Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA343331 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:C-type lectin-like domain (CTLD) encoding genes are highly diverse in C. elegans, comprising a clec gene family of 283 members. Since vertebrate CTLD proteins have characterized functions in defense responses against pathogens and since expression of C. elegans clec genes is pathogen-dependent, it is generally assumed that clec genes function in C. elegans immune defenses. In this study we challenged this assumption and focused on the C. elegans clec gene clec-4, whose expression is highly upregulated upon infection with various pathogens. We tested the involvement of clec-4 in the defense response to infection with Pseudomonas aeruginosa PA14, Bacillus thuringiensis BT18247, and the natural pathogen Serratia rubidaea MYb237. Contrary to our expectation clec-4(ok2050) mutant worms were not more susceptible to pathogen infection than wildtype worms. To explore potential redundant function between different C. elegans clec genes, we investigated expression of several clec-4 paralogs, finding that clec-4, clec-41, and clec-42 expression shows similar infection-dependent changes and co-localizes to the intestine. We found that only clec-42 is required for the C. elegans defense response to BT18247 infection and that clec-4 genetically interacts with clec-41 and clec-42. The exact role of clec-4 in pathogen defense responses however remains enigmatic. Our results further indicate that a complex interplay between different clec genes regulates C. elegans defense responses.
2019-12-31 | GSE110913 | GEO
Project description:The neuronal G protein-coupled receptor NMUR-1, a homolog to the mammalian neuromedin U receptor, has been implicated in the specificity of Caenorhabditis elegans innate immune response against pathogen infections. NMUR-1 controls C. elegans transcription activity by regulating transcription factors, which, in turn control the expression of distinct defense genes. This study further investigates the role of NMUR-1 at the protein level in regulating innate immune responses against pathogens Salmonella enterica and Enterococcus faecalis by utilizing mass spectrometry-based quantitative proteomics. We found that NMUR-1 regulates a class of proteins responsible for transmembrane transport during infection. Specifically, a group of proteins forming F1FO ATP synthase responsible for ATP biosynthesis is downregulated in NMUR-1 loss of function mutants during both S. enterica and E. faecalis infections. ATP measurements further revealed that nmur-1 mutants have reduced ATP production in response to both S. enterica and E. faecalis infections. Functional assays demonstrated that inhibiting F1FO ATP synthase using RNA interference or chemical modification mimicked the survival phenotypes of the untreated nmur-1 knockout mutants on S. enterica and E. faecalis. These findings provide valuable insights into the mechanism by which NMUR-1 regulates energy homeostasis at the protein level as part of an innate immune response against specific pathogens.
2025-10-02 | PXD045826 | Pride
Project description:piRNA expression regulates pathogenesis in a Caenorhabditis elegans model of Lewy body disease
| PRJNA622394 | ENA
Project description:Expression analysis of C. elegans genes kin-1 and crh-1 mutant
| PRJNA175021 | ENA
Project description:Expression analysis of C. elegans genes daf-9 and daf-12 mutant
| PRJNA177847 | ENA
Project description:Tocotrienol Rich Fraction (TRF) Modulates Genes Expression in Oxidative Stress-Induced Caenorhabditis elegans
| PRJNA393168 | ENA
Project description:Determination of nutrient-responsive genes in C. elegans
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Project description:C. elegans immune response to Staphylococcus aureus, 4 hour exposure
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Project description:Yilmaz2016 - Genome scale metabolic model -
Caenorhabditis elegans (iCEL1273)
This model is described in the article:
A Caenorhabditis elegans
Genome-Scale Metabolic Network Model.
Yilmaz LS, Walhout AJ.
Cell Syst 2016 May; 2(5): 297-311
Abstract:
Caenorhabditis elegans is a powerful model to study
metabolism and how it relates to nutrition, gene expression,
and life history traits. However, while numerous experimental
techniques that enable perturbation of its diet and gene
function are available, a high-quality metabolic network model
has been lacking. Here, we reconstruct an initial version of
the C. elegans metabolic network. This network model
contains 1,273 genes, 623 enzymes, and 1,985 metabolic
reactions and is referred to as iCEL1273. Using flux balance
analysis, we show that iCEL1273 is capable of representing the
conversion of bacterial biomass into C. elegans biomass
during growth and enables the predictions of gene essentiality
and other phenotypes. In addition, we demonstrate that gene
expression data can be integrated with the model by comparing
metabolic rewiring in dauer animals versus growing larvae.
iCEL1273 is available at a dedicated website
(wormflux.umassmed.edu) and will enable the unraveling of the
mechanisms by which different macro- and micronutrients
contribute to the animal's physiology.
This model is hosted on
BioModels Database
and identified by:
MODEL1604210000.
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2016-11-03 | MODEL1604210000 | BioModels
Project description:LIN-42, the Caenorhabditis elegans PERIOD homolog, negatively regulates microRNA transcription
| PRJNA251425 | ENA