Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325325 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3657720.fastq.gz | Fastqsanger.gz | |||
| SRR3657711.fastq.gz | Fastqsanger.gz | |||
| SRR3657721.fastq.gz | Fastqsanger.gz | |||
| SRR3657712.fastq.gz | Fastqsanger.gz | |||
| SRR3657722.fastq.gz | Fastqsanger.gz |
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Project description:Recent revelations into microRNA function suggest that microRNAs serve as a key player in a robust adaptive response against stress in animals through their fine-tuning capability in gene expression. However, it remains largely unclear how a microRNA-modulated downstream mechanism contributes to the process of homeostatic adaptation. Here we show that loss of an intestinally expressed microRNA gene mir-60 in the nematode C. elegans promotes adaptive response against oxidative stress; animals lacking mir-60 dramatically extend lifespan under a mild and long-term oxidative stress condition, while they do not increase resistance against a strong and transient oxidative stress exposure. We found that canonical stress responsive factors, such as DAF-16/FOXO, are dispensable for mir-60 loss to enhance oxidative stress resistance. Gene expression profiles revealed that genes encoding lysosomal proteases and those involved in the xenobiotic metabolism and pathogen defense response are up-regulated by the mir-60 loss. Detailed genetic studies and computational microRNA target prediction suggest that endocytosis components and a bZip transcription factor gene zip-10, which functions in innate immune response, are directly modulated by miR-60 in the intestine. Our findings suggest that the mir-60 loss facilitates adaptive response against chronic oxidative stress by ensuring the maintenance of cellular homeostasis.
2016-09-27 | GSE83239 | GEO
Project description:Downstream targets of let-60 Ras in Caenorhabditis elegans
| PRJNA91919 | ENA
Project description:Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP
2007-07-13 | GSE8462 | GEO
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.
To cite BioModels Database, please use:
BioModels Database:
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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.
2016-11-03 | MODEL1604210000 | BioModels
Project description:Transcriptome analysis for Caenorhabditis elegans based on novel expressed sequence tags
| PRJNA79387 | ENA