Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA982578 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25036040_1.fastq.gz | Fastqsanger.gz | |||
| SRR25036040_2.fastq.gz | Fastqsanger.gz | |||
| SRR25036041_1.fastq.gz | Fastqsanger.gz | |||
| SRR25036041_2.fastq.gz | Fastqsanger.gz |
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Project description:The root of Vicatia thibetica de Boiss is a Chinese herb medicine with homology of medicine and food. We first report that HLB01 (the extract of Vicatia thibetica de Boiss root) extends lifespan and promotes healthy parameters in Caenorhabditis elegans (C. elegans). In doxorubicin-induced senescent mice, HLB01 counteracts senescence associated biomarkers significantly, including AST, ALT, p21 and γH2AX. Interestingly, HLB01 promotes the level of collagen in C. elegans and mammalian cell systemically, which might be one of the essential factors to exert anti-aging effects of HLB01. In addition, HLB01 can scavenge free radical to perform antioxidant ability. Lifespan extension of HLB01 also dependent on DAF-16 and HSF-1 to perform oxidative stress resistance and heat stress resistance. Taken together, these data indicate that HLB01 extends lifespan and healthspan of C. elegans, resists doxorubicin‐induced senescence in mice via collagen promoting, antioxidant and stress resistance.
2021-03-06 | GSE168322 | GEO
Project description:we used Caenorhabditis elegans as a model organism, to investigate the effect of mannose on the lifespan. Using nematode RNAi methods, RT-PCR, RNA-seq and other experimental method, we explored the possible mechanism for how mannose change the lifespan of Caenorhabditis elegans.
2023-09-01 | GSE192579 | GEO
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.
2017-04-20 | MODEL1704200000 | BioModels
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.
2017-04-20 | MODEL1704200001 | BioModels
Project description:Background: We here show that inhibitors of mitochondrial complex I promote physical activity, stress resistance as well as lifespan of Caenorhabditis elegans despite normal food uptake, i.e. in the absence of DR. Dietary restriction (DR) extends lifespan and promotes metabolic health in evolutionary distinct species. The RNA-seq data comprises 4 age groups (1, 5, 10 and 20 days after L4) and 2 different conditions (rotenone and normal feeding (DMSO)) Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2013-04-16 | GSE46051 | GEO
Project description:Background: We here show that inhibitors of mitochondrial complex I promote physical activity, stress resistance as well as lifespan of Caenorhabditis elegans despite normal food uptake, i.e. in the absence of DR. Dietary restriction (DR) extends lifespan and promotes metabolic health in evolutionary distinct species. The RNA-seq data comprises 4 age groups (1, 5, 10 and 20 days after L4) and 2 different conditions (rotenone and normal feeding (DMSO)) 22 samples: mRNA profiles of 1-day, 5-day and 10-day old worms as triplicates for each, rotenone and solvent control treatment; mRNA profiles of 20-day old worms as duplicates for each, rotenone and solvent control treatment
2013-04-16 | E-GEOD-46051 | biostudies-arrayexpress
Project description:To elucidate the molecular mechanism underlying lifespan reduction induced by PM2.5 exposure in Caenorhabditis elegans, we performed global gene expression profiling by RNA-sequencing technology, and compared the gene expression pattern change induced by PM2.5 exposure.
2023-02-22 | GSE214215 | GEO
Project description:The C. elegans lifespan in the presence of Bacillus licheniformis caused induction of a large number of genes associated with anti-aging activiy including beta-oxidation Inaddition, these results indicate the B. licheniformis enhances the lifespan of Caenorhabditis elegans through serotonin signaling
2015-11-05 | GSE63056 | GEO
Project description:Dietary restriction (DR) is the most effective and reproducible intervention to extend lifespan in divergent species1. In mammals, two regimens of DR, intermittent fasting (IF) and caloric restriction (CR), have proven to extend lifespan and reduce the incidence of age-related disorders2. An important characteristic of IF is that it can increase lifespan, even when there is little or no overall decrease in calorie intake2. The molecular mechanisms underlying IF-induced longevity, however, remain largely unknown. Here we establish an IF regimen that effectively extends the lifespan of Caenorhabditis elegans, and show that a nutrient-related signalling molecule, the low molecular weight GTPase Cel-Rheb, has a dual role in lifespan regulation; Cel-Rheb is required for the IF-induced longevity, whereas inhibition of Cel-Rheb mimics the CR effects. We also show that Cel-Rheb exerts its effects in part via the insulin/IGF-like signalling effector DAF-16 in IF, and that Cel-Rheb is required for fasting-induced nuclear translocation of DAF-16. We find that HSP-12.6, a DAF-16 target, functions to mediate the IF-induced longevity. Furthermore, our analyses demonstrate that most of fasting-induced upregulated genes require Cel-Rheb function for their induction, and that Cel-Rheb/Cel-TOR signalling is required for the fasting-induced downregulation of an insulin-like peptide, INS-7. These findings identify the essential role of signalling via Cel-Rheb in IF-induced longevity and gene expression changes, and suggest a molecular link between the IF-induced longevity and the insulin/IGF-like signalling pathway. Experiment Overall Design: We examined fasting-induced changes of the gene expression profiles in Caenorhabditis elegans. We performed the genome-wide analysis by using Affymetrix GeneChip oligonucleotide microarrays, and examined the effect of downregulation of Cel-Rheb and Cel-TOR by RNAi on the expression profiles. Five independent experiments were performed with wild type N2. Synchronized worms under six conditions (control-fed, control-fasting, Rheb RNAi-fed, Rheb RNAi-fasting, TOR RNAi-fed, and TOR RNAi-fasting) were collected and frozen with liquid nitrogen at day 4 of adulthood. Total RNA was extracted with Sepasol(R)-RNA â Super (Nacalai tesque), and purified with RNeasy Mini Kit (Qiagen), according to manufactureâs instructions. Synthesis of cDNA, in vitro transcription and biotin labelling cRNA, and hybridization to the C. elegans Genome Array (Affymetrix) were performed according to Affymetrix protocols. Hybridized arrays were scanned using an Affymetrix GeneChip Scanner. Scanned chip images were analyzed with GeneSpring GX 7.3.1 (Agilent Technologies).
2009-01-13 | E-GEOD-9682 | biostudies-arrayexpress
Project description:Suppression of Transcriptional Drift Extends C. elegans Lifespan by Postponing the Onset of Mortality
| PRJNA268148 | ENA