Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression Data of Reactive Oxygen Species Signalling in C. elegans

ABSTRACT: We have shown that worms that possess mutations in two electron transport chain subunits live longer due to mtROS signalling. Wild type worms can also live longer by treatment with the pro-oxidant paraquat. Paraquat treatment is not additive to the mutations in the ETC subunits. We aimed to determine the underlying changes in gene expression that were common to both paraquat treatment and the two mutations. We also have shown genetically that the mtROS signal that leads to extended lifespan is dependent on CED-4. We generated double mutants that lack functional CED-4 with the two mutations in the ETC subunits. We have found that a large number of gene expression changes by mtROS signalling are reverted by loss of CED-4. Young adult C. elegans were grown using a 4-hour synchronized lay and harvested by hand picking. At least three biological repeats were obtained for each condition. Worm RNA was extracted and prepared for hybridization to Affymetrix chips. We compared the gene expression patterns of genetic mutants and the wild type treated with paraquat all against a wild type control. We sought to obtain a common pattern of expression between two genetic mutants, isp-1 and nuo-6, and paraquat treatment.

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Siegfried Hekimi

PROVIDER: E-GEOD-54024 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression Data of Reactive Oxygen Species Signalling in C. elegans

Project description:We have shown that worms that possess mutations in two electron transport chain subunits live longer due to mtROS signalling. Wild type worms can also live longer by treatment with the pro-oxidant paraquat. Paraquat treatment is not additive to the mutations in the ETC subunits. We aimed to determine the underlying changes in gene expression that were common to both paraquat treatment and the two mutations. We also have shown genetically that the mtROS signal that leads to extended lifespan is dependent on CED-4. We generated double mutants that lack functional CED-4 with the two mutations in the ETC subunits. We have found that a large number of gene expression changes by mtROS signalling are reverted by loss of CED-4.

2014-05-08 | GSE54024 | GEO

Proteome dysregulation induced by 5-fluoro-2′-deoxyuridine (FUdR) in C. elegans

Project description:The effect of 5-fluoro-2′-deoxyuridine (FUdR) on the proteome of C. elegans (wild type and glp-1/skn-1 mutants) was studied. Total protein extracts were obtained from the wild type and mutant worms subjected to the FUdR or control treatment and relative protein levels assessed by shotgun proteomics (TMT).

2024-07-18 | PXD045805 | Pride

One-day thermal regime extends lifespan

Project description:Environmental factors such as temperature can modulate animal’s lifespan. However, the underlying mechanisms remain largely undefined. Through proteomic analysis of C. elegans at different time points (young adult, middle age, and old age) and under two temperature conditions (20°C and 25°C), we found that temperature affects C. elegans lifespan largely by modulating the proteostasis. Surprisingly, although animals live shorter at the higher temperature, we found that worms cultured at 25°C for one day at early adulthood promotes the protein homeostasis by decreasing the synthesis and increasing the degradation, suggesting the beneficial effects. Consistent with the finding, animals shifting from 20°C to 25°C for 24 hours between the larval L4 to adult Day 3 stages indeed live longer and are more resistant to stresses. Furthermore, we found that the one-day thermal induced lifespan extension is mediated by the FOXO transcriptional factor DAF-16. These results reveal an unexpected and complicated mechanism underlying the temperature effects on aging, which could potentially aid to develop strategies for treating aging related diseases.

2023-03-11 | PXD024916 | Pride

Investigating impacts of mycothiazole and its synthetic derivative on mitochondrial function and aging in C. elegans

Project description:Small molecule inhibitors of mitochondrial electron transport chain (ETC) hold significant promise in the field of mitochondrial research and aging biology. In this study, we studied two molecules: mycothiazole (MTZ) - isolated from the marine sponge P. mycofijiensis and its semisynthetic acetylated derivative 8-O-acetylmycothiazole (8-OAc) as efficient alternatives for their high efficiency to inhibit ETC complex I function. Similar to rotenone, a widely used complex I inhibitor, these two compounds showed anticancer activity and strikingly demonstrate a lack of toxicity to non-cancer cells, a highly beneficial feature in the development of anti-cancer therapeutics. Furthermore, experiments with these small molecules in vivo utilizing C.elegans demonstrate their additional utilization to aging studies. We observed that both molecules have the ability to induce a mitochondria-specific unfolded protein response (UPRMT) pathway, which extends lifespan of worms when applied in their adult stage. Interestingly, we also found that these two molecules employ different pathways to extend lifespan in worms, where MTZ utilize the transcription factors, ATFS-1 and HSF-1, which are involved in the UPRMT and heat shock response (HSR) pathways, respectively. In opposition,8-OAc only required HSF-1 and not ATFS-1. This observation elucidates an important insight into the functional roles of various protein subunits of ETC complexes and their regulatory mechanisms associated with aging.

2024-01-01 | E-MTAB-13546 | biostudies-arrayexpress

Transcription profiling of C. elegans wildtype and gas-1 mitochondrial mutants

Project description:Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. Experiment Overall Design: 5 biological replicates of wildtype and electron transport chain (ETC) mutant C. elegans were used as sources of total RNA, each for hybridization to a single Affymetrix whole-genome microarray. Comparison of the data was intended to reveal metabolic pathways downstream of the mutation.

2008-04-07 | E-GEOD-9896 | biostudies-arrayexpress

Ribosomal and tRNA Biogenesis Interact to Control Hypoxic Injury and Translation

Project description:Protein translation is an essential cellular process, but paradoxically, it can also promote aging and other stresses. In a screen for mutations that protect C. elegans from hypoxic stress, we isolated multiple genes that impact translation, including a ribosomal RNA helicase gene, ddx-52, tRNA biosynthesis genes, and a gene controlling amino acid availability. To better define the mechanisms whereby these genes control hypoxic injury, we performed a second screen for genetic suppressors of the ddx-52(lf) phenotypes. This screen identified multiple genes involved in ribosome biogenesis. Surprisingly, the suppressor mutations were able to restore normal hypoxic sensitivity and protein synthesis to the tRNA biosynthesis mutants, but not to the mutant reducing amino acid uptake. Proteomic characterization of the mutants demonstrated that reduced tRNA biosynthetic activity produces a corresponding reduction in ribosomal structural subunits. Our study uncovers an uncharacterized regulatory interaction between ribosomal biogenesis and tRNA abundance controlling translation and hypoxic survival. A proteomic analysis of a threonyl-tRNA synthetase mutant with and without the ribosomal biogenesis suppressors revealed an uncharacterized feedback mechanism whereby disruption of tRNA aminoacylation results in a corresponding reduction in ribosomal subunits, thereby explaining the ability of enhanced ribosomal biogenesis to suppress reduced tRNA aminoacylation.

2022-02-15 | PXD017267 | Pride

Brugia malayi glycophosphatidylinositol-anchored proteome

Project description:A proteomics strategy was used to identify putative GPI-APs from adult B. malayi. Three different sample types were prepared for analysis. Firstly, intact adult worms were treated with PI-PLC to enzymatically release and solubilize the protein away from the lipid moiety. A mock-treatment with no PI-PLC was performed as a negative control. The samples derived from treatment of the intact worms have been named “Surface” but it should be noted that the proteins could originate from any exposed surface like the mouth, vagina, or rectum of the worm. Secondly, a membrane fraction of B. malayi adult female worms was prepared by ultracentrifugation of a total lysate in a sucrose buffer to separate membrane proteins from soluble proteins. This membrane fraction was also treated with PI-PLC or mock-treated without PI-PLC as a negative control. Lastly, a GPI-AP enriched sample was prepared by performing a series of organic solvent partitions to extract GPI-APs from a membrane fraction. This sample was not treated with PI-PLC. Proteins in all three samples types were digested with trypsin and the resulting peptides analyzed by LC-MS/MS.

2019-11-12 | PXD014949 | Pride

NAD+ and PPAR-modifying drugs in a C. elegans model of respiratory chain complex I deficiency

Project description:The gas-1(fc21) mutation affects the 49 kD subunit of complex I, decreasing the rate of complex I-dependent oxidative phosphorylation. This is a model for human mitochondrial respiratory chain disease. NAD+ and PPAR-modifying drugs may confer benefits with respect to lifespan in these short-lived mutant worms. Analysis of gas-1(fc21) electron transport chain complex I mutants treated either starting in development or in young adulthood only with nicotinic acid (1 mM), resveratrol (50 microM), rosiglitazone (5 mM) or fenofibrate (14 microM) is presented. The goal is to detect transcriptional changes in clusters of genes using gene set enrichment analysis to explain treament effects in these mutant worms. Four biological replicates were performed for each treatment condition (nicotinic acid, resveratrol, rosiglitazone, and fenofibrate) for each drug beginning either in development or in young adulthood for gas-1 mutant worms, i.e., 8 treated samples in total. At most one outlier was excluded from each analysis. Untreated N2 and gas-1 in each of the control solvents (S-basal, for nicotinic acid, and 1% DMSO, for resveratrol, rosiglitazone, and fenofibrate) were also analyzed; at least 3 replicates of each were included. These were used as sources of total RNA, each for hybridization to a single Affymetrix whole-genome microarray. Analysis was performed to reveal transcriptional changes related to mutantion and/or drug treatment effects.

2014-08-13 | E-GEOD-57626 | biostudies-arrayexpress

Worms spun in centrifuge at elevated g values

Project description:Worms spun at higher than normal g values for 4 days on 20G centrifuge vs. worms kept at 1 X G. Both are mixed stage cultures. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment Physical Characteristics: worms kept at increased g values for 4 days (x g value) stimulus_or_stress_design

2013-06-22 | E-GEOD-38877 | biostudies-arrayexpress

Whole worm proteomics after optogenetically induced mechanical muscle stress (OptIMMuS)

Project description:This project includes 16 samples of transgenic C. elegans whole worm lysate after mechanical stress in 4 replicates of 4 conditions. Transgenic C. elegans strains expressing the optogenetic channelrhodopsin mutant ChR2(C128S;H134R)-FLAG in body wall muscle cells (PP3189 hhIs251[myo-3p::ChR2(C128S,H134R)-FLAG::unc-54 3'UTR, Cbrunc-119(+)]) were used to contract the worms’ muscles by blue light illumination to induce mechanical muscle stress. The optogenetic channel is activated by adding the cofactor all-trans retinal (ATR) to it’s food source E. coli OP50. In this experiment, we compared the treatment condition (1) worms after 8 h of illumination on plates with ATR (light plus ATR) to three control conditions: (2) illumination on plates without ATR (light minus ATR), (3) worms kept in the dark on plates with ATR (dark plus ATR), and (4) worms kept in the dark on plates without ATR (dark minus ATR).

2024-07-16 | PXD045078 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data