Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA313027 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity
| PRJNA314583 | ENA
Project description:Disruption of physiological homeostasis elicits cellular stress response and behavioral changes of the animal. We recently showed that mitochondrial stress induces aversive associative memory for food bacteria that C. elegans inherently prefers without stress. Depletion of atp-2 by RNA interference in the non-neural tissues causes mitochondrial disruption and induces bacterial avoidance in C. elegans. Our transcriptome provide several metabolic pathways that may are critical for aversive memory. Among these pathwaies, we found that peroxisomal β-oxidation mediates serotonergic neuron,NSM, to promote stress-induced aversive memory.
2024-03-25 | GSE241240 | GEO
Project description:Animals integrate metabolic, developmental, and environmental information before committing key resources to reproduction. In C. elegans, adult animals reallocate key fat stores from intestinal cells to the germline via lipoproteins to promote reproduction. I identified the evolutionarily conserved homeodomain transcription factor CEH-60/PBX as a potent regulator of lipid homeostasis, longevity, and stress response pathways. To gain a comprehensive view of CEH-60 transcriptional activity, I profiled the transcriptomes of ceh-60 mutants by mRNA-Seq and identified genome-wide CEH-60 binding sites by ChIP-Seq. These approaches revealed that several homeostatic pathways are directly controlled by the CEH-60 transcription factor. CEH-60 functions cooperatively with UNC-62/MEIS in the intestine to directly activate lipoprotein genes while simultaneously repressing genes involved in stress responses, including the innate immune and oxidative stress responses. Thus in wild-type animals, CEH-60 serves as a molecular switch that promotes reproduction (i.e., lipoproteins) while repressing stress response and longevity pathways. This study identifies a new key regulator of fat metabolism, longevity, and stress response pathways during normal C. elegans development.
2019-04-04 | GSE112979 | GEO
Project description:Mitochondrial stress during development causes widespread changes in chromatin structure to promote mitochondrial unfolded protein response (UPRmt), perpetuating an early response across a lifetime results in lifespan extension. We found that the nucleosome remodeling and deacetylase (NuRD) complex interact with the transcription factor DVE-1 to initiate the global chromatin condensation and induce the UPRmt in animals experienced with mild mitochondrial dysfunction. The condensed chromatin structure can be well maintained into later life that is beneficial for lifespan extension. Moreover, overexpression of the core component of the NuRD complex is sufficient to induce the UPRmt response and longevity in C. elegans. Thus, a transient mitochondrial stress response during early development is established and propagated into later life through the NuRD-dependent chromatin remodeling pathway to extend lifespan.
2020-07-31 | GSE143904 | GEO
Project description:Animals integrate metabolic, developmental, and environmental information before committing key resources to reproduction. In C. elegans, adult animals reallocate key fat stores from intestinal cells to the germline via lipoproteins to promote reproduction. I identified the evolutionarily conserved homeodomain transcription factor CEH-60/PBX as a potent regulator of lipid homeostasis, longevity, and stress response pathways. To gain a comprehensive view of CEH-60 transcriptional activity, I profiled the transcriptomes of ceh-60 mutants by mRNA-Seq and identified genome-wide CEH-60 binding sites by ChIP-Seq. These approaches revealed that several homeostatic pathways are directly controlled by the CEH-60 transcription factor. CEH-60 functions cooperatively with UNC-62/MEIS in the intestine to directly activate lipoprotein genes while simultaneously repressing genes involved in stress responses, including the innate immune and oxidative stress responses. Thus in wild-type animals, CEH-60 serves as a molecular switch that promotes reproduction (i.e., lipoproteins) while repressing stress response and longevity pathways. This study identifies a new key regulator of fat metabolism, longevity, and stress response pathways during normal C. elegans development.
2019-04-04 | GSE112978 | GEO
Project description:To identify ATFS-1 target genes during mitochondrial stress
| PRJNA269110 | ENA
Project description:Lipid biosynthesis coordinates a Mitochondrial to Cytosolic Stress Response
| PRJNA326871 | ENA
Project description:Transgenerational inheritance of mitochondrial stress adaptation in C. elegans
| PRJNA339523 | ENA
Project description:ATFS-1 mediates a protective transcription program during mitochondrial stress
| PRJNA167341 | ENA
Project description:Hypoxia-inducible transcription factor HIF is the key regulator of hypoxia response. It is conserved from human to the model organism C. elegans. The homolog of HIF in C. elegans is HIF-1. In C. elegans, there are six alternative splicing isoforms for HIF-1. Isoform a (HIF1a) is the predominant one with important biological functions for stress response and longevity. Here, by performing chromatin immunoprecipitation DNA-sequencing (ChIP-seq), we identified the direct targets for HIF-1a at whole genome level.
2023-04-15 | GSE228846 | GEO