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ABSTRACT:
PROVIDER: PRJNA1285594 | ENA |
REPOSITORIES: ENA
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Project description:Infection of Pseudomonas donghuensis HYS strain and its fur deletion mutant in Caenorhabditis elegans was conducted to assess changes in the expression profile of Caenorhabditis elegans, and potential core virulence factors were identified by measuring the gene expression levels of the HYS colonizing the nematode's intestine. Preliminary studies indicate that P. donghuensis HYS exhibits significant toxicity towards Caenorhabditis elegans, yet the underlying mechanisms of this pronounced toxicity remain unclear. Previous work identified several virulence factors contributing to the toxicity of HYS through detection and functional validation; however, the molecular mechanisms responsible for its strong toxicity have not been elucidated. Therefore, we aim to analyze the mechanisms underlying HYS's pronounced toxicity by examining the responses of infected Caenorhabditis elegans. The Ferric uptake regulator (Fur) is responsible for maintaining iron homeostasis in Gram-negative bacteria, and given that HYS possesses a greater iron uptake capacity than other common species in the same genus, such as Pseudomonas aeruginosa, we hypothesize that Fur may play a critical role in the strong toxicity exhibited by HYS. Consequently, we infected Caenorhabditis elegans with both HYS and its fur deletion mutant and analyzed the changes in the expression profile of Caenorhabditis elegans. We observed a significant reduction in toxicity following the deletion of fur, indicating that Fur regulates core virulence factors. To identify these core virulence factors, we conducted transcriptomic sequencing of the pathogenic bacteria under various conditions and performed a screening for virulence factors.
2025-06-04 | GSE291743 | GEO
Project description:Iron overload, characterized by accumulation of iron in tissues, induces a multiorgan toxicity whose mechanisms are not fully understood. Using cultured cell lines, Caenorhabditis elegans, and mice, we found that ferroptosis occurs in the context of iron-overload-mediated damage. Exogenous oleic acid protected against iron-overload-toxicity in cell culture and Caenorhabditis elegans by suppressing ferroptosis. In mice, oleic acid protected against FAC-induced liver lipid peroxidation and damage. Oleic acid changed the cellular lipid composition, characterized by decreased levels of polyunsaturated fatty acyl phospholipids and decreased levels of ether-linked phospholipids. The protective effect of oleic acid in cells was attenuated by GW6471 (a PPAR-? antagonist), as well as in Caenorhabditis elegans lacking the nuclear hormone receptor NHR-49 (a PPAR-? functional homologue). These results highlight ferroptosis as a driver of iron-overload-mediated damage, which is inhibited by oleic acid. This monounsaturated fatty acid represents a potential therapeutic approach to mitigating organ damage in iron overload individuals.
2025-05-06 | PXD045642 | Pride
Project description:Iron overload, characterized by accumulation of iron in tissues, induces a multiorgan toxicity whose mechanisms are not fully understood. Using cultured cell lines, Caenorhabditis elegans, and mice, we found that ferroptosis occurs in the context of iron-overload-mediated damage. Exogenous oleic acid protected against iron-overload-toxicity in cell culture and Caenorhabditis elegans by suppressing ferroptosis. In mice, oleic acid protected against FAC-induced liver lipid peroxidation and damage. Oleic acid changed the cellular lipid composition, characterized by decreased levels of polyunsaturated fatty acyl phospholipids and decreased levels of ether-linked phospholipids. The protective effect of oleic acid in cells was attenuated by GW6471 (a PPAR- antagonist), as well as in Caenorhabditis elegans lacking the nuclear hormone receptor NHR-49 (a PPAR- functional homologue). These results highlight ferroptosis as a driver of iron-overload-mediated damage, which is inhibited by oleic acid. This monounsaturated fatty acid represents a potential therapeutic approach to mitigating organ damage in iron overload individuals.
2023-10-02 | GSE243891 | GEO
Project description:Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans
| PRJNA144879 | ENA
Project description:Nucleus-Independent Transgenerational Small RNA Inheritance in Caenorhabditis elegans
| PRJNA1018494 | ENA
Project description:Biomolecular condensates, such as stress and germ granules, often contain sub-compartments. For instance, the Caenorhabditis elegans germ granule, which localizes near the outer nuclear membrane of germ cell nuclei, is composed of at least four ordered compartments, each housing distinct sets of proteins and RNAs. How these compartments form and why they are spatially ordered remains poorly understood. Here, we show that the conserved RNA helicase DDX-19 defines another compartment of the larger C. elegans germ granule, which we term the D compartment. The D compartment exhibits properties of a liquid condensate and forms between the outer nuclear pore filament and other compartments of the germ granule. Two nuclear pore proteins, NPP-14 and GLEL-1, are required for its formation, suggesting that the D compartment localizes adjacent to the outer nuclear membrane via interactions with the nuclear pore. The loss of DDX-19, NPP-14, or GLEL-1 leads to functional defects, including aberrant formation of the other four germ granule compartments, a loss of germline immortality, and dysregulation of small RNA-based transgenerational epigenetic inheritance programs. Hence, we propose that a function of the D compartment is to anchor larger germ granules to nuclear pores, enabling germ granule compartmentalization and promoting transgenerational RNA surveillance.
2025-02-09 | PXD056752 | Pride
Project description:Effective toxicological testing of the vast number of new and existing chemicals currently in use will require efficient and cost effective methods. We evaluated the utility of a simple, low cost toxicity testing system employing the nematode Caenorhabditis elegans to identify toxicologically relevant changes in gene expression. Dichlorvos and fenamiphos, which are organophosphorous pesticides that inhibit acetylcholinesterase were chosen as model toxicants to test the usefulness of the C. elegans toxicity testing system, and mefloquine, which appears to perturb neuronal Ca++ homeostasis, provided an out-group for analysis. Keywords: gene expression array-based (RNA / in situ oligonucleotide)
2009-06-03 | GSE12298 | GEO