RNA-sequencing analysis of Drosophila yki tumor tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE154404 | GEO | 2020/11/25
REPOSITORIES: GEO
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Project description:Purpose: Flies with Yki gut tumors is a widely used Drosophila model of cancer cachexia. Since cancer cachexia is a multi-organ syndrome, its investigation requires understanding how tumors induce metabolic dysfunction in peripheral organs. To address this, we performed a body-wide single-cell transcriptome analysis of Yki tumor model flies. Methods: snRNA-seq analysis of whole-body flies (without heads) with and without Yki gut tumors. Results: The data provides information of transcriptome alternations related to tumor-induced cachexia, including expression of metabolic genes and tumor-host organ communications. Conclusions: Cachexia phenotypes in Yki tumor model flies originated from metabolic dysregulation in peripheral organs that induced by tumor secreted factors.
2025-02-21 | GSE229526 | GEO
Project description:RNA-sequencing analysis of Drosophila yki tumor tissue
| PRJNA646198 | ENA
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 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: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:Purpose: Activation of yki or Ras signaling pathways in ISCs causes overproliferation and ISC reprogramming. To gain insight into yki- and Ras-induced ISC reprogramming and gene expression, we performed a transcriptomic analysis of adult midgut with overexpression of yki-3SA or Ras1A in the ISCs.
2018-04-27 | GSE113728 | GEO
Project description:In order to investigate the underlying molecular mechanism of Yki-regulated tracheal progenitor migration and proliferation, genomic chromatin immunoprecipitation (ChIP-seq) was performed to identify loci bound by Yki in trachea.The peaks we observed included multiple Yki binding sites in the promoter and intronic regions of expanded (ex) and Diap1, which are well-characterized direct target genes of Yki. Other Yki targets are regulators in cell migration, cell cycle, and cell adhesion, and include hnt, which is a regulator of cell cycle in follicle cells.Yki occupancy was also pronounced in the promoter region of two heparan sulfate proteoglycans (HSPGs), Dally and Dally-like protein (Dlp) , which together with Ex and Diap1 belong to the cell migration GO cluster. Significant ChIP-seq peaks were observed in the region of N-cadherin (Ncad), a cell adhesion molecule that promotes cell migration and Matrix metalloproteinase-1 (MMP-1), a component of the extracellular matrix. Together, these results suggest that Yki activates various targets that function in cell cycle, cell migration and cell adhesion.
2022-04-22 | GSE184856 | GEO
Project description:Purpose: localized aberrant cell proliferation induced by activation of Yki in ISCs impairs muscle functions. To gain insight into the cross talk between intestine and muscle, we performed a transcriptomic analysis of thoracic muscles in ISC overproliferation flies. Methods: To extract total RNAs for RNA-Seq experiment, we used 10 thoraces dissected out from both esg-Gal4, tub-Gal80ts, UAS-GFP/+ (Con) and esg-Gal4, tub-Gal80ts, UAS-GFP/UAS-Yki-act (Yki) flies incubated for 8 days at 29°C. After assessing RNA quality with Agilent Bioanalyzer, mRNAs were enriched by poly-A pull-down. Then, sequencing libraries constructed with Illumina TruSeq RNA prep kit were sequenced using Illumina HiSeq2000 at the Columbia Genome Center (http://systemsbiology.columbia.edu/genome-center). We multiplexed samples in each lane, which yields targeted number of single-end 100 bp reads for each sample, as a fraction of 180 million reads for the whole lane. Sequence reads were mapped back to the Drosophila genome (flybase genome annotation version r5.51) using Tophat. With the uniquely mapped reads, we quantified gene expression levels using Cufflinks (FPKM values). Next, we performed data normalization on the read counts and applied a negative binomial statistical framework using the Bioconductor package DESeq to quantify differential expression between experimental and control data. Results: Gene list enrichment analysis of the downregulated muscle transcriptome by ISCs Yki overexpressioin revealed a striking enrichment of multiple metabolic processes impinging on carbohydrate metabolism, amino acid metabolism, metabolism of vitamins and cofactors, and metabolism of xenobiotics by cytochrome P450. Interestingly, target genes of Foxo, a transcription factor inhibited by insulin/IGF signaling, are enriched in the upregulated muscle transcriptome of ISCs Yki overepxression flies. In particular, induction of InR and Thor, well-characterized targets of Foxo, are validated with qPCR. Conclusions: Our study represents ISCs overproliferation induced by Yki overepxression remotedly regulates muscle function and gene expression probally via modulation of insulin signaling in muscle. Our results show that RNA-seq offers a comprehensive evaluation of signaling network and biological process in organ communication. Thoraces mRNA profiles of both esg-Gal4, tub-Gal80ts, UAS-GFP/+ (Con) and esg-Gal4, tub-Gal80ts, UAS-GFP/UAS-Yki-act (Yki) flies incubated for 8 days at 29°C were generated by deep sequencing, in replicate, using Illumina HiSeq2000.
2015-02-01 | E-GEOD-65325 | biostudies-arrayexpress
Project description:Anorexia is frequently observed during cancer and associated with increased morbidity and mortality. Our previous work has shown the presence of transcription factors in the hypothalamus of anorectic tumor-bearing rats. The aim of the present study was, therefore, to assess expression of neuropeptides, neurotransmitter-synthesizing enzymes and receptors in this structure. Morris hepatoma 7777 cells injected subcutaneously in Buffalo rats provoked a 15% reduction in food intake and 10% lower body weight when the tumor represented 1-2% of body mass. Real-time PCR showed that tumor-bearing rats did not display the increase in hypothalamic agouti-related peptide mRNA observed in food-restricted weight-matched animals. These findings indicate that blunted hypothalamic AgRp mRNA expression underlies cancer-associated anorexia.
2010-04-10 | GSE18688 | GEO
Project description:Anorexia is frequently observed during cancer and associated with increased morbidity and mortality. Our previous work has shown the presence of transcription factors in the ventral striatum of anorectic tumor-bearing rats. The aim of the present study was, therefore, to assess expression of neuropeptides, neurotransmitter-synthesizing enzymes and receptors in this structure. Morris hepatoma 7777 cells injected subcutaneously in Buffalo rats provoked a 15% reduction in food intake and 10% lower body weight when the tumor represented 1-2% of body mass. Mircorarrays and real-time PCR revealed increased ventral striatal prostaglandin D synthase expression in food-restricted animals compared to anorectic tumor-bearing rats. These findings indicate that reduced ventral striatal prostaglandin D synthesis underlies cancer-associated anorexia.
2010-04-10 | GSE18687 | GEO