Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of EcR RNAi on wandering third instar larval fat body gene expression in Drosophila melanogaster

ABSTRACT: We compared ecdysone receptor (EcR)-dependent gene expression in the Drosophila fat body on 0.15 M sucrose and 0.5 M sucrose high-sugar diets in order to gain insight into the role of this gene during caloric overload. Phenotypic analyses showed an increased severity of EcR RNAi phenotypes with increasing dietary sugar concentration. Because EcR is a transcription factor, we performed RNA-seq studies to identify transcriptional targets that might underlie insulin resistance downstream of EcR RNAi.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE110432 | GEO | 2018/02/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of Seven-up RNAi on wandering third instar larval fat body gene expression in Drosophila melanogaster

Project description:We compared Seven-up-dependent gene expression in the Drosophila fat body on control and high-sugar diets in order to gain insight into the role of this gene during caloric overload. Phenotypic analyses showed an increased severity of Seven-up RNAi phenotypes with increasing dietary sugar concentration. Because Seven-up is a transcription factor, we performed RNA-seq studies to identify transcriptional targets that might underlie insulin resistance downstream of Seven-up RNAi. Our data support a model where Seven-up promotes insulin signaling by inhibiting ecdysone receptor target gene expression.

2018-04-01 | GSE95800 | GEO

Direct and widespread role for the nuclear receptor EcR in mediating the response to ecdysone in Drosophila

Project description:Ecdysone signaling has long been studied as a paradigm for how hormones can synchronize development events in tissues throughout the animal. At the genetic level, ecdysone acts through its receptor, EcR, which has been classically thought to act at a relatively small number of canonical, ecdysone-responsive genes which then go on to activate the effectors of cellular processes. However, in spite of the decades of work studying EcR, the understanding of how EcR promotes changes in gene expression genome-wide in vivo remains incomplete. To examine EcR’s role in promoting changes in gene expression, we use a tissue-specific GAL4 driver to knockdown EcR throughout wing development and perform RNAseq on both WT wings and EcR-RNAi wings at -6h after puparium formation (APF) and +6hAPF. We find that EcR is required to promote thousands of gene expression changes genome-wide. To determine whether EcR is directly effecting these changes, we perform CUT&RUN in wings to identify EcR binding sites genome-wide. We find that EcR directly binds thousands of sites genome-wide, including many genes important for wing development. Collectively, these data suggest that EcR does not only act the top of a signaling cascade, but, instead, directly effects the response to ecdysone at multiple levels.

2019-04-24 | GSE124254 | GEO

EcR mutant midgut comparison

Project description:Comparisons between EcR mutant midgut and a reference control sample from mixed-stage normal midgut Keywords = Drosophila, ecdysone, network, genomic, microarray, organogenesis, EcR, midgut, central nervous system, salivary gland, epidermis, imaginal disc, development

2010-06-05 | E-GEOD-540 | biostudies-arrayexpress

EcR mutant midgut comparison

2003-07-23 | GSE540 | GEO

Opportunistic binding of EcR to open chromatin drives tissue-specific developmental responses [RNA-seq]

Project description:In Drosophila, the ecdysone steroid hormone is essential for coordinating developmental timing across physically separated tissues. Ecdysone directly impacts genome function through its receptor, a heterodimer of the EcR and Usp proteins. Ligand binding to EcR triggers a transcriptional cascade, including activation of a set of primary response transcription factors. The hierarchical organization of this pathway has left the direct role of EcR in mediating ecdysone responses obscured. Here, we investigate the role of EcR in controlling tissue-specific ecdysone responses, focusing on two tissues that diverge in their response to rising ecdysone titers: the larval salivary gland, which undergoes programmed destruction, and the wing imaginal disc, which initiates metamorphosis. We find that EcR functions bimodally, with both gene repressive and activating functions, even at the same developmental stage. We find that EcR DNA binding profiles are highly tissue-specific, and transgenic reporter analyses demonstrate that EcR plays a direct role in controlling enhancer activity. Despite a strong correlation between tissue-specific EcR binding and tissue-specific open chromatin, we find that EcR does not control chromatin accessibility at genomic targets. We conclude that EcR contributes extensively to tissue-specific ecdysone responses. However, control over access to its binding sites is subordinated to other transcription factors.

2022-09-12 | GSE202809 | GEO

Opportunistic binding of EcR to open chromatin drives tissue-specific developmental responses [FAIRE-seq]

2022-09-12 | GSE202808 | GEO

Opportunistic binding of EcR to open chromatin drives tissue-specific developmental responses [CUT&RUN]

2022-09-12 | GSE202807 | GEO

Effect of transgenic RNAi on wandering third instar larval fat body gene expression in Drosophila melanogaster

Project description:We compared four transcription factor knockdowns using transgenic RNAi expressed in the larval fat body. FOXO, Tfb1, p53, and Stat92E-dependent gene expression in the Drosophila fat body was quantified on control and high-sugar diets in order to generate expression profiles via RNA-seq. These expression data were used to build a gene regulatory network to predict novel roles for these and other genes during caloric overload.

2018-03-13 | GSE111728 | GEO

Effect of high-sugar feeding on wandering third instar larval fat body gene expression in Drosophila melanogaster

Project description:We compared gene expression in the Drosophila fat body on control and high-sugar diets in order to gain insight into the role of this organ during caloric overload. Differential expression analysis revealed changes in gene expression suggestive of a role for CoA metabolism in the ability to tolerate high-sugar feeding. This led us to perform biochemical and mutant studies supporting a model where CoA is limiting in the face of caloric overload.

2016-01-27 | GSE76214 | GEO

FRUM and EcR-regulated expression during Drosophila development

Project description:In Drosophila, male-specific FRU (FRUM) is required to establish the potential for courtship behaviors, but the downstream effectors of FRUM during development are largely unknown. A microarray-based approach identified genes that are differentially expressed as a consequence of FRUM in pupae, in both whole body and CNS tissues. Genes were also identified that are sex-differentially expressed in CNS tissues. The FRUM-regulated sets were significantly overrepresented with genes also regulated by the ecdysone regulatory pathway. Two EcR isoforms (EcRA and EcRB1) are expressed in FRUM-expressing neurons during distinct periods of metamorphosis. Males with abrogated EcRA function in FRUM-expressing neurons aggressively court other males. Transcriptional profiles of mutants with abrogated EcRA function in the fru circuit demonstrate that EcR and FRUM regulate common gene sets, including the early gene broad. These results demonstrate a novel role for EcR in specifying male courtship behavior through its actions specifically in the FRUM neural circuitry.

2009-09-21 | GSE11752 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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