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Characterization of the genes that were regulated by infection with Malassezia furfur

ABSTRACT: In the present study, we investigated the pathogenicity of infection with Malassezia furfur using Caenorhabditis elegans as a model animal. The lifespan of the adult C. elegans infeted with Malassezia furfur was significantly longer than that of uninfected animals (control). Transcriptional profiling comparing infected- and uninfected animals suggested that genes related to the innate immunity were upregulated by infection with Malassezia furfur.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE260976 | GEO | 2025/03/06

REPOSITORIES: GEO

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Project description:Gebauer2016 - Genome-scale model of Caenorhabditis elegans metabolism (without bacteria) This model is one of the two versions of ElegCyc presented in the paper. It describes the metabolism of a worm raised in a medium without bacteria. This model is described in the article: A Genome-Scale Database and Reconstruction of Caenorhabditis elegans Metabolism. Gebauer J, Gentsch C, Mansfeld J, Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N, Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C. Cell Syst 2016 May; 2(5): 312-322 Abstract: We present a genome-scale model of Caenorhabditis elegans metabolism along with the public database ElegCyc (http://elegcyc.bioinf.uni-jena.de:1100), which represents a reference for metabolic pathways in the worm and allows for the visualization as well as analysis of omics datasets. Our model reflects the metabolic peculiarities of C. elegans that make it distinct from other higher eukaryotes and mammals, including mice and humans. We experimentally verify one of these peculiarities by showing that the lifespan-extending effect of L-tryptophan supplementation is dose dependent (hormetic). Finally, we show the utility of our model for analyzing omics datasets through predicting changes in amino acid concentrations after genetic perturbations and analyzing metabolic changes during normal aging as well as during two distinct, reactive oxygen species (ROS)-related lifespan-extending treatments. Our analyses reveal a notable similarity in metabolic adaptation between distinct lifespan-extending interventions and point to key pathways affecting lifespan in nematodes. This model is hosted on BioModels Database and identified by: MODEL1704200000. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:Gebauer2016 - Genome-scale model of Caenorhabditis elegans metabolism (with bacteria) This model is one of the two versions of ElegCyc presented in the paper. It describes the metabolism of a worm raised in a medium with bacteria This model is described in the article: A Genome-Scale Database and Reconstruction of Caenorhabditis elegans Metabolism. Gebauer J, Gentsch C, Mansfeld J, Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N, Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C. Cell Syst 2016 May; 2(5): 312-322 Abstract: We present a genome-scale model of Caenorhabditis elegans metabolism along with the public database ElegCyc (http://elegcyc.bioinf.uni-jena.de:1100), which represents a reference for metabolic pathways in the worm and allows for the visualization as well as analysis of omics datasets. Our model reflects the metabolic peculiarities of C. elegans that make it distinct from other higher eukaryotes and mammals, including mice and humans. We experimentally verify one of these peculiarities by showing that the lifespan-extending effect of L-tryptophan supplementation is dose dependent (hormetic). Finally, we show the utility of our model for analyzing omics datasets through predicting changes in amino acid concentrations after genetic perturbations and analyzing metabolic changes during normal aging as well as during two distinct, reactive oxygen species (ROS)-related lifespan-extending treatments. Our analyses reveal a notable similarity in metabolic adaptation between distinct lifespan-extending interventions and point to key pathways affecting lifespan in nematodes. This model is hosted on BioModels Database and identified by: MODEL1704200001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Characterization of the genes that were regulated by infection with Malassezia furfur

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