Project description:To investigate the accumulation of non coding small RNAs we performed high throughput RNA sequencing on size selcted total RNA from malaria parasite Plasmodium falciparum
Project description:This experiment characterizes the transcriptome of the human malaria parasite, P. falciparum at 8 different stages of the intraerythrocytic cycle Examination of polyA selected RNA in Plasmodium falciparum 3D7 strain at 8 different stages using RNA-seq
Project description:This experiment characterizes the localisation of H2A.Z, H3K9ac and H3K4me3 in the epigenome of the human malaria parasite, P. falciparum at 4 different stages of intraerythrocytic development.
Project description:This experiment characterizes the transcriptome of the human malaria parasite, P. falciparum at 8 different stages of the intraerythrocytic cycle
Project description:This experiment characterizes the localisation of H2A.Z, H3K9ac and H3K4me3 in the epigenome of the human malaria parasite, P. falciparum at 4 different stages of intraerythrocytic development. Examination of H2A.Z, H3K9ac, H3K4me3 and mono-nucleosomal input in 3D7 strain at 4 different stages and H2A in 3D7 strain at 1 stage using native ChIP-seq
Project description:The human malaria parasite Plasmodium falciparum employs intricate post-transcriptional regulatory mechanisms in different stages of its life cycle. Despite the importance of post-transcriptional regulation, key elements of these processes, namely RNA binding proteins (RBPs), are poorly characterized. In this study, the RNA binding properties of P. falciparum proteins were characterized including two putative members of the Bruno/CELF family of RBPs (PfCELF1 and PfCELF2), dihydrofolate reductase-thymidylate synthase (PfDHFR-TS), and adenosine deaminase (PfAda).The mRNA targets of these P. falciparum proteins were investigated by ribonomics using DNA microarrays.
Project description:The mRNA 5â² cap is normally essential for eukaryotic mRNA translation, stabilization and transport and both the cap and eIF4E are important elements of post-transcriptional gene regulation. To further our understanding of mRNA translation in the human malaria parasite Plasmodium falciparum, we have investigated the parasite translation initiation factor eIF4E and its interaction with 5â² capped mRNA. We have purified P. falciparum eIF4E as a recombinant protein and demonstrated that it has canonical mRNA 5â² cap binding activity. We used this protein to purify P. falciparum full-length 5â² capped mRNAs from total parasite RNA. Microarray analysis comparing total and eIF4E-purified 5â² capped mRNAs shows that a subset of 34 features were more than two-fold under-represented in the purified RNA sample, including 19 features representative of nuclear transcripts. The uncapped nuclear transcripts may represent a class of mRNAs targeted for storage and cap removal. Keywords: total RNA vs purified capped mRNA The microarray data were obtained from four hybridizations using RNA from two independent GST-PfeIF4E purifications from separate malaria cultures.
Project description:Investigation of whole genome gene expression level changes in Plasmodium falciparum 3D7 delta-PfPuf2 mutant, compared to the wild-type strain 3D7. The mutation engineered into this strain render tanslational control. The mutants analyzed in this study are further described in Miao J, Li J, Fan Q, Li X, Li X, Cui L.2010. The Puf-family RNA-binding protein PfPuf2 regulates sexual development and sex differentiation in the malaria parasite Plasmodium falciparum. J Cell Sci. 123(7):1039-49 (PMID 20197405).
Project description:To help malaria parasites survive unpredictable host immune responses, it is known that genes for surface proteins express stochastically in Plasmodium falciparum. Here, we demonstrate that gene expression for intracellular metabolic functions may be preordained and insensitive to specific metabolic perturbations. In a tightly-controlled, large microarray study involving over 100 hybridizations to isogenic drug-sensitive and drug-resistant parasites, the lethal antifolate WR99210 failed to over-produce RNA for the biochemically and genetically proven target dihydrofolate reductase-thymidylate synthase (DHFR-TS). Beyond the target, this transcriptional obstinacy carried over to the rest of the parasite genome, including genes for target pathways of folate and pyrimidine metabolism. Even 12 hours after commitment to death, the transcriptome remained faithful to evolutionarily entrained paths. A system-wide transcriptional disregard for metabolic perturbations in malaria parasites may contribute to selective vulnerabilities of the parasite to lethal antimetabolites. While large protective metabolic responses were not detected, DNA microarrays helped capture small, but reproducible drug-dependent perturbations within hours of drug exposure. In addition, in Plasmodium cells that had adapted to long-term drug exposure, DNA microarrays revealed new, large genome-wide transcriptional adjustments in the hard-wired transcriptional program itself. Keywords: Plasmodium falciparum treated with pyrimethamine RNA from pyrimethamine-treated parasite vs RNA from untreated control, Pyr-sensitive TM4/8.2 parasite strain, pyrimethamine concentration at IC50 and treated for 2 h, 4 h, and 8 h, microarray data were obtained from at least four hybridizations using RNA from at least two independent parasite cultures
Project description:To help malaria parasites survive unpredictable host immune responses, it is known that genes for surface proteins express stochastically in Plasmodium falciparum. Here, we demonstrate that gene expression for intracellular metabolic functions may be preordained and insensitive to specific metabolic perturbations. In a tightly-controlled, large microarray study involving over 100 hybridizations to isogenic drug-sensitive and drug-resistant parasites, the lethal antifolate WR99210 failed to over-produce RNA for the biochemically and genetically proven target dihydrofolate reductase-thymidylate synthase (DHFR-TS). Beyond the target, this transcriptional obstinacy carried over to the rest of the parasite genome, including genes for target pathways of folate and pyrimidine metabolism. Even 12 hours after commitment to death, the transcriptome remained faithful to evolutionarily entrained paths. A system-wide transcriptional disregard for metabolic perturbations in malaria parasites may contribute to selective vulnerabilities of the parasite to lethal antimetabolites. While large protective metabolic responses were not detected, DNA microarrays helped capture small, but reproducible drug-dependent perturbations within hours of drug exposure. In addition, in Plasmodium cells that had adapted to long-term drug exposure, DNA microarrays revealed new, large genome-wide transcriptional adjustments in the hard-wired transcriptional program itself. Keywords: Plasmodium falciparum treated with pyrimethamine RNA from pyrimethamine-treated parasite vs RNA from untreated control, Pyr-sensitive TM4/8.2 strain, pyrimethamine concentration at IC50 and treated for 0 h and 24 h, microarray data were obtained from at least four hybridizations using RNA from at lease two independent parasite cultures