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

ABSTRACT: 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))

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE185490 | GEO | 2021/10/08

REPOSITORIES: GEO

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RNA-Seq of Notch-stimulated overgrowing Drosophila melanogaster wing imaginal discs

Project description:Aim: mRNA profile of 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) results in mRNA expression changes that, while partly overlapping with Notch only (N), and with scrib mutation only (S), are unique to the combination

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

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Single-cell transcriptomic analysis of the scrib mutant wing imaginal discs

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

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

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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.

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

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

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