Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome-wide regulation of host m6A mRNA methylation by malaria parasite infection

ABSTRACT: N6-Methyladenosine (m6A) modification has been found to play important roles in diverse pathogen infections and host responses, here we report host m6A mRNA transcriptome profiles regulated by the infections of two strains of malaria parasite Plasmodium yoelii (N67 and N67C). We showed that malaria infection can regulate host m6A mRNA modification and reprogram host m6A mRNA methylome by mediating corresponding m6A catalytic enzyme levels. Our data suggested m6A modification as a significant transcriptome-wide mark during host-malaria interactions.

ORGANISM(S): Mus musculus

PROVIDER: GSE150546 | GEO | 2021/05/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome Survey of Malaria Parasite Liver Stages

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

2008-01-07 | GSE8125 | GEO

5-methylcytosine modification-mediated mRNA stabilization is associated with sexual development of malaria parasites [BisRNA-seq]

Project description:5-methylcytosine (m5C) is emerging as an important epi-transcriptome modification involving RNA stability and translation efficiency in various biological processes. However, it remains unclear how m5C contributes to the dynamic regulation of transcriptome during the development of Plasmodium. Here, we identified the presence of 5-methylcytosine (m5C) modification in rodent (P. yoelii) and human (P. falciparum) malaria parasites transcriptome and depicted a comprehensive characterization landscape of m5C mRNA modification at single-nucleotide resolution (RNA-BisSeq) from asexual replicating stage to gametocyte development. Through transcriptome-wide profiling of mRNA m5C modification, we found that m5C modified mRNA displayed higher stability than non-m5C modified mRNA during the development of Plasmodium. We identified Plasmodium ortholog of NSUN2 as an mRNA m5C methyltransferase in malaria parasites. LC–MS/MS and RNA-BisSeq analysis revealed a large decrease in mRNA m5C modification at transcriptome-wide level upon Nsun2 knockout. Absence of Nsun2 severely reduced gametocyte production in either rodent (P. yoelii) or human (P. falciparum) malaria parasites. Meanwhile, some genes related to gametocytogenesis displayed a great reduction of m5C modification. Together, our data provides comprehensive mRNA m5C profiles in Plasmodium genus and reveals m5C modification-mediated mRNA stability as a novel mechanism regulating sexual differentiation of a unicellular eukaryote.

2022-02-08 | GSE159126 | GEO

5-methylcytosine modification-mediated mRNA stabilization is associated with sexual development of malaria parasites [Half-life]

2022-02-08 | GSE159125 | GEO

5-methylcytosine modification-mediated mRNA stabilization is associated with sexual development of malaria parasites [RNA-seq]

2022-02-08 | GSE159124 | GEO

Strain-specific Innate Immune Signaling Pathways Determine Malaria Parasitemia Dynamics and Host Mortality

Project description:Malaria infection triggers vigorous host immune responses; however, the parasite ligands, host receptors and the signaling pathways responsible for these reactions remain unknown or controversial. Malaria parasites primarily reside within red blood cells (RBCs), thereby hiding themselves from direct contact and recognition by host immune cells. Host responses to malaria infection are very different from those elicited by bacterial and viral infections and the host receptors recognizing parasite ligands have been elusive. Here we investigated mouse genome-wide transcriptional responses to infections with two strains of Plasmodium yoelii (N67 and N67C) and discovered differences in innate response pathways corresponding to strain-specific disease phenotypes. Using in vitro RNAi gene knockdown and knockout mice, we demonstrated that a strong IFN-I response triggered by RNA Polymerase III and melanoma differentiation-associated protein 5 (MDA5), not Toll-like receptors (TLRs), binding of parasite DNA/RNA contributed to a decline of parasitemia in N67-infected mice. We showed that conventional dendritic cells were the major sources of early IFN-I, and that surface expression of phosphatidylserine (PS) on infected RBC (iRBC) might promote their phagocytic uptake, leading to the release of parasite ligands and the IFN-I response in N67 infection. In contrast, an elevated inflammatory response mediated by CD14/TLR and p38 signaling played a role in disease severity and early host death in N67C-infected mice. In addition to identifying cytosolic DNA/RNA sensors and signaling pathways previously unrecognized in malaria infection, our study demonstrates the importance of parasite genetic backgrounds in malaria pathology and provides important information for studying human malaria pathogenesis. Spleen RNA from mice, 4 days post infection with Plasmodium yoelii (strain N67 or N67C), or mock infection (N). Replicates from 6 individual mice per condition.

2014-01-13 | E-GEOD-51329 | biostudies-arrayexpress

Host cell transcripts during malaria liver stage infection reveals a coordinated and sequential set of biological events

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

Malaria parasite hijacks host complement C3 to facilitate its transmission

Project description:Host-derived factors are sucked into midgut of mosquitoes during natural malaria transmission, but their influence on malaria transmission is largely unknown. We reported that mouse complement C3 taken into mosquitoes significantly promoted malaria transmission either in laboratory or in field. This effect was attributed to the reduction of microbiota abundance in mosquito midgut by host-derived C3 through direct lyses the predominant symbiont bacteria Elizabethkingia anopheles. Elizabethkingia anopheles symbiont bacteria were demonstrated to be detrimental to malaria sexual stages in mosquitoes. Strikingly, the promoted effect of host C3 on malaria transmission was confirmed by laboratory mosquitoes membrane-feeding on Plasmodium falciparum. Therefore, we reveal a novel strategy of malaria parasite to utilize host complement C3 to promote its transmission, and the administration of C3 inhibitor would provide us a novel strategy to control malaria transmission.

2024-08-01 | GSE271070 | GEO

Interferon-mediated innate immune responses against malaria parasite liver stages

Project description:Identification of innate immune responses in the livers of mice infected with liver-stage arresting, transgenic, Plasmodium yoelii parasites.

2013-03-05 | GSE44831 | GEO

Extensive Transcriptional and Translational Regulation Occur During the Maturation of Malaria Parasite Sporozoites

Project description:These data were used to assess gene expression and dynamics between oocyst sporozoites and salivary gland sporozoites for both Plasmodium falciparum and Plasmodium yoelii.

2019-10-01 | GSE113582 | GEO

Inner membrane complex proteomics reveals a palmitoylation cascade regulating intraerythrocytic development of malaria parasite

Project description:Malaria is caused by infection of the erythrocytes by the parasites Plasmodium. Inside the erythrocytes, the parasites grow and multiply via schizogony, an unconventional cell division mode. The Inner Membrane Complex (IMC), an organelle located beneath the plasma membrane of the parasites, is essential for schizogony, serving as the platform for protein anchorage. However, the protein compositions of IMC and their localization determinants remain unclear. Here we used biotin ligase (TurboID)-based proximity labelling and quantitative mass spectrometry to compile the proteome of the schizont IMC of rodent malaria parasite Plasmodium yoelii. In total, the IMC proteome consisting of 488 proteins were identified. 19 of the 22 selected candidates were confirmed to localize in the IMC, indicating good reliability. In light of the existing palmitome of Plasmodium falciparum, 136 proteins of the P. yoelii IMC proteome are potentially palmitoylated. We further identified DHHC2 the major resident palmitoyl-acyl-transferase of the IMC. Conditional depletion of DHHC2 led to defective schizont segmentation and growth arrest in vitro and in vivo. DHHC2 was found to palmitoylate two critical IMC proteins CDPK1 and GAP45 for their IMC localization. In summary, this study reports a comprehensive inventory of P. yoelii IMC proteins and demonstrates a central role of DHHC2 governing IMC localization of proteins during the schizont development.

2022-07-01 | PXD028193 |

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data