Viral factors inhibit TOR pathway
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB29401 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2860625_1.fastq.gz | Fastqsanger.gz | |||
| ERR2860625_2.fastq.gz | Fastqsanger.gz | |||
| ERR2860626_1.fastq.gz | Fastqsanger.gz | |||
| ERR2860626_2.fastq.gz | Fastqsanger.gz | |||
| ERR2860627_1.fastq.gz | Fastqsanger.gz |
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Project description:Polydnaviruses (PDVs) are obligate symbionts of endoparasitoid wasps, which exclusively attack the larval stages of their lepidopteran hosts. The Polydnavirus is injected by the parasitoid female during oviposition to selectively infect host tissues by the expression of viral genes without undergoing replication. Toxoneuron nigriceps bracovirus (TnBV) is associated with Toxoneuron nigriceps (Hymenoptera: Braconidae) wasp, an endoparasitoid of the tobacco budworm larval stages, Heliothis virescens (Lepidoptera: Noctuidae). Previous studies showed that TnBV is responsible for alterations in host physiology. The arrest of ecdysteroidogenesis is the main alteration which occurs in last (fifth) instar larvae and, as a consequence, prevents pupation. TnBV induces the functional inactivation of H. virescens prothoracic glands (PGs), resulting in decreased protein synthesis and phosphorylation. Previous work showed the involvement of the PI3K/Akt/TOR pathway in H. virescens PG ecdysteroidogenesis. Here, we demonstrate that this cellular signaling is one of the targets of TnBV infection. Western blot analysis and enzyme immunoassay (EIA) showed that parasitism inhibits ecdysteroidogenesis and the phosphorylation of the two targets of TOR (4E-BP and S6K), despite the stimulation of PTTH contained in the brain extract. Using a transcriptomic approach, we identified viral genes selectively expressed in last instar H. virescens PGs, 48 h after parasitization, and evaluated expression levels of PI3K/Akt/TOR pathway genes in these tissues. The relative expression of selected genes belonging to the TOR pathway (tor, 4e-bp, and s6k) in PGs of parasitized larvae was further confirmed by qRT-PCR. The down-regulation of these genes in PGs of parasitized larvae supports the hypothesis of TnBV involvement in blocking ecdysteroidogenesis, through alterations of the PI3K/Akt/TOR pathway at the transcriptional level.
| S-EPMC6275226 | biostudies-literature
Project description:gnp_blan06_torpten - rnai tor time course - The impact of the TOR pathway on growth and stress responses. Modification of translational and transcriptional profiles in Tor-inducible RNAi mutants and identification of TOR targets.
2011-01-07 | GSE25701 | GEO
Project description:ra03-07_tor - tor - Study of 2 TOR mutants (7817 Strong, 7846 weak) - Mutant vs wild type on different nitrogen conditions (10mM=control and 100uM) Keywords: treated vs untreated comparison,wt vs mutant comparison
2007-06-20 | GSE7987 | GEO
Project description:gnp_blan06_torpten - rnai tor time course - The impact of the TOR pathway on growth and stress responses. Modification of translational and transcriptional profiles in Tor-inducible RNAi mutants and identification of TOR targets. 28 dye-swaps - normal vs. rnai mutant comparison.
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Project description:fapesp-bra-inra-10-01_bioen_hypocotyl - dark hypocotyls tor rnai - Transcriptional comparison between 2 TOR RNAi mutants versus GUS control. - Sowing after 24h imbibition at 4°C in the dark, on MS1/5, no sucrose, 10 mM ethanol, 8 g/l agar, vertical growth with 3h light, 6 days growth in the dark (20°C), hypocotyls were harvested under green light ; cotyledons and root were removed.
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Project description:gnp_blan06_torpten - overexpression of pten2a - The impact of the TOR pathway on growth and stress responses. - Comparaison control versus overexpressor. The overexpressor has a male phenotype of sterility.
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Project description:gnp_blan06_torpten - overexpression of pten2a - The impact of the TOR pathway on growth and stress responses. - Comparaison control versus overexpressor. The overexpressor has a male phenotype of sterility. 3 dye-swap - gene knock in (transgenic)
2010-11-30 | E-GEOD-24902 | biostudies-arrayexpress
Project description:The Tor kinase is one of the major regulatory nodes in a eukaryotic cell and until now, little is known about this kinase in filamentous fungi. Here, we analysed the Tor kinase in Aspergillus fumigatus, which is the most important airborne fungal pathogen of humans and the main causative agent of invasive aspergillosis. Because deletion of the single tor gene of A. fumigatus was apparently lethal, we generated a conditional lethal tor mutant. This was achieved by fusing the tor gene with the inducible xylose promoter and replacing the endogenous tor gene by the inducible xylp-tor gene cassette. The generated transgenic strain opened up the possibility to activate or silence the tor gene under controlled conditions. Since we did not observe any effect of rapamycin on Tor of A. fumigatus, the generation of the inducible Tor gene was even more valuable for an in-depth analysis of the Tor kinase. By LC-MS/MS analyses of mycelial proteins we identified the regulatory network of Tor. Tor controls a variety of genes and proteins involved in nutrient sensing, stress response, cell cycle progression, protein biosynthesis and degradation. Tor is a major kinase responsible for protein import into the mitochondria, and consequently responsible for the correct function of most processes occurring into these organelles, e.g. respiration and ornithine metabolism. Regulation of iron acquisition by Tor was found to be independent of the HapX transcription factor.
2022-02-28 | PXD001601 | Pride
Project description:The target of rapamycin (TOR) pathway is an evolutionarily conserved signal transduction system that is activated by varying nutrient and environmental signals and governs a plethora of eukaryotic biological processes, but its role in Cryptococcus neoformans remains elusive. In this study, we investigated the TOR pathway by functionally characterizing two Tor-like kinases, Tor1 and Tlk1, in C. neoformans. We successfully deleted TLK1, but not TOR1. TLK1 deletion did not result in any evident in vitro phenotypes, suggesting that Tlk1 is mainly dispensable for the growth of C. neoformans. We further demonstrated that Tor1, but not Tlk1, is essential and the target of rapamycin by constructing and analyzing conditionally regulated strains and sporulation analysis of heterozygous mutants in the diploid strain background. To analyze the functions of Tor1 in more detail, we constructed constitutive TOR1 overexpression strains. Tor1 negatively regulated thermotolerance and the DNA damage response, which are two important virulence factors of C. neoformans. We also found that TOR1 overexpression reduced Mpk1 phosphorylation, which is required for cell wall integrity and thermoresistance, and Rad53 phosphorylation, which governs the DNA damage response pathway. Tor1 is localized to the cytoplasm but enriched in the vacuole membrane. Phosphoproteomics and transcriptomics revealed that Tor1 regulates a variety of biological processes, including metabolic processes, cytoskeleton organization, ribosome biogenesis, autophagy, and stress response. TOR inhibition by rapamycin caused actin depolarization in a Tor1-dependent manner. Finally, screening rapamycin-sensitive and -resistant kinase and transcription factor mutants revealed that the TOR pathway may crosstalk with a number of signaling pathways, including the Hog1 pathway. In conclusion, our study demonstrates that a single Tor1 kinase plays a variety of roles in the fungal meningitis pathogen C. neoformans.
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