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ABSTRACT: Genome-wide binding of Yki and GAF in embryos and wing imaginal discs

PROVIDER: PRJNA184674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR504946.fastq.gz	Fastqsanger.gz
	SRR504947.fastq.gz	Fastqsanger.gz
	SRR504948.fastq.gz	Fastqsanger.gz
	SRR504949.fastq.gz	Fastqsanger.gz
	SRR504950.fastq.gz	Fastqsanger.gz

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Genome-wide binding of Sd and Yki in imaginal discs

Project description:The transcription cofactor Yki drives growth and proliferation in part by controlling mitochondrial network formation. To determine if Yki and Sd are directly bound to DNA corresponding to mitochondrial genes, we used chromatin immunoprecipitation and whole genome tiling arrays (ChIP-chip) to identify regions bound by these factors in eye-antenna and wing imaginal discs. The supplementary .bed files contain all Yki or Sd binding sites (called at 5% FDR) in wing or eye-antenna imaginal discs, as well as shared Sd+Yki sites and associated target genes. Wing or eye-antenna imaginal discs ChIPped for Yki or Sd-GFP vs. input DNA from corresponding imaginal discs.

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Genome-wide binding of Sd and Yki in imaginal discs

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Project description:Promoter proximal pausing (PPP) of RNA Polymerase II has emerged as a crucial rate-limiting-step in the regulation of gene expression. Regulation of PPP is brought about by complexes 7SK snRNP, P-TEFb (Cdk9/cycT) and the Negative Elongation Factor (NELF) which are highly conserved from Drosophila to humans. Here we show that RNAi-mediated depletion of bin3 or Hexim of the 7SK snRNP complex or depletion of individual components of the NELF complex enhance Yki-driven growth leading to neoplastic transformation of Drosophila wing imaginal discs. We also show that increased CDK9 expression cooperates with Yki, in driving neoplastic growth. Interestingly, over-expression of CDK9 on its own or in the background of depletion of one of the components of 7SK snRNP or the NELF complex necessarily and specifically needed Yki over-expression to cause tumorous growth. Genome-wide gene expression analyses suggested that deregulation of protein homeostasis is associated with tumorous growth of wing imaginal discs. As both Fat/Hippo/Yki pathway and PPP are highly conserved, our observations may provide insights into mechanisms of oncogenic function of YAP, the orthologue of Yki in human.

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Genome-wide binding of Yki and GAF in embryos and wing imaginal discs [ChIP-Seq]

Project description:The Hippo pathway regulates metazoan growth, acting through the transcriptional co-activators Yorkie (in Drosophila) and Yap and Taz (in vertebrates). Much attention has been focused on upstream regulators of Yorkie and its homologues. In contrast, the mechanisms by which they actually promote transcription have remained poorly understood. Genome-wide chromatin binding experiments support extensive functional overlap between Yorkie and GAF. Chromatin binding identifies thousands of Yorkie sites, the majority of which are associated with elevated transcription, based on genome-wide analysis of mRNA and histone H3K4Me3 modification. Our studies establish a molecular basis for transcriptional activation by Yorkie and implicate it as a global regulator of transcriptional activity in Drosophila. This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. This dataset was generated in collaboration with Ken Irvine at HHMI/Rutgers University and Richard S. Mann at Columbia University. It contains ChIP-seq data (Illumina) for multiple transcription factor antibodies in Drosophila embryos and larval wing imaginal discs.

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