmoDB version 6.1) as well as in all upsB var promoters.In addition,PfTRZ was enriched at seven additional, intra-chromosomal sites and called in the PfTRZ-HA ChIP-seq only.

2016-07-15 | GSE76537 | GEO

Discovery of telomere repeat-binding factor in the malaria parasite Plasmodium falciparum

Project description:ChIP-seq experiments were performed for the putative telomere repeat-binding factor (PfTRF) in the malaria parasite Plasmodium falciparum strain 3D7. The gene encoding this factor (PF3D7_1209300) was endogenously tagged with either a GFP- or a 3xHA-tag and these transgenic parasite lines were used in ChIP-sequencing experiments. Sequencing of the ChIP and input libraries showed enrichment of PfTRF at all telomere-repeat containing chromosome ends (reference genome Plasmodium falciparum 3D7 from PlasmoDB version 6.1) as well as in all upsB var promoters.In addition,PfTRF was enriched at seven additional, intra-chromosomal sites and called in the PfTRF-HA ChIP-seq only. Plasmodium falciparum 3D7 parasites were generated with -GFP or -3xHA C-terminal tagged TRF (PF3D7_1209300). Nuclei were isolated from formaldehyde cross-linked schizont-stage transgenic parasites and used to prepare chromatin. Chromatin immunoprecipitations were performed using mouse anti-GFP (Roche Diagnostics, #11814460001) or rat anti-HA 3F10 (Roche Diagnostics, #12158167001). Sequencing libraries were prepared according to a Plasmodium-optimized library preparation procedure including KAPA polymerase-mediated PCR amplification.

2016-07-15 | E-GEOD-76537 | biostudies-arrayexpress

Bulk RNA-seq of the human malaria parasite Plasmodium falciparum 3D7 cultured under different iron conditions

Project description:Background: Host iron deficiency is protective against severe malaria as the human malaria parasite Plasmodium falciparum depends on free iron from its host to proliferate. Due to the absence of transferrin, ferritin, ferroportin, and a functional heme oxygenase, the parasite’s essential pathways of iron acquisition, storage, export, and detoxification differ from those in humans and may thus be excellent targets for therapeutic development. However, the proteins involved in these processes in P. falciparum remain largely unknown. Experimental design: To identify iron-regulated mechanisms and putative iron transporters in the human malaria parasite Plasmodium falciparum 3D7, we carried out whole-transcriptome profiling using bulk RNA-sequencing. The parasites were cultured either using erythrocytes from a donors with high, medium (healthy) or low iron status (experiment 1); or with red blood cells from another healthy donor in the presence or absence of 0.7 µM hepcidin, a specific ferroportin inhibitor and iron-regulatory hormone (experiment 2). This concentration of hepcidin was reported to reduce binding of ferrous iron to ferroportin by 50% in vitro (39). Samples from three biological replicates each were harvested at the ring and trophozoite stage (6 – 9 and 26 – 29 hours post invasion, hpi) during the second intra-erythrocytic developmental cycle under the conditions specified.

2024-04-08 | E-MTAB-13411 | biostudies-arrayexpress

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