Notch targets in DmD8 and KC Drosophila cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE9964 | GEO | 2009/02/17
SECONDARY ACCESSION(S): PRJNA103977
REPOSITORIES: GEO
Similar Datasets
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)
2009-02-17 | GSE9965 | GEO
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
Project description:During hematopoiesis, Notch regulates both the emergence of stem and progenitor cells and the subsequent cell fate choices and differentiation. To investigate how Notch drives cells to differentiate we have used a genome-wide approach to identify direct Notch targets in Drosophila Kc cells. These data are the results from Su(H) ChIP-Chip experiments to identify genomic regions occupied by Su(H) after Notch activation in Kc cells.
2013-03-08 | GSE43132 | GEO
Project description:During hematopoiesis, Notch regulates both the emergence of stem and progenitor cells and the subsequent cell fate choices and differentiation. To investigate how Notch drives cells to differentiate we have used a genome-wide approach to identify direct Notch targets in Drosophila Kc cells. These data are the results from Su(H) ChIP-Chip experiments to identify genomic regions occupied by Su(H) after Notch activation in Kc cells. 3 replicates of Su(H) ChIP after 30 min. Notch activation..
2013-03-08 | E-GEOD-43132 | biostudies-arrayexpress
Project description:Several co-repressors interact directly with the DNA-binding protein CSL [Su(H) in Drosophila] and are proposed to keep target genes silenced in the absence of Notch activity. To investigate co-repressor activity in the context of this well defined signalling pathway, we analysed the genome-wide binding profile of the best-characterized CSL co-repressor in Drosophila, Hairless, in Kc cells and in wing imaginal discs. The binding profile in wing discs of a second CSL interacting repressor, SMRTER, was also analysed. There was significant overlap between Hairless and Su(H), both in Kc cells and in wing discs, where they were predominantly found in chromatin with active enhancer marks. The Hairless complex was widely present at some Notch regulated enhancers in the wing disc,but no binding was detected at others, indicating that it is not essential for silencing per se. Analysis of target enhancers confirmed differential requirements for Hairless. SMRTER binding significantly overlapped with Hairless, rather than complementing it, and many enhancers were apparently co-bound by both factors. Our analysis indicates that the actions of Hairless and SMRTER gate the enhancers to Notch activity and to Ecdysone signalling respectively, to ensure that the appropriate levels and timing of target gene expression are achieved.
2017-12-31 | GSE97598 | GEO
Project description:This randomized phase I/II clinical trial is studying the side effects and best dose of gamma-secretase/notch signalling pathway inhibitor RO4929097 when given together with vismodegib and to see how well they work in treating patients with advanced or metastatic sarcoma. Vismodegib may slow the growth of tumor cells. Gamma-secretase/notch signalling pathway inhibitor RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving vismodegib together with gamma-secretase/notch signalling pathway inhibitor RO4929097 may be an effective treatment for sarcoma.
| 2091475 | ecrin-mdr-crc
Project description:Several co-repressors interact directly with the DNA-binding protein CSL [Su(H) in Drosophila] and are proposed to keep target genes silenced in the absence of Notch activity. To investigate co-repressor activity in the context of this well defined signalling pathway, we analysed the genome-wide binding profile of the best-characterized CSL co-repressor in Drosophila, Hairless, in Kc cells and in wing imaginal discs. The binding profile in wing discs of a second CSL interacting repressor, SMRTER, was also analysed. There was significant overlap between Hairless and Su(H), both in Kc cells and in wing discs, where they were predominantly found in chromatin with active enhancer marks. The Hairless complex was widely present at some Notch regulated enhancers in the wing disc,but no binding was detected at others, indicating that it is not essential for silencing per se. Analysis of target enhancers confirmed differential requirements for Hairless. SMRTER binding significantly overlapped with Hairless, rather than complementing it, and many enhancers were apparently co-bound by both factors. Our analysis indicates that the actions of Hairless and SMRTER gate the enhancers to Notch activity and to Ecdysone signalling respectively, to ensure that the appropriate levels and timing of target gene expression are achieved.
2017-12-31 | GSE97597 | GEO
Project description:Several co-repressors interact directly with the DNA-binding protein CSL [Su(H) in Drosophila] and are proposed to keep target genes silenced in the absence of Notch activity. To investigate co-repressor activity in the context of this well defined signalling pathway, we analysed the genome-wide binding profile of the best-characterized CSL co-repressor in Drosophila, Hairless, in Kc cells and in wing imaginal discs. The binding profile in wing discs of a second CSL interacting repressor, SMRTER, was also analysed. There was significant overlap between Hairless and Su(H), both in Kc cells and in wing discs, where they were predominantly found in chromatin with active enhancer marks. The Hairless complex was widely present at some Notch regulated enhancers in the wing disc,but no binding was detected at others, indicating that it is not essential for silencing per se. Analysis of target enhancers confirmed differential requirements for Hairless. SMRTER binding significantly overlapped with Hairless, rather than complementing it, and many enhancers were apparently co-bound by both factors. Our analysis indicates that the actions of Hairless and SMRTER gate the enhancers to Notch activity and to Ecdysone signalling respectively, to ensure that the appropriate levels and timing of target gene expression are achieved.
2017-12-31 | GSE97599 | GEO
Project description:Several co-repressors interact directly with the DNA-binding protein CSL [Su(H) in Drosophila] and are proposed to keep target genes silenced in the absence of Notch activity. To investigate co-repressor activity in the context of this well defined signalling pathway, we analysed the genome-wide binding profile of the best-characterized CSL co-repressor in Drosophila, Hairless, in Kc cells and in wing imaginal discs. The binding profile in wing discs of a second CSL interacting repressor, SMRTER, was also analysed. There was significant overlap between Hairless and Su(H), both in Kc cells and in wing discs, where they were predominantly found in chromatin with active enhancer marks. The Hairless complex was widely present at some Notch regulated enhancers in the wing disc,but no binding was detected at others, indicating that it is not essential for silencing per se. Analysis of target enhancers confirmed differential requirements for Hairless. SMRTER binding significantly overlapped with Hairless, rather than complementing it, and many enhancers were apparently co-bound by both factors. Our analysis indicates that the actions of Hairless and SMRTER gate the enhancers to Notch activity and to Ecdysone signalling respectively, to ensure that the appropriate levels and timing of target gene expression are achieved.
2017-12-31 | GSE97601 | GEO
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.
2012-12-31 | GSE35719 | GEO