Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential Gene expression of C. elegans larvae following tunicamycin treatment in the absence of manf-1

ABSTRACT: Microarray analysis was performed to evaluate the changes in gene expression that are associated with manf-1 deficiency with and without exposure to tunicamycin. RNA was isolated from four groups, (wildtype (N2) and manf-1 mutant (tm3603) L1 stage larve with and without 5 hours exposure to tunicmycin (5microgram/milliliter)) for transcriptomic profiles analysis

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE118294 | GEO | 2019/06/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

The neurotrophic factor MANF regulates autophagy and lysosome function to promote proteostasis in Caenorhabditis elegans

Project description:Mesencephalic astrocyte-derived neurotrophic factor (MANF) is the only neurotrophic factor to be conserved between C. elegans and humans. MANF is a unique neutrotophic factor, as it is a resident ER protein in cells that express it and has a role in regulating ER stress response to tunicamycin exposure and pathogenic Pseudomonas exposure. We sought to further understand the role of MANF by comparing a deletion allele, an overexpression line, and the wild-type in this RNAseq experiment.

2024-10-03 | GSE278675 | GEO

Differential Gene expression of C. elegans larvae following tunicamycin treatment in the absence of manf-1

Project description:Differential Gene expression of C. elegans larvae following tunicamycin treatment in the absence of manf-1

| PRJNA485127 | ENA

Expression profile analysis of Drosophila melanogaster embryonic and larval MANF mutants together with paternal rescue and overexpression conditions

Project description:To find out possible pathways and processes influenced by DmMANF we compared the changes in MANF null and overexpressing animals. We used two developmental stages of Drosophila, st 17 embryos and 29-50 hrs after egg laying (AEL) larvae. The timing were decided according to the lethality of MANF mutants with or without maternal contribution of MANF. Maternal and zygotic MANF mutants (MANFmzD96) were compared to paternal rescue and wild type embryos of the same age. Zygotic MANF mutants (MANFD96) with maternal contribution were compared to wild type and MANF ectopic overexpression larvae harvested well before the average lethality occured (75 hrs AEL). The changes in expression profiles were more drastic in MANFmzD96 embryos than in MANFD96 larvae. Gene ontology annotations were analyzed and clustered by DAVID. The major result was alterations in membranes, changes in membrane transporter expressions and disturbed intracellular membrane traffic. The results were verified by qPCR and transmission electron microscopy. Two developmental stages - 21-24 hrs and 29-50 hrs AEL of MANFD96 mutants without and with maternal contribution were compared to wild type (Wmix means crossed w1118 x w- ) and with paternal rescue or ectopic overexpression of MANF respectively by Drosophila Agilent microarray expression platform.

2012-04-19 | E-GEOD-28820 | biostudies-arrayexpress

MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.

Project description:Mesencephalic astrocyte-derived neurotrophic factor (MANF) is the only human neurotrophic factor with an evolutionarily-conserved C. elegans homolog, Y54G2A.23 or manf-1. MANF is a small, soluble, endoplasmic-reticulum (ER)-resident protein that is secreted upon ER stress and promotes survival of target cells such as neurons. However, the role of MANF in ER stress and its mechanism of cellular protection are not clear and the function of MANF in C. elegans is only beginning to emerge. In this study, we show that depletion of C. elegans manf-1 causes a slight decrease in lifespan and brood size; furthermore, combined depletion of manf-1 and the IRE-1/XBP-1 ER stress/UPR pathway resulted in sterile animals that did not produce viable progeny. We demonstrate upregulation of markers of ER stress in L1 larval nematodes, as measured by hsp-3 and hsp-4 transcription, upon depletion of manf-1 by RNAi or mutation; however, there was no difference in tunicamycin-induced expression of hsp-3 and hsp-4 between wild-type and MANF-deficient worms. Surprisingly, larval growth arrest observed in wild-type nematodes reared on tunicamycin is completely prevented in the manf-1 (tm3603) mutant. Transcriptional microarray analysis revealed that manf-1 mutant L1 larvae exhibit a novel modulation of innate immunity genes in response to tunicamycin. The hypothesis that manf-1 negatively regulates the innate immunity pathway is supported by our finding that the development of manf-1 mutant larvae compared to wild-type larvae is not inhibited by growth on P. aeruginosa. Together, our data represent the first characterization of C. elegans MANF as a key modulator of organismal ER stress and immunity.

| S-EPMC7336501 | biostudies-literature

Expression profile analysis of Drosophila melanogaster embryonic and larval MANF mutants together with paternal rescue and overexpression conditions

2012-04-20 | GSE28820 | GEO

Effect of Tunicamycin on Bovine Capillary Endothelial Cells

Project description:GPT inhibitor Tunicamycin develops ER stress causing anti-angiogenic response in breast tumor microvasculature due to unfolded protein response-mediated apoptosis. cDNA microarray identified 123 and 454 differentially regulated genes with 10 genes overlapping between 3h and 32 h of Tunicamycin treatment. Alg-2 expression is inconsistent but not the Dpms. Evidences support that Tunicamycin completely destroys DPMS activity in capillary endothelial cells without affecting its protein or the mRNA levels but by knocking down the phosphorylation. DPMS’ contribution to developing upr during ER stress has therefore been evaluated because of its inherent regulatory property of GPT. FTIR spectroscopy confirmed protein denaturation. Restablishing the phosphorylation status helps the DPMS regaining its activity. As a result, ER stress is reduced reversing apoptosis and bringing more cells into cycling with normal cellular morphology. Furthermore, differential expression of DPMS in breast tumor microvasculature during Tunicamycin therapy raises its potential as a tumor prognostic marker in the clinic.

2017-11-15 | GSE33729 | GEO

Gene expression profile of MANF-deficient Cx3cr1+ macrophages during muscle regeneration

Project description:RNA sequencing analysis of MANF-deficient macrophages revealed changes in key cellular processes.

2023-02-13 | GSE224983 | GEO

Rat (Rattus norvegicus) RNA-Seq containing SHAM, STROKE and MANF groups

Project description:Samples from three groups, SHAM operated group and two STROKE operated groups treated two days post operation with AAV1-eGFP control and AAV1-MANF treatment were sequenced and analysed for differential gene expression

2020-04-12 | E-MTAB-8339 | biostudies-arrayexpress

Gene expression profile in Liver of young and old mice with MANF overexpression

Project description:MANF overexpression in old mice had a beneficial effect in the liver and restored expression levels of several metabolic genes.

2019-03-01 | GSE123115 | GEO

Ribosome profiling of Tunicamycin-treated and -untreated 17Cl1 cells

Project description:Ribosome profiling (RiboSeq) analysis of murine 17 clone 1 (17Cl-1) cells with and without Tunicamycin treatment. Tunicamycin is known to induce the unfolded protein response, and the objective of this work was to assess the impact of Tunicamycin on cellular translation. Additionally, we sought to assess the impact of differing library preparation methods by using three separate approaches: flash freezing, 1X Cycloheximide, and 100X Cycloheximide.

2021-11-09 | E-MTAB-5391 | biostudies-arrayexpress

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