Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence and absence of arsenite
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE46257 | GEO | 2013/04/23
SECONDARY ACCESSION(S): PRJNA198476
REPOSITORIES: GEO
Similar Datasets
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls 4 samples: 2 mRNA profiles of C.elegans 48h after L4 exposed to Arsenite; 2 mRNA profiles of C.elegans 48h after L4 as controls (H20). The N2 wild type (var. Bristol) strain was used.
2013-04-23 | E-GEOD-46257 | biostudies-arrayexpress
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. Worms were exposed to 100nM Arsenite 48h after L4. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2021-10-19 | GSE110845 | GEO
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: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:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species. 24 samples: 12 mRNA profiles of C.elegans: 6 without GlcN and 6 with GlcN supplementaion; 12 mRNA profiles of M.musculus: 6 without GlcN and 6 with GlcN supplementaion
2014-03-07 | E-GEOD-54853 | biostudies-arrayexpress
Project description:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species.
2014-03-07 | GSE54853 | GEO
Project description:Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ.
2012-02-03 | GSE35360 | GEO
Project description:Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. The global transcriptome was compared in Caenorhabditis elegans mutant strain GE24, pha-1(e2123) exposed to 0, 0.2 and 2.0 mM HuminFeed® (HF) or Huminfeed-Hydroquinone (HF-HQ). Nematodes were harvested as 3 or 11 day old adults (for HF) or 3 day old adults (for HF-HQ).
2012-02-03 | E-GEOD-35360 | biostudies-arrayexpress
Project description:The potential environmental risk of single-walled carbon nanotubes (SWCNTs) is evaluated using Caenorhabditis elegans (C. elegans) as an ecotoxicological animal model. Highly soluble amide-modified SWCNTs (a-SWCNTs) are used in the present study so that the dose-response impact of SWCNTs could be studied. mechanisms. a-SWCNTs are efficiently taken up by worms during feeding and cause significant toxicity in worms, including retarded growth, shortened lifespan and defective embryogenesis. Genome-wide gene expression analysis is performed to investigate the toxic molecular We examined the effect of different concentrations of a-SWCNTs (0, 100, 250 and 500 μg/mL) on the growth of C. elegans. We measured the body length of worms reaching the L4 stage after a-SWCNT exposure for 48 hr at 22°C. Compared to the untreated worms, we found that the average length of worms exposed to a-SWCNTs (500 μg mL-1) was significantly shorter than the untreated groups. In addition, the dose of a-SWCNTs also caused retarded growth, reduced lifespan and defective embryogenesis in worms. Genome-wide gene expression analysis using an Affymetrix GeneChip was performed to further investigate the molecular basis of these defects.
2012-10-11 | E-GEOD-41486 | biostudies-arrayexpress
Project description:Sirtuins, a family of histone deacetylases, have a fiercely debated role in regulating lifespan of different species. Contrasting recent observations, we here find that overexpression of sir-2.1, the orthologue of mammalian SirT1, does extend C. elegans lifespan. Sirtuins are known to convert NAD+ into nicotinamide (NAM). We here find that NAM and its metabolite, 1-methylnicotinamide (MNA), extend C. elegans lifespan, also in the absence of sir-2.1. Consistently, impairment of sir-2.1 prevents extension of lifespan by nicotinic acid (NA), a NAD+ precursor. Taken together, sirtuins extend lifespan by promoting formation of MNA to generate a phase I - mediated ROS signal, providing an unexpected mechanistic role for sirtuins beyond histone deacetylation. 9 samples: 3 mRNA profiles of C.elegans 48h after L4 exposed to nicotinic acid; 3 mRNA profiles of C.elegans 48h after L4 exposed to 1-MNA; 3 mRNA profiles of C.elegans 48h after L4 as controls (H20)
2013-08-09 | E-GEOD-49662 | biostudies-arrayexpress