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

ABSTRACT: 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.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Sarah Bray

PROVIDER: E-GEOD-41426 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Su(H) bound regions in Su(H) 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 Su(H)-expressing Drosophila wing discs. 3 independent replicates. Immuno Precipitation perfomed with Su(H) antibody on chromatin isolated from wing discs overexpressing Su(H) (UAS-GFP:Su(H) expressed by the patched[559.1]-Gal4 driver) and compared to the total input DNA. Samples from replicate #1 and #2 were labelled with Cy5 and replicate #3 as dye-swap with Cy3.

2013-12-31 | E-GEOD-41425 | biostudies-arrayexpress

Gene expression changes in Nicd induced wing disc hyperplasia

Project description:The outcome of Notch proliferation on proliferation depends on the context. In Drosophila wing imaginal discs Notch activation causes hyperplasia despite having localized inhibitory effects on proliferation. To understand te underlying mechanisms we have used genomic strategies to identify the Notch-Su(H) target genes during wing discs hyperplasis. these data are the results from expression profiling the RNAs from hyperplastic wing discs overexpressing Nicd. Direct comparison of third instar lavae wing imaginal disc Nicd (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with UAS-Nicd; FRT82B) vs control (abxUbxFLPase; Act>y>Gal4, UAS GFP; FRT82B tubGal80 with FRT82B ). 4 Biological replicates, the 2nd replicate was performed as a dye-swap.

2013-12-31 | E-GEOD-41428 | biostudies-arrayexpress

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

2013-12-31 | GSE41426 | GEO

Gene expression changes in Nicd induced wing disc hyperplasia

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Gene expression changes in Su(H) induced wing disc hyperplasia

Project description:The outcome of Notch activation of proliferation depends on cellular context. In Drosophila wing discs Notch pathway overactivation results in hyperplasia. To understand the mechanisms we have used genomic strategies to indetify the Notch-S(H) target genes directly regulated in wing disc hyperplasia. These data are the results from expression profiling the RNAs from hyperplastic wing discs overexpressing Su(H). Direct comparison of Giant third instar lavae wing imaginal disc (UAS-GFP:Su(H) expressed by the patched[559.1]-Gal4 driver) vs control (UAS-NLS-GFP expressed by the patched[559.1]-Gal4 driver). 3 Biological replicates, the 3rd replicate was performed as a dye-swap.

2013-12-31 | E-GEOD-41427 | biostudies-arrayexpress

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ChIP-chip from Kc cells with Su(H) antibodies after 30 minutes Notch activation

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

Gene expression changes in Su(H) induced wing disc hyperplasia

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Su(H) ChIP-on-chip of Notch-stimulated overgrowing Drosophila melanogaster wing imaginal discs

Project description:Aim: Su(H) chromatin occupancy profiling by ChIP on larval wing imaginal discs of Drosophila melanogaster to study the cooperation between Notch activation and loss of epithelial polarity (scrib mutation) during neoplastic growth. Results: The combination of Notch activation and scribble mutation (NS) does not lead to a general redeployment of Su(H) binding as compared to individual conditions (Notch only (N), and scrib mutation only (S))

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Genome -wide profile of SMRTER binding in Drosophila wing imaginal discs

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.

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