ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE22650 | GEO | 2010/07/28
SECONDARY ACCESSION(S): PRJNA128013
REPOSITORIES: GEO
Similar Datasets
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 3 replicates of Twist ChIP after30 min. Notch activation.
2010-07-27 | E-GEOD-22650 | 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: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
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 Su(H) antibody and compared to the total input DNA. Samples from replicates #1 and #2 were labelled with Cy5, and replicate #3 was labelled with Cy3 as a dye-swap. For time point 10M-bM-^@M-^Y, only 2 biological replicates were obtained.
2012-12-31 | E-GEOD-35719 | biostudies-arrayexpress
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
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 | GSE35715 | 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. 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
Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist
2013-12-12 | GSE53222 | GEO
Project description:Background: The basic helix-loop-helix transcription factor TWIST1 (Twist) is involved in embryonic cell lineage determination and mesodermal differentiation. There is evidence to indicate that Twist expression plays a role in breast tumor formation and metastasis, but the role of Twist in dysregulating pathways that drive the metastatic cascade is unclear. Importantly, the genes and pathways dysregulated by Twist in cell lines and mouse models have not been validated against data obtained from patient samples. Methods: We over-expressed the human Twist gene in non-metastatic MCF-7 breast cancer cells to generate the estrogen-independent metastatic breast cancer cell line MCF-7/Twist. These cells were then inoculated in the mammary fat pad of female severe compromised immunodeficient mice, which subsequently formed xenograft tumors that metastasized to the lungs. Microarray data was collected from both in vitro (MCF-7 and MCF-7/Twist cell lines) and in vivo (primary tumors and lung metastases) models of Twist expression. Our data was compared to publically available gene signatures of different subtypes, classes, and grades of human breast cancers. Results: Our data establishes a Twist over-expressing mouse model of breast cancer, which metastasizes to the lung and replicates some of the ontogeny of human breast cancer progression. Gene profiling data, following Twist expression, exhibited novel metastasis driver genes as well as cellular maintenance genes that were synonymous with the metastatic process. We demonstrated that the genes and pathways altered in the transgenic cell line and metastatic animal models generated, parallel many of dysregulated gene pathways observed in human breast cancers. Conclusions: Analogous gene expression patterns observed in both in vitro and in vivo Twist preclinical models of breast cancer metastasis and public patient data sets supports the functional role of Twist in promoting breast tumor metastasis. Our data indicates that genetic dysregulation of Twist at the cellular level drives alterations in related gene pathways in the Twist metastatic mouse model which are comparable to changes seen in breast cancer patient samples. Lastly, we have identified novel genes and pathways that could be further investigated as targets for drugs to ultimately treat metastatic breast cancer.
2017-01-13 | GSE87705 | GEO