Expression data from Drosophila melanogaster wing disc - YAP/Yki vs YAP/Yki+dTcf/Pan-RNA RNAi conditions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493740 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Determine the genes controlled by dTcf/Pan involved in tumor formation manuscript dTcf/Pangolin suppresses growth and tumor formation in Drosophila
2018-09-29 | GSE120607 | GEO
Project description:Wing imaginal discs were dissected to generate body wall and wing/hinge fragments. Targets from three biological replicates of each were generated and the expression profiles were determined using Affymetrix Drosophila Genechip 1 arrays. Comparisons between the sample groups allow the identification of genes with localized expression patterns. Keywords = Drosophila, wing disc, spatially restricted transcripts Keywords: repeat sample
2003-01-08 | GSE93 | GEO
Project description:Throughout Metazoa, developmental processes are controlled by a surprisingly limited number of conserved signaling pathways. Precisely how these signaling cassettes were assembled in early animal evolution remains poorly understood, as do the molecular transitions that potentiated the acquisition of their myriad developmental functions. Here we analyze the molecular evolution of the proto-oncogene YAP/Yorkie, a key effector of the Hippo signaling pathway that controls organ size in both Drosophila and mammals. Based on heterologous functional analysis of evolutionarily distant Yap/Yorkie orthologs, we demonstrate that a structurally distinct interaction interface between Yap/Yorkie and its partner TEAD/Scalloped became fixed in the eumetazoan common ancestor. We then combine transcriptional profiling of tissues expressing phylogenetically diverse forms of Yap/Yorkie with ChIP-seq validation in order to identify a common downstream gene expression program underlying the control of tissue growth in Drosophila. Intriguingly, a subset of the newly-identified Yorkie target genes are also induced by Yap in mammalian tissues, thus revealing a conserved Yap-dependent gene expression signature likely to mediate organ size control throughout bilaterian animals. Combined, these experiments provide new mechanistic insights while revealing the ancient evolutionary history of Hippo signaling. We sought to define the downstream target genes of selected Yap variants by performing RNA sequencing analysis (RNA-seq) on total RNA isolated from GMR-Gal4>Yap eye discs. Transcriptional profiles were generated in triplicate from eye imaginal disks with either endogenous Yki, or GMR-Gal4 over-expressed Yki, Trichoplax Yap, Monosiga Yap, or Monisiga Yap+TEAD domain, using deep sequencing via Illumina Hi Seq.
2014-03-01 | E-GEOD-54600 | biostudies-arrayexpress
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.
2012-10-03 | E-GEOD-26678 | biostudies-arrayexpress
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
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.
2020-06-07 | GSE151935 | GEO
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).
2013-12-31 | GSE41427 | GEO
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.
2013-12-31 | GSE41426 | GEO
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.
2012-10-03 | GSE26678 | GEO
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.
2013-12-31 | GSE41425 | GEO