Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1208452 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Virulence is a key trait under selection during host-parasite coevolution. In order to obtain increased fitness, parasites are predicted to increase their ability to circumvent and overcome host immunity. A particular challenge for pathogens are external immune systems, found among various invertebrates. Such external immune systems are chemical defence systems comprised of highly potent antimicrobial compounds released by prospective hosts into the environment. We carried out a coevolution experiment with the entomopathogenic fungus, Beauveria bassiana, and the red flour beetle, Tribolium castaneum, which has a well-documented external immune system. Surprisingly, after just seven transfers of experimental evolution we saw a significant increase in virulence in all B. bassiana. This increase in virulence was mainly the result of the B. bassiana isolates evolving resistance to the external immune defences of the T. castaneum beetles, but not obviously through the increased production of toxins or other harmful substances. Furthermore, transcriptomic analyses of B. bassiana RNA-seq data implicates up-regulation of genes responsible for resistance to oxidative stress underlying the observed resistance. We conclude that external immunity acts as a powerful selective force for virulence evolution, with an increase in virulence being achieved apparently entirely by overcoming these defences, most likely due to elevated oxidative stress resistance.
2017-03-09 | GSE71570 | GEO
Project description:EtROP2 is a virulence determinant produced by Eimeria tenella in host cells, during and early after cell invasion. We compared transcriptomic analyses of avian cells transfected either by control plasmid or by plasmid allowing EtROP2 expression. We used an avian epithelial cell model developed in our lab (Clec213). Transfected avian cells were FACS sorted by fluorescent marker in order to reduce background noise from non-transfected cells. This analysis allowed us to assess EtROP2 effect on host cell transcription and possibly identify host signalling pathways modified by the parasite. These signalling pathways will pave the way to the identification of potential host protein targeted by parasite virulence factors.
2023-05-26 | GSE205391 | GEO
Project description:The most severe form of human malaria is caused by Plasmodium falciparum. Its virulence is closely linked to the increase in rigidity and cytoadhesion of infected erythrocytes, which obstruct blood flow to vital organs. Unlike other human-infecting Plasmodium species, P. falciparum exports a family of 18 ‘FIKK’ serine/threonine kinases into the host cell. We reveal substantial species-specific phosphorylation of erythrocyte proteins by P. falciparum, but not by Plasmodium knowlesi, which does not export FIKK kinases. By systematic deletion of all FIKK kinases combined with large-scale quantitative phosphoproteomics we identify unique phosphorylation fingerprints for each kinase, including phosphosites on parasite virulence factors and host cell proteins. Despite their non-overlapping target sites, a network analysis reveals that some FIKKs may act in the same pathways. Only deletion of the non-exported kinase FIKK8 resulted in reduced parasite growth, suggesting the exported FIKKs may support functions important for survival within the host. We show that one kinase, FIKK4.1, mediates both cytoskeletal rigidification and trafficking of the adhesin and key virulence factor PfEMP1 to the host cell surface. This establishes the FIKK family as important drivers of parasite evolution and malaria pathology.
2020-04-17 | PXD015833 | Pride
Project description:Toxoplasma gondii is an obligate intracellular protozoan parasite which, upon invasion of host cells, injects virulence factors that are known to induce dramatic alterations in host cell signaling. Although much work has been directed at understanding the impact of specific secreted proteins on host cell function, dissecting the host response to injected virulence factors has been complicated by the fact that injection is rapidly followed by invasion, establishment of a parasitophorous vacuole in the host cell cytoplasm, secretion of parasite proteins from other specialized organelles, and remodeling of the host cell cytoskeleton Here, we describe the global macrophage transcriptional response to secreted proteins and show that injection of rhoptry contents alone is sufficient to trigger a dramatic host cells response. We further define modules of genes that are regulated in a parasite strain-specific manner by activation of the host transcription factor, STAT6. Our approach leverages transgenic parasites that express mCherry and inject Cre-recombinase along with normal virulence factors into the cytoplasm of host cells. Primary macrophages were recovered from transgenic reporter mice (Ai6) that express the ZsGreen1 fluorochrome when exposed to cre recombinase, allowing for the identification of a unique population of cells into which T. gondii injects virulence factors but does not infect (uninfected-injected, or U-I). Transcriptional profiling of these U-I cells compared to infected cells or uninfected controls from the same cultures was carried out, using bone marrow derived macrophages (BMDM) from either WT or STAT6-/- mice. This data allows us to interrogate the outcomes T. gondii induced STAT signaling in both infected and U-I cell populations, and to resolve effects of injected virulence factors, like ROP16, from those changes induced by infection.
2019-03-01 | GSE55892 | GEO
Project description:Parasites are strong drivers of evolutionary change and the genetic variation of both host and parasite populations can co-evolve as a function of the parasite's virulence and the host's immune resistance. The role of transcriptome variation in specific interactions between host and parasite genotypes has been less studied and can be confounded by high genotypic variability in natural populations. We have analysed gene expression between two inbred lines of a self-fertilising fish experimentally infected with a parasite under controlled conditions, in order to estimate the role of the genotype in the transcriptome responses to infection using RNA-seq.
2018-02-14 | GSE101084 | GEO
Project description:Toxoplasma gondii secretes various virulence effector molecules into host cells to disrupt host interferon-γ (IFN-γ)-dependent immunity. Among the effectors, ROP18 directly phosphorylates and inactivates IFN-inducible GTPases, such as immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs), leading to subversion of IFN-inducible GTPase-induced cell-autonomous immunity. The modes of action of ROP18 have been studied extensively; however, little is known about the molecular mechanism of how ROP18 is produced in the parasite itself. Here, we report a role of T. gondii transcription factor IWS1 in ROP18 mRNA expression in the parasite. Compared with wild-type virulent type I T. gondii, IWS1-deficient parasites showed dramatically increased loading of IRGs and GBPs onto the parasitophorous vacuole membrane (PVM). Moreover, IWS1-deficient parasites displayed decreased virulence in wild-type mice but retained normal virulence in mice lacking the IFN-γ receptor. Furthermore, IWS1-deficient parasites showed severely decreased ROP18 mRNA expression. Ectopic expression of ROP18 in IWS1-deficient parasites restored the decreased loading of effectors onto the PVM and in vivo virulence in wild-type mice. Taken together, these data demonstrate that T. gondii IWS1 regulates ROP18 mRNA expression to determine fitness in IFN-γ-activated host cells and mice.
2023-01-30 | GSE204926 | GEO
Project description:The development and outcome of cerebral malaria (CM) reflects a complex interplay between parasite-expressed virulence factors and host response to infection. To simultaneously analyze transcriptional programs in both parasite and host over the course of infection, we created microarrays to concurrently detect transcripts in the genomes of both Plasmodium berghei and mouse. Analysis of RNA from brain, lung, liver, and spleen of mice infected with P. berghei ANKA showed that parasite gene expression is readily detected in whole organ RNA. Comparison of CM-susceptible (C57BL/6) and CM-resistant (BALB/c) mice showed that both host and parasite display distinct organ-specific transcriptional signatures in susceptible versus resistant animals. Host genes whose expression differs between CM-resistant and CM-susceptible mice, at either baseline or induced by infection, tend to relate to humoral and immune response, complement activation, or cell-cell interactions, suggesting differences in immune function that may directly underlie protection from or susceptibility to CM. P. berghei, in contrast, displayed differential expression of genes related to apparent biosynthestic activities, with the majority of transcriptional activity observed in the lung. These data show that analysis of host and parasite gene expression profiles by hybridizing infected host samples to a single microarray is feasible, and can facilitate dissection of complex host-pathogen interactions. Keywords: Time course, Disease state analysis
2006-11-24 | GSE5672 | GEO
Project description:High temperature events can disrupt species interactions, including those among hosts, symbionts, and natural enemies. Understanding the genetic and physiological processes underlying these disruptions is a critical scientific challenge in this era of anthropogenic climate change. We explore how high temperatures disrupt the interactions among an herbivorous insect host, Manduca sexta, its insect parasitoid, Cotesia congregata, and the parasitoid’s symbiotic virus. In this system, high temperatures kill developing parasitoids, but not hosts. We evaluated the physiological and transcriptomic causes of thermal mismatch in ecological interactions using parasitoid egg in vitro experiments, immunological assays, and RNAseq. We found that high temperatures disrupt the capacity of the parasitoid’s symbiotic virus to immunosuppress the host insect, resulting in thermal mismatch and death of the parasitoid. At the transcriptomic level, key viral genes involved in suppressing host immune pathways showed reduced expression, driven by the virus’s circular genomic structure. This work is among the first to demonstrate the genetic and physiological mechanisms by which a symbiont limits the ecological functioning of host-parasite dynamics, and provides a framework for understanding how molecular processes give rise to ecological outcomes in response to high temperature events caused by climate change.
2024-08-04 | GSE273477 | GEO
Project description:The normally virulent type-I RH parasite is rendered avirulent when lacking ROP5. The avirulent phenotype is a consequence of interaction with the host innate immune system. We sought to understand if ROP5 alters host gene expression in order to escape host defenses. We saw no gene expression differences between host cells infected with wt (RH∆ku80) or RH∆ku80∆rop5 parasites. We have included uninfected HFF samples that were harvested in parallel with the infected samples.
2012-09-13 | GSE32104 | GEO
Project description:We have 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). Here we are repeating the experiment but using a more virulent strain of the parasite: P. chabaudi CB, to study further how mosquito transmission regulates parasite virulence. 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/
2014-08-27 | E-ERAD-289 | biostudies-arrayexpress