PfAP2-I-GFP anti-GFP and anti-IgG ChIP-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Plasmodium falciparum
PROVIDER: GSE80293 | GEO | 2017/06/01
SECONDARY ACCESSION(S): PRJNA318518
REPOSITORIES: GEO
Similar Datasets
Project description:Obligate intracellular parasites must efficiently invade host cells in order to mature and be transmitted. For the malaria parasite Plasmodium falciparum, invasion of host red blood cells (RBCs) is essential. Here we describe a parasite-specific transcription factor belonging to the Apicomplexan Apetala 2 (ApiAP2) family that is responsible for regulating the expression of a subset of merozoite genes involved in RBC invasion (PfAP2-I). Our genome-wide analysis by ChIP-seq shows that PfAP2-I interacts with a specific DNA motif in the promoters of these genes. msp5 transcription levels decrease when the PfAP2-I DNA-binding motif is mutated in PfAP2-I-GFP parasites, showing that PfAP2-I must bind the DNA motif in order for msp5 to be transcribed.
2016-12-31 | GSE77809 | GEO
Project description:Obligate intracellular parasites must efficiently invade host cells in order to mature and be transmitted. For the malaria parasite Plasmodium falciparum, invasion of host red blood cells (RBCs) is essential. Here we describe a parasite-specific transcription factor belonging to the Apicomplexan Apetala 2 (ApiAP2) family that is responsible for regulating the expression of a subset of merozoite genes involved in RBC invasion (PfAP2-I). Our genome-wide analysis by ChIP-seq shows that PfAP2-I interacts with a specific DNA motif in the promoters of these genes. msp5 transcription levels decrease when the PfAP2-I DNA-binding motif is mutated in PfAP2-I-GFP parasites, showing that PfAP2-I must bind the DNA motif in order for msp5 to be transcribed.
2016-12-31 | GSE77807 | GEO
Project description:PfAP2-I-GFP-msp5MUT vs PfAP2-I-GFP 3D7
| PRJNA311596 | ENA
Project description:In the malaria parasite Plasmodium falciparum, the switch from asexual multiplication to sexual differentiation into gametocytes is essential for transmission to mosquitos. One of the key determinants of sexual commitment is the transcription factor PfAP2-G, which has been proposed to orchestrate this crucial cell fate decision by driving expression of gametocyte genes. We show conclusively that PfAP2-G is a transcriptional activator of gametocyte genes and identify the earliest known markers expressed during commitment. Remarkably, we also find that in sexually committed cells, PfAP2-G is associated with the promoters of genes important for red blood cell invasion and activates them through its interactions with a second transcription factor. We thus demonstrate an intriguing transcriptional link between the apparently opposing processes of red blood cell invasion and gametocytogenesis that is coordinated by the master regulator PfAP2-G. This finding has important implications for the development of new anti-malarial drugs that block the invasion of red blood cells by sexually committed cells, thereby preventing parasite transmission.
2019-02-08 | GSE121312 | GEO
Project description:In the malaria parasite Plasmodium falciparum, the switch from asexual multiplication to sexual differentiation into gametocytes is essential for transmission to mosquitos. One of the key determinants of sexual commitment is the transcription factor PfAP2-G, which has been proposed to orchestrate this crucial cell fate decision by driving expression of gametocyte genes. We show conclusively that PfAP2-G is a transcriptional activator of gametocyte genes and identify the earliest known markers expressed during commitment. Remarkably, we also find that in sexually committed cells, PfAP2-G is associated with the promoters of genes important for red blood cell invasion and activates them through its interactions with a second transcription factor. We thus demonstrate an intriguing transcriptional link between the apparently opposing processes of red blood cell invasion and gametocytogenesis that is coordinated by the master regulator PfAP2-G. This finding has important implications for the development of new anti-malarial drugs that block the invasion of red blood cells by sexually committed cells, thereby preventing parasite transmission.
2019-02-08 | GSE120990 | GEO
Project description:In this study we have investigated PfAP2-HC (PF3D7_1456000), a protein that was identified by co-immunoprecipitation with PfHP1 coupled with liquid chromatography-tandem mass spectrometry. PfAP2-HC belongs to the ApiAP2 family, the main transcription factor family in Apicomplexan parasites. We have confirmed that AP2-HC colocalises with HP1 with the use of immunofluorescence assays and chromatin immunoprecipitation-sequencing. We show that PfAP2-HC is not required for heterochromatin maintenance and inheritance with the use of PfAP2-HC Kock out and knockdown. We show with transcriptome-wide microarray time course analysis that PfAP2-HC does not act as a transcription factor in blood stage parasites. We demonstrate that the AP2 domain is dispensable for heterochromatin targeting by introducing a premature stop codon before the AP2 domain. We show that PfAP2-HC binding to heterochromatin dependents on PfHP1. and PfAP2-HC is likely not involved in de novo heterochromatin formation
2020-11-04 | GSE154840 | GEO
Project description:In the malaria parasite Plasmodium falciparum, the switch from asexual multiplication to sexual differentiation into gametocytes is essential for transmission to mosquitos. One of the key determinants of sexual commitment is the transcription factor PfAP2-G, which has been proposed to orchestrate this crucial cell fate decision by driving expression of gametocyte genes. We show conclusively that PfAP2-G is a transcriptional activator of gametocyte genes and identify the earliest known markers expressed during commitment. Remarkably, we also find that in sexually committed cells, PfAP2-G is associated with the promoters of genes important for red blood cell invasion and activates them through its interactions with a second transcription factor. We thus demonstrate an intriguing transcriptional link between the apparently opposing processes of red blood cell invasion and gametocytogenesis that is coordinated by the master regulator PfAP2-G. This finding has important implications for the development of new anti-malarial drugs that block the invasion of red blood cells by sexually committed cells, thereby preventing parasite transmission.
2019-02-11 | GSE120448 | GEO
Project description:The pathogenicity of the malaria parasites results from their ability to invade and remodel red blood cells (RBCs), expressing antigenic variant proteins for immune evasion and survival, and then to egress from the host cell. These sequential processes require concerted actions of a large number of proteins during the intraerythrocytic developmental cycle (IDC)(Boddey and Cowman, 2013; Cowman et al., 2017; Tan and Blackman, 2021), but the molecular basis of the required regulation is only partially understood. Here, we have characterized an essential Apicomplexan AP2 (ApiAP2) transcription factor (we refer to it as PfAP2-MRP; Master Regulator of Pathogenesis) that shows two peaks of expression during the IDC at 16- and 40-hour post-invasion (h.p.i.). When expression of PfAP2-MRP at 40 h.p.i. was disrupted using an inducible gene knockout approach, ∆PfAP2-MRP parasites unable to form mature merozoites and egress from the host RBCs owing to strong down-regulation of several known egress- and invasion-associated genes, in addition to several novel hypothetical genes thought to be involved in these key life cycle processes. Disruption of PfAP2-MRP expression at 16 h.p.i. results in transcriptional activation of the majority of silenced var genes observed at both bulk and single-cell level. This is also reflected by a significantly higher level of immuno-recognition of the exported proteins on the ∆PfAP2-MRP parasite-infected RBCs by pooled sera from malaria-exposed individuals from an endemic region. In addition, overexpression of many early gametocyte marker genes was also observed in ∆PfAP2-MRP parasites at both 40 h.p.i., and at 16 h.p.i. PfAP2-MRP directly regulates these genes by binding to their promoter region or indirectly through 14 other downstream AP2 transcription factors. Taken together, we conclude that PfAP2-MRP is an upstream transcriptional regulator that participates in mutually exclusive expression patterns shown by the var family of genes and is a critical determinant of parasite's growth during the IDC.
2024-01-26 | PXD030308 | Pride
Project description:RNA-immunoprecipitation of mTRAN1-GFP
| PRJEB63171 | ENA
Project description:Malarial parasite pathogenicity results from its ability to invade and remodel red blood cells (RBCs), expressing antigenic variant proteins for immune evasion and survival, and then to egress from the host cell. These sequential processes require concerted actions of a large number of proteins during the intraerythrocytic developmental cycle (IDC), but the molecular basis of the required regulation is only partially understood. Here, we have characterized an essential Apicomplexan AP2 (ApiAP2) transcription factor (we refer to it as PfAP2-P; Pathogenesis) that shows two peaks of expression during the IDC at 16- and 40-hour post invasion (h.p.i.). When expression of PfAP2-P at 40 h.p.i. was disrupted using an inducible gene knockout approach, ∆PfAP2-P parasites unable to form mature merozoites and egress from the host RBCs owing to strong down-regulation of several known egress- and invasion-associated genes, in addition to several novel hypothetical genes of thought to be involved in these key life cycle processes during the IDC. Disruption of PfAP2-P expression at 16 h.p.i. results in transcriptional activation of virtually majority of silenced var genes observed at both bulk and single cell level. This is also reflected by significantly higher level of recognition of the exported proteins on the ∆PfAP2-P parasite-infected RBCs by pooled sera from malaria-exposed individuals from endemic region. In addition, over-expression of many early gametocyte marker genes was also observed in ∆PfAP2-P parasites at both 40 h.p.i., and at 16 h.p.i. PfAP2-P directly regulates these genes by binding to their promoter region or indirectly through 14 other down-stream AP2 transcription factors. Taken together, we conclude that PfAP2-P is an upstream transcriptional regulator that participates in mutually exclusive expression pattern shown by the var family of genes and a critical determinant of parasite’s growth during the IDC.
2023-08-07 | GSE191025 | GEO