Plasmodium falciparum 3D7
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ABSTRACT:
PROVIDER: PRJNA231046 | ENA |
REPOSITORIES: ENA
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Project description:The dry season is a major challenge for Plasmodium falciparum parasites in many malaria endemic regions, where water availability limits mosquitoes to only part of the year. How P. falciparum bridges two transmission seasons months apart, without being cleared by the host or compromising host survival is poorly understood. Here we show that low levels of P. falciparum parasites persist in the blood of asymptomatic Malian individuals during the 5- to 6-month dry season, rarely causing symptoms and minimally affecting the host immune response. Parasites isolated during the dry season are transcriptionally distinct from those of subjects with febrile malaria in the transmission season, reflecting longer circulation within each replicative cycle, of parasitized erythrocytes without adhering to the vascular endothelium. Low parasite levels during the dry season are not due to impaired replication, but rather increased efficiency of splenic clearance of longer-circulating infected erythrocytes. We propose that P. falciparum virulence in areas of seasonal malaria transmission is regulated so that the parasite decreases its endothelial binding capacity, allowing increased splenic clearance and enabling several months of subclinical parasite persistence.
2020-08-20 | GSE148125 | GEO
Project description:Plasmodium falciparum blood stage parasites: control vs PfTRF-depleted parasites
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Project description:Transmission of Plasmodium spp. from a human host to a mosquito vector requires that some parasites abandon the asexual replicative cycle in the blood, associated with all clinical symptoms of malaria, and convert into non-replicative sexual precursors called gametocytes. The sexual conversion rate (i.e., the proportion of parasites that convert at each cycle) is variable, which enables parasites to adjust the balance between sexual and asexual development to the conditions of the human blood environment. Under some specific types of stress, parasites enhance sexual conversion rates to increase their relative investment in transmission. Sexual conversion is orchestrated by the master regulator AP2-G, a transcription factor of the ApiAP2 family. In Plasmodium falciparum, the species that produces the vast majority of human malaria cases and deaths, activation of ap2-g expression requires the GDV1 protein, which displaces heterochromatin from the ap2-g promoter. An antisense long noncoding RNA (lncRNA) encoded in the same locus as GDV1, named gdv1-as, is a negative regulator of GDV1 expression, but how the expression of this lncRNA is regulated or how specific types of stress enhance sexual conversion is not known. Here we show that environmental induction of sexual conversion is initiated by activation of gdv1 expression in a process dependent on the AP2-HS transcription factor, previously described as the activator of the malarial protective HS response. Next, GDV1 activates the expression of its own repressor, gdv1-as, by removing heterochromatin from its putative promoter. This positive-negative regulatory feedback loop limits GDV1 activation to a short burst of expression. This same mechanism operates for stimulation of sexual conversion by different environmental conditions, and AP2-HS is also needed for the activation of metabolic pathways that compensate depletion of phospholipid precursors. These findings provide new insight on the mechanisms underlying the fundamental developmental decision of malaria parasites and explain their plasticity to increase the investment in transmission when the conditions of the environment are unfavourable.
2026-07-27 | GSE298061 | GEO
Project description:Transmission of Plasmodium spp. from a human host to a mosquito vector requires that some parasites abandon the asexual replicative cycle in the blood, associated with all clinical symptoms of malaria, and convert into non-replicative sexual precursors called gametocytes. The sexual conversion rate (i.e., the proportion of parasites that convert at each cycle) is variable, which enables parasites to adjust the balance between sexual and asexual development to the conditions of the human blood environment. Under some specific types of stress, parasites enhance sexual conversion rates to increase their relative investment in transmission. Sexual conversion is orchestrated by the master regulator AP2-G, a transcription factor of the ApiAP2 family. In Plasmodium falciparum, the species that produces the vast majority of human malaria cases and deaths, activation of ap2-g expression requires the GDV1 protein, which displaces heterochromatin from the ap2-g promoter. An antisense long noncoding RNA (lncRNA) encoded in the same locus as GDV1, named gdv1-as, is a negative regulator of GDV1 expression, but how the expression of this lncRNA is regulated or how specific types of stress enhance sexual conversion is not known. Here we show that environmental induction of sexual conversion is initiated by activation of gdv1 expression in a process dependent on the AP2-HS transcription factor, previously described as the activator of the malarial protective HS response. Next, GDV1 activates the expression of its own repressor, gdv1-as, by removing heterochromatin from its putative promoter. This positive-negative regulatory feedback loop limits GDV1 activation to a short burst of expression. This same mechanism operates for stimulation of sexual conversion by different environmental conditions, and AP2-HS is also needed for the activation of metabolic pathways that compensate depletion of phospholipid precursors. These findings provide new insight on the mechanisms underlying the fundamental developmental decision of malaria parasites and explain their plasticity to increase the investment in transmission when the conditions of the environment are unfavourable.
2026-07-27 | GSE298024 | GEO
Project description:Transmission of Plasmodium spp. from a human host to a mosquito vector requires that some parasites abandon the asexual replicative cycle in the blood, associated with all clinical symptoms of malaria, and convert into non-replicative sexual precursors called gametocytes. The sexual conversion rate (i.e., the proportion of parasites that convert at each cycle) is variable, which enables parasites to adjust the balance between sexual and asexual development to the conditions of the human blood environment. Under some specific types of stress, parasites enhance sexual conversion rates to increase their relative investment in transmission. Sexual conversion is orchestrated by the master regulator AP2-G, a transcription factor of the ApiAP2 family. In Plasmodium falciparum, the species that produces the vast majority of human malaria cases and deaths, activation of ap2-g expression requires the GDV1 protein, which displaces heterochromatin from the ap2-g promoter. An antisense long noncoding RNA (lncRNA) encoded in the same locus as GDV1, named gdv1-as, is a negative regulator of GDV1 expression, but how the expression of this lncRNA is regulated or how specific types of stress enhance sexual conversion is not known. Here we show that environmental induction of sexual conversion is initiated by activation of gdv1 expression in a process dependent on the AP2-HS transcription factor, previously described as the activator of the malarial protective HS response. Next, GDV1 activates the expression of its own repressor, gdv1-as, by removing heterochromatin from its putative promoter. This positive-negative regulatory feedback loop limits GDV1 activation to a short burst of expression. This same mechanism operates for stimulation of sexual conversion by different environmental conditions, and AP2-HS is also needed for the activation of metabolic pathways that compensate depletion of phospholipid precursors. These findings provide new insight on the mechanisms underlying the fundamental developmental decision of malaria parasites and explain their plasticity to increase the investment in transmission when the conditions of the environment are unfavourable.
2026-07-27 | GSE339382 | 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