Plasmodium falciparum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA374799 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5259140.fastq.gz | Fastqsanger.gz | |||
| SRR5259131.fastq.gz | Fastqsanger.gz | |||
| SRR5259141.fastq.gz | Fastqsanger.gz | |||
| SRR5259132.fastq.gz | Fastqsanger.gz | |||
| SRR5259134.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Malaria is caused by Plasmodium parasites that proliferate through iterative cycles of intra-erythrocytic replication. During each cycle a small number of parasites differentiate into gametocytes, the only forms able to infect the mosquito vector and transmit malaria. Sexual commitment is triggered by activation of AP2-G, the master transcriptional regulator of gametocytogenesis. Heterochromatin protein 1 (HP1)-dependent silencing of ap2-g prevents sexual conversion and secures proliferation. Here, we identify gametocyte development 1 (GDV1) as the first upstream activator of the sexual differentiation pathway in P. falciparum. Induction of GDV1 expression is sufficient to activate AP2-G expression and sexual differentiation. We found that GDV1 targets heterochromatin and triggers HP1 eviction preferentially at ap2-g and other gametocyte-specific genes. We further demonstrate that GDV1-dependent activation of ap2-g is controlled via a gdv1 antisense RNA. In summary, we identify GDV1 as an unprecedented cell fate decision factor that induces sexual differentiation by antagonizing HP1-dependent gene silencing.
2018-05-04 | GSE94901 | GEO
Project description:Malaria transmission requires the conversion of some asexual parasites into sexual forms termed gametocytes. The initial stages of sexual development, including sexually-committed schizonts and sexual rings, remain poorly characterized, in part because only a subset of parasites undergo sexual development and they are morphologically identical to their asexual counterparts. Here we present a system based on conditional expression of PfAP2-G, the master regulator of sexual conversion, for controlled sexual induction. Induction resulted in ~90% sexual conversion, which enables the characterization of early sexual stages without further purification. Transcriptomic analysis identified the alterations that follow pfap2-g activation, including identification of genes that are down-regulated. We also show that the inducible system enables the characterization of committed stages at the phenotypic level. Altogether, the inducible lines will facilitate the study of the initial stages of sexual development, which is important for the development of new strategies to stop malaria transmission.
2020-06-10 | GSE135005 | GEO
Project description:Malaria transmission requires the conversion of some asexual parasites into sexual forms termed gametocytes. The initial stages of sexual development, including sexually-committed schizonts and sexual rings, remain poorly characterized, in part because only a subset of parasites undergo sexual development and they are morphologically identical to their asexual counterparts. Here we present a system based on conditional expression of PfAP2-G, the master regulator of sexual conversion, for controlled sexual induction. Induction resulted in ~90% sexual conversion, which enables the characterization of early sexual stages without further purification. Transcriptomic analysis identified the alterations that follow pfap2-g activation, including identification of genes that are down-regulated. We also show that the inducible system enables the characterization of committed stages at the phenotypic level. Altogether, the inducible lines will facilitate the study of the initial stages of sexual development, which is important for the development of new strategies to stop malaria transmission.
2020-06-10 | GSE135002 | GEO
Project description:The sexual stages are vital phases in malaria parasite transmission and are the targets of various interventions such as transmission blocking vaccines. The molecular mechanisms underlying sexual development, however, remain poorly understood. We report mappping of a determinant previously linked to a male gametocyte development defect in the P. falciparum Dd2 parasite to an 82 kb region on chromosome 12. In order to find a critical gene in this region, we compared gene expression pattern in sexual stage of the parasite between Dd2 and its normal gametocyte-producing ancestor W2 clones. The region contains a sexual stage specific gene (pfmdv 1) that is expressed substantially at a lower level in the Dd2 than in W2 parasite. Disruption of pfmdv 1 results in a dramatic reduction in mature gametocytes, especially male gametocytes, with the majority of sexually committed parasites arrested at stage-I. The pfmdv-1 knockout parasites show an enlarged nucleus, often with separation of the inner and outer nuclear membranes and presence of multi-membrane vesicles in red blood cell cytoplasm. Mosquito infectivity of the knockout parasites is also greatly reduced, but not completely lost, suggesting presence of compensatory mechanisms in the sexual development pathways. Data include Day 8 gametocytes of male defective Dd2 and parental W2 clones of Plasmodium falciparum. The series includes three biological repeats. Keywords: repeat sample
2010-06-10 | E-GEOD-2265 | biostudies-arrayexpress
Project description:In the malaria parasite Plasmodium falciparum, changes in the distribution of heterochromatin at specific loci regulate the expression of clonally variant genes (CVGs), which play fundamental roles in host-parasite interactions. In addition to differences in heterochromatin between individual parasites associated with variant expression of CVGs, changes in heterochromatin distribution associated with different developmental stages have been described. However, while stage II/III gametocytes (sexual precursors) have an altered distribution of heterochromatin compared with asexual blood stages, it is unclear if heterochromatin changes already occur at the very early stages of sexual development. Here we used a transgenic parasite line in which sexual conversion can be conditionally induced to characterise the changes in heterochromatin distribution associated with the earliest stages of sexual development. We found that there were essentially no changes in sexual rings or stage I gametocytes compared with asexual blood stages, and remodelling of heterochromatin started at stage II or III of gametocyte development, with changes similar to those previously described in parasites of a different genetic background. Therefore, global redistribution of heterochromatin does not appear to play a role in the initial steps of sexual development. We also found that, for several genes, changes in expression associated with sexual development precede changes in the heterochromatin at their locus.
2024-10-09 | GSE252334 | GEO
Project description:Differentiation from asexual blood stages to sexual gametocytes is required for transmission of malaria parasites from the human to the mosquito host. Preventing gametocyte commitment and development would block parasite transmission, but the underlying molecular mechanisms behind these processes remain poorly understood. Here, we report that the ApiAP2 transcription factor, PfAP2-G2 (PF3D7_1408200) plays a critical role in the maturation of Plasmodium falciparum gametocytes. PfAP2-G2 binds to the promoters of a wide array of genes that are expressed at many stages of the parasite life cycle. Interestingly, we also find binding of PfAP2-G2 within the gene body of almost 3000 genes, which strongly correlates with the location of H3K36me3 and several other histone modifications as well as Heterochromatin Protein 1 (HP1), suggesting that occupancy of PfAP2-G2 in gene bodies may serve as an alternative regulatory mechanism. Disruption of pfap2-g2 does not impact asexual development, parasite multiplication rate, or commitment to sexual development but the majority of sexual parasites are unable to mature beyond stage III gametocytes. The absence of pfap2-g2 leads to overexpression of 28% of the genes bound by PfAP2-G2 and none of the PfAP2-g2 bound are downregulated, suggesting that it is a repressor. We also find that PfAP2-G2 interacts with chromatin remodeling proteins, a microrchidia (MORC) protein, and another ApiAP2 protein (PF3D7_1139300). Overall our data demonstrate that PfAP2-G2 is an important transcription factor that establishes an essential gametocyte maturation program in association with other chromatin-related proteins.
2021-02-01 | GSE160924 | GEO
Project description:Differentiation from asexual blood stages to sexual gametocytes is required for transmission of malaria parasites from the human to the mosquito host. Preventing gametocyte commitment and development would block parasite transmission, but the underlying molecular mechanisms behind these processes remain poorly understood. Here, we report that the ApiAP2 transcription factor, PfAP2-G2 (PF3D7_1408200) plays a critical role in the maturation of Plasmodium falciparum gametocytes. PfAP2-G2 binds to the promoters of a wide array of genes that are expressed at many stages of the parasite life cycle. Interestingly, we also find binding of PfAP2-G2 within the gene body of almost 3000 genes, which strongly correlates with the location of H3K36me3 and several other histone modifications as well as Heterochromatin Protein 1 (HP1), suggesting that occupancy of PfAP2-G2 in gene bodies may serve as an alternative regulatory mechanism. Disruption of pfap2-g2 does not impact asexual development, parasite multiplication rate, or commitment to sexual development but the majority of sexual parasites are unable to mature beyond stage III gametocytes. The absence of pfap2-g2 leads to overexpression of 28% of the genes bound by PfAP2-G2 and none of the PfAP2-g2 bound are downregulated, suggesting that it is a repressor. We also find that PfAP2-G2 interacts with chromatin remodeling proteins, a microrchidia (MORC) protein, and another ApiAP2 protein (PF3D7_1139300). Overall our data demonstrate that PfAP2-G2 is an important transcription factor that establishes an essential gametocyte maturation program in association with other chromatin-related proteins.
2021-02-01 | GSE160923 | GEO
Project description:Malaria parasites go through major transitions during their complex life cycle, yet the underlying differentiation pathways remain obscure. Here we apply single cell transcriptomics to unravel events that initiate sexual development in preparation for transmission of the parasite from human to mosquito. This proof-of-concept study provides a template to capture transcriptional diversity in heterogeneous parasite populations, with major implications for our understanding of parasite biology and the ongoing malaria elimination campaign.
2017-03-11 | GSE96066 | GEO
Project description:The sexual stages are vital phases in malaria parasite transmission and are the targets of various interventions such as transmission blocking vaccines. The molecular mechanisms underlying sexual development, however, remain poorly understood. We report mappping of a determinant previously linked to a male gametocyte development defect in the P. falciparum Dd2 parasite to an 82 kb region on chromosome 12. In order to find a critical gene in this region, we compared gene expression pattern in sexual stage of the parasite between Dd2 and its normal gametocyte-producing ancestor W2 clones. The region contains a sexual stage specific gene (pfmdv 1) that is expressed substantially at a lower level in the Dd2 than in W2 parasite. Disruption of pfmdv 1 results in a dramatic reduction in mature gametocytes, especially male gametocytes, with the majority of sexually committed parasites arrested at stage-I. The pfmdv-1 knockout parasites show an enlarged nucleus, often with separation of the inner and outer nuclear membranes and presence of multi-membrane vesicles in red blood cell cytoplasm. Mosquito infectivity of the knockout parasites is also greatly reduced, but not completely lost, suggesting presence of compensatory mechanisms in the sexual development pathways. Data include Day 8 gametocytes of male defective Dd2 and parental W2 clones of Plasmodium falciparum. The series includes three biological repeats. Keywords: repeat sample
2005-05-01 | GSE2265 | GEO
Project description:For malaria transmission, the parasite must undergo sexual differentiation into mature gametocytes. However, the molecular basis for this critical transition in the parasites life cycle is unknown. Six previously uncharacterized genes, Pfg14.744, Pfg14.745, Pfg14.748, Pfg14.763, Pfg14.752 and Pfg6.6 that are members of a 36 gene Plasmodium falciparum-specific subtelomeric superfamily were found to be expressed in parasites that are committed to sexual development as suggested by co-expression of Pfs16 and Pfg27. Northern blots demonstrated that Pfg14.744 and Pfg14.748 were first expressed before the parasites differentiated into morphologically distinct gametocytes, transcription continued to increase until stage II gametocytes were formed and then rapidly decreased. Immunofluorescence assays indicated that both proteins were only produced in the subpopulation of ring stage parasites that are committed to gametocytogenesis and both localized to the parasitophorous vacuole (PV)b of the early ring stage parasites. As the parasites continued to develop Pfg14.748 remained within the parasitophorous vacuole, while Pfg14.744 was detected in the erythrocyte. The 5' flanking region of either gene alone was sufficient to drive early gametocyte specific expression of green fluorescent protein (GFP). In parasites transfected with a plasmid containing the Pfg14.748 5' flanking region immediately upstream of GFP, fluorescence was observed in a small number of schizonts the cycle before stage I gametocytes were observed. This expression pattern is consistent with commitment to sexual differentiation prior to merozoite release and erythrocyte invasion. Further investigation into the role of these genes in the transition from asexual to sexual differentiation could provide new strategies to block malaria transmission.
2014-10-16 | GSE62364 | GEO