Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA297595 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ATFS-1 mediates a protective transcription program during mitochondrial stress
| PRJNA167341 | ENA
Project description:To identify ATFS-1 target genes during mitochondrial stress
| PRJNA269110 | ENA
Project description:We previously reported that the RNA endonculease HOE-1 (RNaseZ/ELAC2) is necessary and sufficient for activation of the mitochondrial unfolded protein response (UPRmt) in C. elegans (PMID: 35451962). To comprehensively assess the broader cellular consequences of increased nuclear activity of HOE-1, we conducted RNA sequencing on day 2 adult wildtype animals vs animals in which endogenous HOE-1 is elevated in the nucleus via perturbation of its nuclear export signal (hoe-1(ΔNES)). Additionally, wildtype and hoe-1(ΔNES) animals were grown on both control and atfs-1 RNAi (ATFS-1 is the central transcription factor for UPRmt) to determine gene expression that is atfs-1 dependent. This analysis revealed that differential gene expression in hoe-1(ΔNES) animals exhibits a strong mitochondrial signature. Notably, gene ontology (GO) analysis of significantly upregulated genes showed a significant overrepresentation of mitochondrial associated genes. Moreover, knockdown of atfs-1 strongly compromised the differentially expressed gene profile. Together these data suggest that increased nuclear activity of HOE-1 preferential impacts expression of mitochondrial genes.
2024-03-13 | GSE261565 | GEO
Project description:The mitochondrial unfolded protein response (UPR mt ) is regulated by the bZIP protein ATFS-1 which promotes mitochondrial protein homeostasis (proteostasis) and mitochondrial biogenesis in Caenorhabditis elegans . Upon mitochondrial perturbation, the ATFS-1-dependent transcriptional program promotes gene expression, leading to mitochondrial recovery. Conversely, atfs-1 -deletion worms harbor dysfunctional mitochondria, are developmentally impaired, and short-lived. However, atfs-1 -deletion worms develop to adults suggesting the presence of other signaling pathways that promote mitochondrial function and biogenesis in the absence of atfs-1 . We hypothesized that additional transcription factors regulate, or promote, mitochondrial function in the absence of atfs-1 . Here, we screened for transcription factors that could reduce the decline in mitochondrial function in the atfs-1 mutants when inhibited. Here, we demonstrate that inhibition of the nuclear hormone receptor NHR-180 re-establishes a functional mitochondrial network in atfs-1(null) worms, increases mtDNA content, and improves the developmental rate of wildtype worms. NHR-180 increases transcription of genes required for cytosolic protein synthesis in response to mitochondrial perturbation. Inhibition of the S6 kinase homolog, rsks-1 , in atfs-1(null) worms leads to a recovery of the mitochondrial network and mtDNA content consistent with nhr-180 regulating expression of protein synthesis components. Consistent with the observations in C. elegans , S6 kinase inhibition also increased mitochondrial biogenesis in mammalian atf5 -knockout cells that harbor severely impaired mitochondria. Intriguingly, nhr-180 or S6 kinase inhibition also rescues mitochondrial dysfunction caused by mutations in multiple genes required for oxidative phosphorylation. Combined, these studies suggest that increased protein synthesis contributes to the mitochondrial dysfunction caused by perturbations in OXPHOS gene expression and suggest a relatively straightforward approach to reducing the impact of mitochondrial dysfunction.
2025-04-04 | GSE290561 | GEO
Project description:To better understand genome coordination and OXPHOS recovery during mitochondrial dysfunction, we examined ATFS-1, a transcription factor that regulates mitochondria-to nuclear communication during the mitochondrial UPR, via ChIP-sequencing. Wildtype worms treated spg-7(RNAi) are analyzed in the presence and absence of ATFS-1 antibody to identify ATFS-1 targets. Individual samples were analyzed. Wildtype worms treated spg-7(RNAi) in the absence of antibody is used as a control.
2015-03-03 | E-GEOD-63803 | biostudies-arrayexpress
Project description:The Argonautes (AGOs) are widely expressed, evolutionarily conserved RNA binding proteins that play an important role in gene expression regulation. The AGOs bind to small regulatory noncoding RNAs such as micro RNAs (miRNAs), short interfering RNAs (siRNAs), Piwi-interacting RNAs (piRNAs) etc. The small regulatory noncoding RNAs serve the function of guiding the AGOs to the right target RNAs by complementary base pairing. Additionally, the AGOs interact with GW182 (TNRC6A/-B/-C) proteins and together with small RNAs, they form an effector ribonucleo protein complex named, RNA Induced Silencing Complex (RISC) that regulates several aspects of transcriptional and post-transcriptional gene expression. ALG-1 (Argonaute Like Gene) and ALG-2 are the AGO proteins in C. elegans that are required for miRNA mediated gene expression regulation. Our efforts towards the characterization of the protein complexes comprised of ALG-1 led to the identification of DPF-3, a conserved protease belonging to clinically relevant Di Peptidyl Peptidase IV family, as the novel interacting partner of ALG-1. We have further explored the role of DPF-3 in AGO regulation.
2025-03-06 | PXD060454 | Pride
Project description:We sequenced the transcriptome of a host (Caenorhabditis elegans) following its interaction with a non-native bacterium (Enterococcus faecalis) that has protective traits against the pathogen, Staphylococcus aureus. We also investigated the impact that the evolutionary history of the protective bacterium has on the transcriptional history of the host. We tested protective bacteria that had either coevolved against the pathogen within C. elegans, or had evolved on its own within C. elegans.
2021-04-20 | GSE151731 | GEO
Project description:CREB regulates Reproductive Aging through Hedgehog/Patched Signaling
| PRJNA598859 | ENA
Project description:Systematic Analysis of Tissue-Restricted miRISCs Reveals a Broad Role for microRNAs in Suppressing Basal Activation of the C. elegans Pathogen Response
| PRJNA153221 | ENA