Ontology highlight
ABSTRACT:
PROVIDER: PRJNA701959 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13990247_1.fastq.gz | Fastqsanger.gz | |||
| SRR13990248_1.fastq.gz | Fastqsanger.gz | |||
| SRR13990249_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Gametocytes are nonreplicative sexual forms that mediate malaria transmission to a mosquito vector. They are generated from asexual blood stage parasites, which proliferate in the circulation. However, it remains largely unknown as to how this transition is genetically regulated. Here, we report that an Apetala2 (AP2) family transcription factor, AP2-G2, regulates the transition as a transcriptional repressor. Disruption of AP2-G2 in the rodent malaria parasites, Plasmodium berghei, did not prevent commitment to the sexual stage but halted their development before manifesting sex-specific morphologies. ChIP-seq analysis revealed that AP2-G2 targets approximately 1,500 genes and recognizes a five-base motif on their promoters. Most of these target genes are required for asexual proliferation in the blood by the parasites, thereby suggesting that AP2-G2 blocks the program for asexual replication of parasites in the blood. DNA microarray analysis showed that the identified targets constituted approximately 70% of the upregulated genes in AP2-G2-depleted parasites, and a promoter assay using a centromere plasmid demonstrated that the binding motif functions as a cis-acting negative regulatory element. These results suggest that global transcriptional repression, which occurs during the initial phase of gametocytogenesis, is an essential step to promote conversion to the sexual stage.
2015-10-01 | GSE66189 | GEO
Project description:Cathepsin C-like protease regulates DNA replication by histone H3 N-terminal clipping in malaria parasites
| PRJEB18114 | ENA
Project description:Gametocytes are nonreplicative sexual forms that mediate malaria transmission to a mosquito vector. They are generated from asexual blood stage parasites, which proliferate in the circulation. However, it remains largely unknown as to how this transition is genetically regulated. Here, we report that an Apetala2 (AP2) family transcription factor, AP2-G2, regulates the transition as a transcriptional repressor. Disruption of AP2-G2 in the rodent malaria parasites, Plasmodium berghei, did not prevent commitment to the sexual stage but halted their development before manifesting sex-specific morphologies. ChIP-seq analysis revealed that AP2-G2 targets approximately 1,500 genes and recognizes a five-base motif on their promoters. Most of these target genes are required for asexual proliferation in the blood by the parasites, thereby suggesting that AP2-G2 blocks the program for asexual replication of parasites in the blood. DNA microarray analysis showed that the identified targets constituted approximately 70% of the upregulated genes in AP2-G2-depleted parasites, and a promoter assay using a centromere plasmid demonstrated that the binding motif functions as a cis-acting negative regulatory element. These results suggest that global transcriptional repression, which occurs during the initial phase of gametocytogenesis, is an essential step to promote conversion to the sexual stage.
2015-10-01 | GSE66188 | GEO
Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 6% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.
2020-04-20 | GSE144976 | GEO
Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 9% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.
2020-04-20 | GSE132643 | GEO
Project description:The intra-erythrocytic developmental cycle (IDC) of malaria parasites is synchronized with the time-of-day hosts feed, but the mechanism underpinning this coordination is unknown. Combining in vivo and in vitro approaches using rodent and human malaria parasites, we reveal that: (i) 57% of P. chabaudi genes exhibit 24 h “circadian” periodicity in expression; (ii) 58% of these genes lose rhythmicity when the IDC is out-of-synchrony with host rhythms; (iii) 9% of P. falciparum genes show circadian expression under free-running conditions; (iv) Serpentine receptor 10 (SR10) is circadian and disrupting it in rodent models shortens the IDC by 2-3 hours; (v) diverse processes, including DNA replication, the ubiquitin and proteasome pathways, are affected by disruption of SR10 and loss of coordination with host rhythms. Our results reveal that malaria parasites are at least in part responsible for scheduling their IDC, explaining the fitness benefits of coordination with host rhythms.
2020-04-20 | GSE132625 | GEO
Project description:Cytotoxicity of DNA-protein crosslinks (DPCs) is ascribed largely to their ability to block the progression of DNA replication fork. DPCs are frequently occurring in cells, either as a consequence of metabolism or exogenous agents. The mechanism of DPCs removal is not completely understood. Here, we characterize SPRTN (DVC1) as specialised DNA-dependent metalloprotease for DPC removal in humans. SPRTN has an N-terminal metalloprotease domain that cleaves various DNA binding substrate during S-phase progression. SPRTN is a part of replisome and removes DPCs during DNA replication fork progression, thus protecting proliferative cells from DPCs toxicity. Ruijs-Aalfs Syndrome (RJALS) patient cells with monogenic mutations in SPRTN are hypersensitive to DPC-inducing agents due to DPC removal defect and DNA replication fork stalling. We propose a model where SPRTN protease forms specialised DNA-replication coupled DPC removal pathway essential for DNA replication fork progression and genome stability. We conclude RJALS is the first human syndrome linked to this pathway
2017-03-29 | MSV000080743 | MassIVE
Project description:Novak1997 - Cell Cycle
Modeling the control of DNA replication in fission yeast.
This model is described in the article:
Modeling the control of DNA replication in fission yeast.
Novak B., Tyson JJ.
Proc. Natl. Acad. Sci. U.S.A. 1997:94(17):9147-52
Abstract:
A central event in the eukaryotic cell cycle is the decision to commence DNA replication (S phase). Strict controls normally operate to prevent repeated rounds of DNA replication without intervening mitoses ("endoreplication") or initiation of mitosis before DNA is fully replicated ("mitotic catastrophe"). Some of the genetic interactions involved in these controls have recently been identified in yeast. From this evidence we propose a molecular mechanism of "Start" control in Schizosaccharomyces pombe. Using established principles of biochemical kinetics, we compare the properties of this model in detail with the observed behavior of various mutant strains of fission yeast: wee1(-) (size control at Start), cdc13Delta and rum1(OP) (endoreplication), and wee1(-) rum1Delta (rapid division cycles of diminishing cell size). We discuss essential features of the mechanism that are responsible for characteristic properties of Start control in fission yeast, to expose our proposal to crucial experimental tests.
This model is hosted on BioModels Database
and identified by: BIOMD0000000007
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000007 | BioModels
Project description:Lifecycle progression of the malaria parasite Plasmodium falciparum requires a finely tuned regulation of gene expression including histone methylation. The histone methyltransferase PfSET10 was previously identified as a histone H3 lysine K4 methyltransferase involved in var gene regulation, making it a prominent antimalarial target. We here investigated the role of PfSET10 in the P. falciparum blood stages in more detail, using tagged PfSET10-knockout (KO) and -knockdown (KD) lines. We demonstrated a nuclear localization of PfSET10 in the P. falciparum blood stages with peak protein levels in schizonts. PfSET10 deficiency resulted in reduced intraerythrocytic growth, but had no effect on gametocyte formation. When the PfSET10-KO line was screened for histone methylation variations, lack of PfSET10 rendered the parasites unable to mark H3K18me1, while no significant changes in the H3K4 methylation status were observed. Comparative transcriptomic profiling of PfSET10-KO schizonts demonstrated the up-regulation of transcripts particularly encoding proteins of erythrocyte invasion and multi gene family proteins, suggesting a suppressive function of the histone methylation mark. TurboID coupled with mass spectrometry further revealed an extensive nuclear PfSET10 interaction network with roles in transcriptional regulation, DNA replication and repair, chromatin remodeling and mRNA processing. Main interactors of PfSET10 included ApiAP2 transcription factors, epigenetic regulators, mediators of RNA polymerase II and DNA replication licensing factors. The combined data pinpoint PfSET10 as a histone H3 lysine K18 methyltransferase regulating DNA and RNA metabolic processes important for intraerythrocytic development of P. falciparum.
2024-09-24 | PXD052931 | JPOST Repository