Ecdysone- and stress-induced expression profile in Kc167 cells
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE3072 | GEO | 2006/08/05
SECONDARY ACCESSION(S): PRJNA93171
REPOSITORIES: GEO
Similar Datasets
Project description:Kc167 cells were mock-treated/treated with combinations of steroid hormone ecdysone and gamma-irradiation, and harvested. The expression profiles were determined using Affymetrix Drosophila Genechip 1 arrays. Comparisons between the sample groups allow the identification of genes with ecdysone- and/or radiation-responsive expression patterns. Experiment Overall Design: 1 set of control, ecdysone, gamma-irradiated, ecdysone + irradiated samples was analyzed.
2008-06-12 | E-GEOD-3072 | biostudies-arrayexpress
Project description:ecdysone treated KC167 cells during Heat Shock and at Room Temperature
2011-08-17 | GSE23824 | GEO
Project description:We used the DamID method to systematically identify the binding sites of Ecdysone Receptor and its heterodimeric partner USP across the whole genome in Drosophila Kc cells. We find that the EcR sites are a subset of the USP sites and that only a proportion are ecdysone regulated from an accompanying ecdysone profiling study. The role of EcR/USP in the ecdysone network appears to be coordinated by the recruitment of many transcription factors as well as signaling molecules. Keywords: DamID, chromatin profiling, DNA microarray In this study we mapped the genomic binding sites of steroid hormone nuclear receptor EcR and USP in Kc167 cells using the DamID method. DamID involves the low level expression of a fusion protein consisting of DNA adenine methyltransferase (Dam) and a chromatin protein of interest. This fusion protein is targeted to the native binding sites of the chromatin protein, where Dam methylates adenines in the surrounding DNA. The methylated DNA fragments were isolated and amplified by selective PCR, labeled with a fluorescent dye and hybridized to whole genome tiling microarrays. In this study,experiments were done with samples obtained from independent experiments and include dye swaps.
2008-05-01 | E-GEOD-9156 | biostudies-arrayexpress
Project description:The changes in transcript titers are described for Drosophila Kc167 cells following 5-48 hr treatment with 20-hydroxyecdysone. Keywords: hormone response RNA from ecdysone-treated cells was compared to RNA from cells treated with carrier alone. A total of 3-13 slides were analyzed for each time point, each from a separate biological sample; dye-swaps were included.
2010-06-21 | E-GEOD-10926 | biostudies-arrayexpress
Project description:Kc167 Cells were plated at 0.5x106/ml and grown at 23.50C. They were treated with 20-HE (Sigma) at a final concentration of 5x10-7M. The reference sample was total RNA isolated at 0 hr. after treatment. The experimental samples were total RNA isolated from cells treated for 1, 3, 6, 12, 24, and 48 hours. Samples were taken at 0hr, 1hr, 3hr, 6hr, 12hr, 24hr and 48hr. Briefly, cells were spun down and Total mRNA was extracted with OligodT (Ambion) nd reverse transcribed in the presence of oligodeothymidine and random hexamers and labeled to the whole genome in-house cDNA microarray and ecdysone responsive genes were identified. Ecdysone responsive genes were identified at each timepoint using a Limma t-test.
2008-06-12 | E-GEOD-11625 | biostudies-arrayexpress
Project description:Steroid hormones control various cellular activities in a context-dependent manner. For example, ecdysone, which acts through a type II nuclear receptor, has seemingly opposite effects in Drosophila wing precursors, promoting proliferation during larval stages, and triggering proliferation arrest at pupariation. We find that wing precursors proliferate normally in the complete absence of the ecdysone receptor (EcR), whether ecdysone is present or not, suggesting that ecdysone overrides a default anti-proliferative activity of the receptor. By contrast, termination of proliferation by high concentration of 20E at the end of larval life requires ligand-induced transcriptional activation by the receptor. The switch from one mode of regulation to the other is determined by ligand level, as measured with a calibrated EcR transcriptional reporter and ex vivo proliferation assays. Accordingly, RNA Seq analysis uncovers distinct transcriptional responses to different doses of ecdysone. Some genes are only activated at high doses (high threshold targets) and likely to comprise genes that stop proliferation at pupariation, when ecdysone titres are high. We find that other target genes respond to all physiological concentrations of ecdysone. Some of these genes are known to promote proliferation and could therefore contribute to the pro-proliferation activity of low-level ecdysone. Finally, we show mathematically and with synthetic reporters that relatively simple combinations of regulatory elements can recapitulate the behaviour of both types of target genes.
2023-08-24 | GSE236166 | GEO
Project description:Coupling immunity and development is essential to ensure survival despite changing internal conditions in the organism. The metamorphosis of the fruit fly represents a striking example of drastic and systemic physiological changes that need to be integrated with the innate immune system. However, the mechanisms that coordinate development and immune cell activity in the transition from larva to adult in Drosophila remain to elucidate. The steroid hormone ecdysone is known to act as a key coordinator of metamorphosis. This hormone activates a nuclear receptor, the Ecdysone Receptor (EcR), which acts as a heterodimer with its partner Ultraspiracle (USP). Together, they activate the transcription of primary response genes, which in turn activate the transcription of a battery of late response genes. We have revealed that regulation of macrophage-like cells (hemocytes) by the steroid hormone ecdysone is essential for an effective innate immune response over metamorphosis. We have shown that in response to ecdysone signalling, hemocytes rapidly up regulate actin dynamics, motility and phagocytosis of apoptotic corpses, and acquire the ability to chemotax to damaged epithelia. Most importantly, individuals lacking ecdysone-activated hemocytes are defective in bacterial phagocytosis and are fatally susceptible to infection by bacteria ingested at larval stages, despite the normal systemic production of antimicrobial peptides. This decrease in survival is comparable to the one observed in pupae lacking immune cells altogether, indicating that ecdysone-regulation is essential to hemocyte immune functions and survival after infection. To better understand the ecdysone regulation of hemocyte activities, we have performed gene expression analysis. In order to identify the genes which expression change at the onset of metamorphosis, we have sorted hemocytes from 3rd instar larvae and from young prepupae and compared their gene expression. Moreover, and in order to identify which genes are regulated by the ecdysone signalling, we have used individuals expressing a dominant negative form of the Ecdysone Receptor specifically in their hemocytes. We have sorted hemocytes from 3rd instar and young prepupae of this genotype to compare their gene expression to the gene expression in larvae and prepupae from the control individuals.
2013-10-25 | GSE49326 | GEO
Project description:Coupling immunity and development is essential to ensure survival despite changing internal conditions in the organism. The metamorphosis of the fruit fly represents a striking example of drastic and systemic physiological changes that need to be integrated with the innate immune system. However, the mechanisms that coordinate development and immune cell activity in the transition from larva to adult in Drosophila remain to elucidate. The steroid hormone ecdysone is known to act as a key coordinator of metamorphosis. This hormone activates a nuclear receptor, the Ecdysone Receptor (EcR), which acts as a heterodimer with its partner Ultraspiracle (USP). Together, they activate the transcription of primary response genes, which in turn activate the transcription of a battery of late response genes. We have revealed that regulation of macrophage-like cells (hemocytes) by the steroid hormone ecdysone is essential for an effective innate immune response over metamorphosis. We have shown that in response to ecdysone signalling, hemocytes rapidly up regulate actin dynamics, motility and phagocytosis of apoptotic corpses, and acquire the ability to chemotax to damaged epithelia. Most importantly, individuals lacking ecdysone-activated hemocytes are defective in bacterial phagocytosis and are fatally susceptible to infection by bacteria ingested at larval stages, despite the normal systemic production of antimicrobial peptides. This decrease in survival is comparable to the one observed in pupae lacking immune cells altogether, indicating that ecdysone-regulation is essential to hemocyte immune functions and survival after infection. To better understand the ecdysone regulation of hemocyte activities, we have performed gene expression analysis. In order to identify the genes which expression change at the onset of metamorphosis, we have sorted hemocytes from 3rd instar larvae and from young prepupae and compared their gene expression. Moreover, and in order to identify which genes are regulated by the ecdysone signalling, we have used individuals expressing a dominant negative form of the Ecdysone Receptor specifically in their hemocytes. We have sorted hemocytes from 3rd instar and young prepupae of this genotype to compare their gene expression to the gene expression in larvae and prepupae from the control individuals. Hemocytes were isolated by FACS from selected 3rd instar larvae (at the late feeding stage) and prepupae (from 1h to 2h after puparium formation - APF) corresponding to two different genotypes: individuals w;HmlDeltaGal4, UAS-GFP/+ that express GFP specifically in hemocytes (genotype control), and individuals w;HmlDeltaGal4; UAS-GFP/UAS-EcRB1DN W650A which hemocytes express an Ecdysone Receptor Dominant Negative construct in addition to the GFP (EcRDN). For each of the four conditions we performed three biological replicates.
2013-10-25 | E-GEOD-49326 | biostudies-arrayexpress
Project description:Steroid hormones act as important developmental switches and their nuclear receptors regulate many genes. However, few hormone-dependent enhancers have been characterized and important aspects of their sequence architecture, cell type-specific activating and repressing functions, or the regulatory roles of their chromatin structure have remained unclear. We used STARR-seq, a recently developed enhancer-screening assay, and ecdysone signaling in two different Drosophila cell types to derive the first genome-wide hormone-dependent enhancer activity maps. We demonstrate that enhancer activation depends on cis-regulatory motif combinations that differ between cell types and can predict cell type-specific ecdysone targeting. Activated enhancers are often not accessible prior to induction. Enhancer repression following hormone treatment is independent of receptor motifs and receptor binding to the enhancer as we show using ChIP-seq, but appears to rely on motifs for other factors, including Eip74. Our strategy is applicable to study signal-dependent enhancers for different pathways and across organisms. STARR-seq was performed in S2 and OSC cells treated with ecdysone in two replicates. DHS-seq before and after treatment was done with single-end sequencing in two replicates. RNA-seq (with and without ecdysone) was performed with a strand-specific protocol using single-end sequencing in two replicates in S2. ChIP-seq (with and without ecdysone) was performed single-end sequencing in two replicates in S2 cells.
2014-03-27 | E-GEOD-47691 | biostudies-arrayexpress
Project description:The changes in transcript titers are described for Drosophila Kc167 cells following 5-48 hr treatment with 20-hydroxyecdysone. Keywords: hormone response
2009-03-20 | GSE10926 | GEO