Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Imaginal discs produce neuropeptide-like precursor 1 to alleviate ER stress in response to warm temperatures

ABSTRACT: In mammals, prolonged heat stress induces an endoplasmic reticulum (ER) stress response that can damage internal organs. In Drosophila, larvae grow and develop into adults faster at warmer temperatures (e.g., 30°C) than at lower temperatures, but with reduced body size and fertility. In this study, we show that the neuropeptide gene neuropeptide-like precursor 1 (Nplp1) alleviates temperature-induced ER stress in imaginal discs. Warm temperatures increase production of a specific Nplp1 splice variant that inhibits PKR-like endoplasmic reticulum kinase (PERK) activation and cell death. Nplp1 inhibits Dilp8 expression through the PERK/ATF4/Yki pathway, thereby enabling imaginal disc growth and ecdysone homeostasis under warm temperature conditions. These findings provide valuable insights into how animals cope with elevated temperatures.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE297273 | GEO | 2025/10/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of N2 and flp-6 Caenorhabditis elegans at 25 °C

Project description:Temperature is a prominent environmental stimulus that influences life span. Previous studies indicate that in Caenorhabditis elegans, thermosensory perception in the AFD neuron maintains life span at warm temperatures. How thermosensation is translated into neuronal signals that shape aging remains elusive. We found that the Caenorhabditis elegans CREB crh-1, as well as several key genes in AFD thermosensory transduction, were specifically required for normal life span at warm temperatures. crh-1 acted in the AFD to increase transcription of the CRE-containing neuropeptide gene flp-6 in a temperature-dependent manner. Both crh-1 and flp-6 were necessary and sufficient for longevity at warm temperatures, and their effects depended on the AIY interneuron. Moreover, flp-6 signaling downregulated ins-7/insulin and several insulin pathway genes, whose activity compromised life span. We postulate that temperature experience is integrated in the thermosensory neurons to generate CREB-dependent neuropeptide signals that antagonize insulin signaling and promote temperature-specific longevity.

2018-05-01 | GSE68464 | GEO

Transcriptional changes associated with endoplasmic reticulum stress in the eye imaginal disc of Drosophila melanogaster

Project description:We obtained transcriptional profiles of third instar eye imaginal disc nuclei with or without endoplasmic reticulum stress using next generation sequencing (NGS). We employed an isolation of nuclei tagged in specific cell type (INTACT) protocol (Ma and Weake, J. of Vis. Exp., 2014) to label nuclear membranes of GMR-GAL4-expressing cells with EGFP. The experimental group also expressed a mutant allele of the membrane visual protein rhodopsin (Rh-1(G69D)), which is known to cause endoplasmic reticulum stress and initiate Unfolded Protein Response (UPR) signaling. The goal of this study was to characterize the transcriptional changes associated with endoplasmic reticulum stress responses in a commonly used platform, the eye imaginal disc.

2021-09-20 | GSE150058 | GEO

Project description:Imaginal discs produce neuropeptide-like precursor 1 to alleviate ER stress in response to warm temperatures.

| PRJNA1262550 | ENA

Neurons shift translational control to secure proteostatic resilience during ER stress

Project description:Proteostasis is essential for survival and particularly important for highly specialized post mitotic cells like neurons. Transient reduction of protein synthesis by protein kinase R–like endoplasmic reticulum (ER) kinase (PERK)-mediated phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) is a major proteostatic survival response during ER stress. Paradoxically, neurons are remarkably tolerant to PERK dysfunction, which suggests the existence of cell type-specific mechanisms that secure proteostatic stress resilience. We employed PERK-deficient neuron and astrocyte monocultures to investigate the mechanisms underlying neuron-specific ER stress resilience in the absence of PERK.

2022-06-13 | GSE200742 | GEO

Endoplasmic reticulum stress sensor protein PERK in hepatic stellate cells promotes the progression of hepatocellular carcinoma via p38δ MAPK/IL-1β axis

Project description:Palmitic acid (PA) absorption from the intestine is increased in metabolic dysfunction-associated steatohepatitis (MASH). It induces endoplasmic reticulum (ER) stress and interleukin-1 beta (IL-1β) production in hepatic stellate cells (HSCs). Protein kinase R-like endoplasmic reticulum kinase (PERK) is an ER stress sensor protein involved in HSC activation and liver fibrosis. However, its role in HSCs during hepatocellular carcinoma (HCC) progression remains unclear. This study clarified the process of IL-1β production via PERK in HSCs and explored the mechanism underlying MASH-related HCC progression. HSCs were treated with PA or transfected with PERK small-interfering RNA (siRNA) or PERK plasmid. Proliferation, scratch, and Transwell assays were performed on HCC cells cultured in the conditioned medium (CM) from HSCs. PA treatment increased PERK and IL-1β expressions in HSCs. PERK knockdown decreased IL-1β expression, while its overexpression increased it in HSCs. The CM from PA-treated HSCs showed elevated IL-1β levels and enhanced HCC cells’ proliferation, migration, and invasion; however, these effects were suppressed by PERK knockdown in HSCs. RNA-sequencing analysis revealed that p38δ mitogen-activated protein kinase (MAPK) is the intermediate molecule between PERK and IL-1β in HSCs. In the tumor microenvironment of MASH-related HCC, PERK in HSCs promotes HCC progression via the p38δ MAPK/IL-1β axis.

2025-06-07 | GSE292002 | GEO

Deficiency of ERO1 and activation of protein translation synergistically impair breast tumor resilience

Project description:Endoplasmic reticulum (ER) stress triggers an adaptive response which fosters tumor cell survival and resilience to stress conditions. Activation of the endoplasmic reticulum stress response, through its PERK branch, promotes the phosphorylation of the α-subunit of translation initiation factor eIF2alpha, thereby repressing general protein translation and selectively augmenting the translation of ATF4 with the downstream CHOP transcription factor and the protein disulfide oxidase ERO1. Here, we show that ISRIB, a small molecule, which inhibits the action of the phosphorylated α-subunit of eIF2, thereby activating protein translation, synergistically interacts with the genetic deficiency of protein disulfide oxidase ERO1 enfeebling tumor growth and spreading. ISRIB represses CHOP signal but surprisingly does not inhibit ERO1. Mechanistically, ISRIB increases the ER protein load with a prominent perturbing effect on ERO1 deficient Triple-Negative breast cells, which have adapted to live with low client protein load, while ERO1 deficiency selectively impairs VEGF-dependent angiogenesis. Strikingly, ERO1-deficient Triple Negative Breast Cancer xenografts have augmented ER stress response and PERK branch. In vivo, ISRIB synergistically with ERO1 deficiency inhibits the growth of Triple-Negative Breast cancer xenografts by impairing proliferation and angiogenesis, while it is not effective on the xenograft counterparts with ERO1. In summary, these results demonstrate that ISRIB together with ERO1 deficiency synergistically shatters a feature of the adaptive ER stress response while ERO1 deficiency selectively impairs angiogenesis in tumors, thereby together promoting tumor cytotoxicity. Therefore, our findings suggest two surprising findings in breast tumors: ERO1 is not regulated via CHOP and ISRIB represents a therapeutic option to efficiently inhibit tumor progression in those tumors with limited ERO1 and high PERK.

2022-07-20 | E-MTAB-11313 | biostudies-arrayexpress

Gene expression profiles of control or PERK siRNA-transfected brown adipocyte during the differentiation

Project description:The area of mitochondria in differentiated brown adipocytes is dramatically increased compared with that in brown pre-adipocytes. The ATP production is switched from the glycolysis pathway to the OXPHOS pathway during brown adipocyte differentiation. Endoplasmic reticulum (ER) is surrounded by mitochondria and the area of contact sites between mitochondria and the ER is increased. ER stress sensor PERK was phosphorylated during differentiation. To elucidate the mitochondria-ER crosstalk signaling mediated by PERK, RNA-sequencing analysis was performed using control siRNA- or PERK siRNA-transfected brown adipocytes.

2020-02-03 | GSE132598 | GEO

Comparative transcriptomic analyses of Spring OilSeed Rape (SOSR)accessions in response to warm temperature.

Project description:Elevated growth temperatures are negatively affecting crop productivity and increasing yield losses. Root traits associated with improved adaptation to rising temperatures are a promising approach to generate new varieties better suited to face the environmental constrains caused by climate change. In this study, we identified various Brassica napus roots traits altered in response to warm temperature. Thus, different combination of changes in specific root traits results in an extended and deeper root system. This overall root growth expansion facilitates root adaptation by maximizing root-soil surface interaction and increasing its ability to explore extended soil areas. We associated these traits to coordinated cellular events, including changes in cell division and elongation rates, that drive the increase in root growth triggered by warm temperature. Comparative genome wide transcriptomic analysis revealed the main genetic determinants of these RSA changes and uncovered the necessity of a tight regulation of the heat shock stress response to adjust root growth to warm temperature. Our work provides a phenotypic, cellular and genetic framework of root response to warming temperatures that will help to harness root adaptation mechanisms for crop yield improvement under the future climatic scenario.

2023-01-25 | GSE173272 | GEO

The eIF2 kinase PERK and the integrated stress response facilitate activation of ATF6 during endoplasmic reticulum stress

Project description:Disruptions of the endoplasmic reticulum (ER) that perturb protein folding cause ER stress and elicit an unfolded protein response (UPR) that involves translational and transcriptional changes in gene expression aimed at expanding the ER processing capacity and alleviating cellular injury. Three ER stress sensors PERK, ATF6, and IRE1 implement the UPR. PERK phosphorylation of eIF2 during ER stress represses protein synthesis, which prevents further influx of ER client proteins, along with preferential translation of ATF4, a transcription activator of the integrated stress response. In this study we show that the PERK/eIF2α~P/ATF4 pathway is required not only for translational control, but also activation of ATF6 and its target genes. The PERK pathway facilitates both the synthesis of ATF6 and trafficking of ATF6 from the ER to the Golgi for intramembrane proteolysis and activation of ATF6. As a consequence, liver-specific depletion of PERK significantly reduces both the translational and transcriptional phases of the UPR, leading to reduced protein chaperone expression, disruptions of lipid metabolism, and enhanced apoptosis. These findings show that the regulatory networks of the UPR are fully integrated, and helps explain the diverse pathologies associated with loss of PERK. 14 gene expression arrays, 3 WT control arrays; 3 lsPERK control arrays; 4 WT Treated arrays; 4 lsPERK treated arrays. Comparison of gene expression profiles for treated vs control in wildtype and knock-out.

2012-01-20 | E-GEOD-29929 | biostudies-arrayexpress

Pharmacological induction of selective endoplasmic reticulum retention as a novel strategy for cancer therapy

Project description:We analysed the difference in the surface proteome of human cells that were either subjected to ER stress (induced by thapsigargin (Tg)) only or were additionally treated with a pharmacological inhibitor against the eIF2α kinase PERK, which is localized in the endoplasmic reticulum. Compared to single ER stress, several important plasma-membrane associated kinases, showed a significant downregulation under PERK inhibition.

2020-03-02 | PXD014709 | 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