Microsampling transcriptomics
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB27301 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Single-cell RNA-sequencing is revolutionising our understanding of seemingly homogeneous cell populations but has not yet been widely applied to single-celled organisms. Transcriptional variation in unicellular malaria parasites from the Plasmodium genus is associated with critical phenotypes including red blood cell invasion and immune evasion, yet transcriptional variation at an individual parasite level has not been examined in depth. Here, we describe the adaptation of a single-cell RNA-sequencing (scRNA-seq) protocol to deconvolute transcriptional variation for more than 500 individual parasites of both rodent and human malaria comprising asexual and sexual life-cycle stages. We uncover previously hidden discrete transcriptional signatures during the pathogenic part of the life cycle, suggesting that expression over development is not as continuous as commonly thought. In transmission stages, we find novel, sex-specific roles for differential expression of contingency gene families that are usually associated with immune evasion and pathogenesis.
2017-02-08 | E-ERAD-611 | biostudies-arrayexpress
Project description:The purpose of this research is to identify and evaluate the global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites and specifically compare the blood stage gene expression profiles of samples derived from previous studies on Plasmodium falciparum, Plasmodium vivax and Plasmodium knowlesi
2016-04-08 | GSE80015 | 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:This study is a collaboration with Phil Spence and Jean Langhorne at NIMR, Mill Hill where Phil is studying the differences in aetiology of rodent malaria when mice are infected by mosquito bite versus intraperitoneal injection of blood stage parasites. The aim is to determining transcriptomic differences using RNA-Seq between parasites transmitted by mosquito and those transmitted by injection. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/Protocol: Mice were bled out at 6 days post-infection, and RNA was extracted from purified parasite populations using Trizol reagent and DNase treated. Poly A+ mRNA was purified from total RNA using oligo dT dyna bead selection and libraries were created using a modified RNA-seq protocol, where RNA was fragmented using Covaris AFA sonication instead of metal ions. The samples were sequenced on an Illumina HiSeq 2000.
2012-11-27 | E-ERAD-95 | biostudies-arrayexpress
Project description:The study of rodent malaria parasites has significantly advanced our understanding of malaria parasite biology and host responses to parasite infections. There are four well-characterized rodent malaria parasite species (Plasmodium yoelii, P. chabaudi, P. berghei, and P. vinckei). Each species also has multiple strains that cause different disease phenotypes. P. yoelii nigeriensis N67C and N67, two isogenic parasites, are particularly intriguing as they differ in virulence and incite different immune responses in mice. The genome of the N67 parasite has been assembled recently, but not that of N67C. This study used PacBio HiFi sequencing data to assemble the N67C genome, compared the two genomes, and performed RNA sequencing to identify polymorphisms and differentially expressed genes (DEGs). Results: The assembled N67C parasite genome consisted of 16 scaffolds and three contigs of approximately 22.5 Mb with 100% and 96.6% completeness based on well-characterized single-copy orthologs specific to the Apicomplexa phylum and the Plasmodium genus, respectively. A comparison between the annotated N67C and N67 genomes revealed 133 single nucleotide polymorphisms (SNPs) and 75 indels. Among the polymorphic sites, an S (N67) to N (N67C) amino acid substitution at position 114 (S114N) in the dihydrofolate reductase-thymidylate synthase (DHFR-TS) confers resistance to pyrimethamine in mice. Additionally, 302 differentially expressed genes (DEGs) were detected after comparing mRNA levels between the two parasites. Starting with the predicted and annotated 5,681 N67C and 5,749 N67 genes, we identified 4,641 orthogroups that included at least one gene from the four P. yoelii parasites (N67, N67C, 17X, and YM), whereas 758 orthogroups showed subspecies or strain-specific patterns. Conclusion: The identification of polymorphic sites between the N67 and N67C genomes, along with the detection of the DEGs, may provide crucial insights into the variations in parasite drug responses and disease severity between these two isogenic parasites. The functional characterization of these genetic differences and candidate genes will deepen our understanding of disease mechanisms and pave the way for developing more effective control measures against malaria.
2024-10-14 | GSE278246 | GEO
Project description:After entering their mammalian host via the bite of an Anopheles mosquito, Plasmodium sporozoites migrate to the liver where they traverse several hepatocytes before invading the one inside which they will develop and multiply into thousands of merozoites. Although this constitutes an essential step in malaria infection, the requirements of Plasmodium parasites in liver cells and how they use the host cell for their own survival and development are poorly understood. To gain new insights into the molecular host-parasite interactions that take place during malaria liver infection, we have used high-throughput microarray technology to determine the transcriptional profile of P. yoelii-infected hepatocytes that were collected from P. yoelii-infected mice 24 and 40 h after infection. This in vivo microarray expression was compared with the microarray analysis of in vitro infected hepatoma cells infected with closely related rodent malaria parasite P. berghei. Differential expression patterns for host genes identify genes and pathways involved in the host response to rodent Plasmodium parasites. Keywords: gene expression
2010-02-24 | GSE14967 | GEO
Project description:In the rodent malaria parasite Plasmodium berghei, we found that an AP2 family transcription factor designated AP2-L plays a critical role in the development of the liver stage. Using DNA microarray analysis we showed that the expression of several genes, including those of parasitophorous vacuole membrane proteins, was significantly decreased in the early liver stage of AP2-L-depleted parasites. Gene expression of P. berghei liver stages was compared between wild type and AP2-L KO parasites. Liver stage parasites were cultured for 24h using HepG2 cells. Ten and seven biologically independent experiments were performed for wild type and AP2-L KO parasites, respectively.
2012-04-30 | E-GEOD-34877 | biostudies-arrayexpress
Project description:A promising strategy to design effective malaria blood-stage vaccines is to induce parasite-specific CD4+ Th1 cell responses, but the regulatory mechanism of which is still largely unknown. Here, we showed that the ATG5-deficiency in myeloid cells significantly inhibit the growth of rodent blood-stage malaria parasites through specifically enhancing parasite-specific CD4+ Th1 cell responses. This effect was independent of ATG5-mediated canonical autophagy and non-canonical autophagy. Mechanistically, the deficiency of ATG5 promoted the survival of inflammatory monocytes (CD11b+F4/80- cells), and sequentially increased the generation of chemokine MCP-1 in parasite-infected mice. The interaction of CD11b+F4/80- cells-derived MCP-1 with CCR2 on CD4+ Th1 cells for its optimized differentiation dependent on Jak2/stat4 pathway. Therefore, we highlight the previously unrecognized role of ATG5 in the modulation of the survival of inflammatory monocytes to produce MCP-1, and the selective promoting effect of MCP-1 on CD4+ Th1 cell differentiation, which shed new lights on effective malaria vaccine designation.
2024-03-01 | GSE228461 | GEO