Project description:Rodent malaria parasite RNA hybridized on Illumina Mouse WG-6 v2.0 Expression BeadChip To investigate whether parasite RNA interfere with mouse beadchip analaysis. Malaria parasite resides in red blood cell, therefore RNA isolated from whole infected blood contains host RNA as well as parasite RNA
Project description:We have shown previously (Reid & Berriman, NAR, 2012) that by simultaneously examining host and parasite gene expression over the course of infection we can determine pairs of genes involved in host-parasite interaction. Here we are producing a high quality dataset which will specifically allow us to exploit this finding to identify genes involved in malaria host-parasite interaction. This has been done in collaboration with Jean Langhorne at NIMR. 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/
Project description:To facilitate pre-eythrocytic malaria vaccine and drug target identification, a comprehensive transcriptome analysis of the parasites liver stages (LS) was undertaken. Green fluorescent protein-tagged Plasmodium yoelii (PyGFP) was used to isolate LS-infected hepatocytes from the rodent host. Genome-wide LS gene expression was profiled and compared to other parasite life cycle stages. The analysis reveals ~2000 genes active during LS development. Keywords: Stage comparison, time course
Project description:Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify if and to what degree circulating hemocytes have altered global expression profiles after infection with the rodent malaria parasite, Plasmodium berghei
Project description:Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify if and to what degree circulating hemocytes have altered global expression profiles after infection with the rodent malaria parasite, Plasmodium berghei Hemocytes were isolated 24-28h after infection using the infectious EGFP-CON P. berghei strain (experiment) or an invasion-deficient, Circumsporozoite- and TRAP-related protein (CTRP) knockout strain with the same genetic background as GFP-CON (CTRPko/GFP, control).
Project description:We use the Plasmodium berghei rodent model to characterize the proteome of the final phase of liver stage development, the merosomes, packets of hepatic merozoites that bud from the host hepatocyte to initiate the blood stage of malaria. Plasmodium berghei WT ANKA strain was used to infect HepG2 hepatoma cells. Samples were fractionated by strong cation exchange, and nano-LC Orbitrap mass spectrometry was used to perform untargeted proteomic profiling of 3 biological replicates. Data was processed using MaxQuant and LFQ. Additional searches were performed to identify peptides from cleaved acetylated PEXELs (protein export elements) to identify proteins putatively exported to the host hepatocyte during liver stage development.
Project description:In the malaria parasite Plasmodium falciparum, epigenetic modifications such as acetylation and methylation play important roles in parasite biology and virulence. Here, we characterised a new epigenetic mark, histone lactylation, recently discovered in humans and also present in Plasmodium. It was found in two human malaria parasites, P. falciparum and the zoonotic macaque parasite P. knowlesi, and was also found in vivo in two rodent malaria models. Histones were lactylated rapidly in response to elevated lactate levels, either exogenously added or endogenously generated by the parasite's own metabolism, and they were rapidly delactylated when lactate levels fell. Thus, this epigenetic mark is well-placed to act as a metabolic sensor, since severe falciparum malaria characteristically leads to hyperlactataemia in infected patients. Mass spectrometry showed that lysines on several parasite histones could be lactylated, and that this was accompanied by lactylation of many non-histone chromatin proteins. Histone lactylation was less abundant and less inducible in P. knowlesi than in P. falciparum, suggesting that P. falciparum may have evolved particular epigenetic responses to this characteristic feature of its pathology. Finally, in the rodent model P. yoelii, hyperlactataemia correlated with parasite transcriptomic programmes that suggested metabolic 'dormancy'.
Project description:The aim was to understand the molecular basis of the parasite response to DR. Transcriptomic analysis of synchronized wildtype parasites, collected with 4h intervals, from mice under the two dietary conditions. We found that WT parasites on DR and control diets have different transcriptomes, with a remarkable general repression of transcription in DR.
Project description:The aim of this study is to explore the role of differences in host genetic background which will supplement our current analysis of a timecourse of P.chabaudi infection in C57BL/6 mice over the peak of parasitemia. We have also published a paper showing that infections using mosquito-transmitted parasites have a quite different effect on the host immune system (Spence et al, Nature, 2013) and using this study we can compare the effects in host and parasite of serially blood passaged parasites versus mosquito transmitted parasites. This is in collaboration with Jean Langhorne at NIMR.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/