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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation

ABSTRACT: The transcription factor Twist is a critical cooperating factor that confers transcriptional specificity to the Notch pathway in muscle progenitor cells (DmD8) ChIP analysis of Twi show that Twist binding is significantly enriched in Notch responsive region in DmD8 cells 3 replicates of Twist ChIP after30 min. Notch activation.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Sarah Bray

PROVIDER: E-GEOD-22650 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Specificity of Notch pathway activation: twist controls the transcriptional output in adult muscle progenitors.

Bernard Fred F Krejci Alena A Housden Ben B Adryan Boris B Bray Sarah J SJ

Development (Cambridge, England) 20100707 16

Cell-cell signalling mediated by Notch regulates many different developmental and physiological processes and is involved in a variety of human diseases. Activation of Notch impinges directly on gene expression through the Suppressor of Hairless [Su(H)] DNA-binding protein. A major question that remains to be elucidated is how the same Notch signalling pathway can result in different transcriptional responses depending on the cellular context and environment. Here, we have investigated the facto ...[more]

PMID: 20610485

Similar Datasets

ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation

Project description:The transcription factor Twist is a critical cooperating factor that confers transcriptional specificity to the Notch pathway in muscle progenitor cells (DmD8) ChIP analysis of Twi show that Twist binding is significantly enriched in Notch responsive region in DmD8 cells

2010-07-28 | GSE22650 | GEO

Drosophila melanogaster

Project description:ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation

| PRJNA128013 | ENA

Notch targets in DmD8 and KC Drosophila cells

Project description:To identify genes upregulated in response to Notch signalling in DmD8 cells. To identify genes upregulated in response to Notch signalling in KC cells. Keywords: Expression analysis at a single timepoint (30' after Notch activation)

2009-02-17 | GSE9964 | GEO

Notch targets in KC Drosophila cells

Project description:To identify genes upregulated in response to Notch signalling in KC cells. Keywords: Expression analysis at a single timepoint (30' after Notch activation) KC cells were obtained from Dr Martin Zeidler. Control versus Notch activated KC cells: mRNA was extracted from KC cells incubated in the absence or presence of EDTA to activate Notch (cells were harvested 30 minutes after addition of EDTA). RNA was isolated using TRIzol (Sigma) and reverse transcription was performed with Superscript III Reverse Transcriptase (Invitrogen) and oligo-dT primers (Sigma). Control and experimental samples were labeled with Cy3 or Cy5, mixed together and hybridized on Drosophila transcriptome long-oligonucleotide microarrays (FlyChip, FL002; http://www.flychip.org.uk/services/core/FL002/). Three biological replicates and dye swaps were performed (5 arrays in total/experiment). Slides were scanned by Genepix 400B dual laser scanner (Axon) and spots were found and quantified by Dapple software.

2010-06-23 | E-GEOD-9965 | biostudies-arrayexpress

Poly(A) mRNA-seq from yw and Twi-mCherry-LEXY(V416L) embryos subjected to different blue light exposure schemes

Project description:Profiling of genes expression changes caused by the conditional perturbation of Twist function during different developmental time windows of Drosophila embryogenesis Twist was depleted from the nucleus continuously or post-gastrulation using the improved blue light-inducible mislocalisation system LEXY(slow). Gene expression changes between dark- and blue light-incubated embryos were profiled 2-4 h and 4-6 h after egg lay. yw embryos serve as a wild-type control. Poly(A) mRNA-seq was performed from three biological replicates for Twi-mCherry-LEXY(V416L) embryos and two biological replicates for yw embryos.

2020-12-11 | E-MTAB-9034 | biostudies-arrayexpress

Profiling of Esg genomic binding in the Drosophila midgut with DamID

Project description:Tissue stem cells divide asymmetrically to self-renew and generate differentiated progeny to maintain tissue homeostasis. Escargot (Esg) is a transcriptional repressor that is expressed in multiple stem cell populations in Drosophila melanogaster. Reduced esg function in intestinal stem cells (ISCs) causes a loss of ISCs and a biased differentiation of the daughter enteroblasts (EBs) toward the enteroendocrine (EE) cell fate. Loss of esg leads to an upregulation of differentiation factors and reduced Notch activity within EBs, indicating that Esg is a pivotal regulator of homeostasis in the intestine, supporting self-renewal to maintain a healthy stem cell pool as well as differentiation of progenitor cells. To identify potential transcriptional targets that mediate these phenotypes, in vivo DamID was used to generate the data deposited herein. 3 biological relicates were performed for Esg (with one dye-swap).

2014-11-18 | E-GEOD-55226 | biostudies-arrayexpress

Drosophila melanogaster

Project description:Notch targets in DmD8 and KC Drosophila cells

| PRJNA103977 | ENA

Su(H) bound regions in Nicd induced wing-disc hyperplasia

Project description:The outcome of Notch activation on proliferation depends on cellular context. In Drosophila wing discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand the underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes directly activated during wing disc hyperplasia. These data are the results from ChIP-Chip experiments to identify genomic regions occupied by Su(H) in hyperplastic Nicd-expressing Drosophila wing discs. 2 independent replicates; Immunoprecipitation perfomed with Su(H) antibody on chromatin isolated from wing discs overexpressing Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) and compared to the total input DNA.

2013-12-31 | E-GEOD-41426 | biostudies-arrayexpress

ChIP-chip time-course from DmD8 cells with Pol II (Ser 2 and Ser 5 phosphorylated) antibody after 0, 10, 20, 30 40, 60 and 100 minutes Notch activation

Project description:Cellular responses to signalling pathways are often highly dynamic, however most analyses of developmental signalling pathways focus on a single endpoint. We have analyzed the temporal changes in transcription following a short Notch activation treatment and related these to the recruitment of the Notch pathway transcription factor, CSL [Suppressor of Hairless, Su(H), in Drosophila], and to the state of RNA Polymerase II (Pol II) binding. A total of 154 genes showed significant differential expression over time and their expression profiles stratified into 14 clusters based on temporal and quantitative differences in their responses. These differences were partially reflected in the profiles of Pol II and Su(H) binding. However, neither could fully account for the different response profiles. Furthermore, the timing of the different responses was unaffected by more prolonged Notch activation. Instead our data suggest that regulatory relationships between genes that segregate into different response clusters can partially account for the stratification. Thus, feed-forward repression, where products of early responding Enhancer of split bHLH genes (E(spl)bHLH) inhibit expression of endogenous repressors, is one mechanism that explains the profile of genes that exhibit delayed up-regulation. E(spl)bHLH genes may therefore be responsible for co-ordinating the Notch response of a wide spectrum of other targets, explaining their critical functions in many developmental and disease contexts. DmD8 cells were collected at 7 time points (0M-bM-^@M-^Y, 10M-bM-^@M-^Y, 20M-bM-^@M-^Y, 30M-bM-^@M-^Y, 40M-bM-^@M-^Y, 60M-bM-^@M-^Y and 100M-bM-^@M-^Y) after a 5 minute Notch stimulation as 3 independent replicates. Immunoprecipitation was performed with Pol II (Ser 2 and Ser 5 phosphorylated) antibody and compared to the total input DNA. Samples from replicates #1 and #3 were labelled with Cy5, and replicate #2 was labelled with Cy3 as a dye-swap.

2012-12-31 | E-GEOD-35715 | biostudies-arrayexpress

Trancriptional regulation by axonal SMN on motor neuron cells

Project description:Muscular atrophy (SMA) is an autosomal recessive disease causing selective motor neuron death by the loss of telomeric survival motor neuron gene, SMN1. Axonal SMN, a-SMN, is a truncated form of SMN, derived from an alternatively spliced SMN1 gene. (Setola, et. al. 2007 PNAS 104, 1959-1964). The cellular clones expressing a-SMN in a tetracycline-dependent manner were isolated from NSC34 by two-step stable transfection, first with the tetracycline-repressor construct and subsequently with the a-SMN cDNA. To identify novel a-SMN target genes, the transcriptome of several a-SMN clones was analyzed and compared with that of parental cells.

2012-01-07 | E-MEXP-3402 | biostudies-arrayexpress

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