The complex role of Naked cuticle in Drosophila wing development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA703379 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13755272_1.fastq.gz | Fastqsanger.gz | |||
| SRR13755272_2.fastq.gz | Fastqsanger.gz | |||
| SRR13755273_1.fastq.gz | Fastqsanger.gz | |||
| SRR13755273_2.fastq.gz | Fastqsanger.gz | |||
| SRR13755274_1.fastq.gz | Fastqsanger.gz |
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Project description:It is of tremendous interests to understand how Wnt signaling is regulated in a precise manner both temporally and spatially. Naked cuticle (Nkd) acts as a negative-feedback inhibitor for Wingless (Wg, a fly Wnt) signaling in Drosophila embryonic development. In the present study, we show that nkd is essential for wing pattern formation, such that both gain and loss of nkd result in the disruption of Wg target expression in larvae stage and abnormal adult wing morphologies. Our results of high-throughput sequencing suggest that nkd have profound effects on Drosophila wing development with several critical signaling pathways involved, we conclude that Nkd inhibits the canonical Wg pathway during Drosophila wing development beyond embryonic stage and may play a mediated role in cross-talk between development-related pathways.
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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.
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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.
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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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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).
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