Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157035 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
2021-10-07 | GSE185339 | GEO
Project description: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))
2021-10-08 | GSE185490 | GEO
Project description:The systemic response to injury in Drosophila melanogaster is characterized by the activation of specific signaling pathways that facilitate the regeneration of wounded tissue and help coordinate wound healing with organism growth. The mechanisms by which damaged tissues influence the development and function of peripheral non-injured tissues is not fully understood. Injury was induced in early third instar larvae via temperature-dependent cell death in wing imaginal discs. Microarray analysis using RNA isolated from injured and control was used to identify genes underlying the systemic injury response. We identified 150 genes which were differentially expressed in response to localized cell death in wing imaginal discs. Upregulated genes were associated biological processes including carnitine biosynthesis, signal transduction and regulation of oxidoreductase activity while terms associated with downregulated genes included wound healing, imaginal disc-derived wing hair outgrowth, and regulation of glutamatergic synaptic transmission. Pathway analysis revealed that wing disc damage led to changes in fatty acid, cysteine, and carnitine metabolism. One gene, 14-3-3ζ, which encodes a known regulator of Ras/MAPK signaling was identified as a potential regulator of transdetermination during tissue regeneration. Our results raise the possibility that immune function and cell proliferation during wing disc repair and regeneration in Drosophila may require the sulfur amino acid cysteine and its’ metabolites, taurine and glutathione, similar to what has been reported during tissue repair in mammals. Further, it seems likely that imaginal disc damage stimulates the mobilization of fatty acids to support the energetically demanding process of tissue regeneration. The roles of additional genes that are differentially regulated following imaginal disc injury remain to be elucidated.
2017-09-30 | GSE94938 | GEO
Project description:Chromatin insulators are DNA protein complexes that mediate inter and intra chromosomal interactions. Boundary Element Associated Factor- 32 (BEAF-32) is an insulator protein predominantly found near gene promoters and thought to play a role in gene expression. We find that mutations in BEAF-32 are lethal, show loss of epithelial morphology in imaginal discs and cause neoplastic growth defects. To investigate the molecular mechanisms underlying this phenotype, we carried out a genome-wide analysis of BEAF-32 localization in wing imaginal disc cells. Mutation of BEAF-32 results in miss-regulation of 3850 genes by at least 1.5-fold, 647 of which are bound by this protein in wing imaginal cells. Up-regulated genes encode proteins such as Bazooka, a determinant of cell polarity; the Insulin receptor-1 and the p70-S6 kinase, involved in the insulin growth factor pathway that can activate various pathways involved in cell proliferation; and the Unpaired 3 ligand of the Janus kinase (JNK) pathway, and its target gene Socs35, which can also activate cell proliferation. The expression of genes involved in DNA homologous end repair and oxidative stress pathways is also increased in BEAF-32 mutants. Among the down-regulated genes are those encoding components of the Wingless pathway, which is required for cell differentiation, and amino acid metabolism. Miss-regulation of these genes explains the unregulated cell growth and neoplastic phenotypes observed in imaginal tissues of BEAF-32 mutants. Here we examine mapping the genomic binding sites and its distribution of BEAF-32, a Drosophila insulator proteins in wing imaginal tissue. We performed ChIP-seq analysis using BEAF-32B.
2012-07-05 | E-GEOD-36735 | biostudies-arrayexpress
Project description:In Drosophila, homozygosity for tumor suppressors, like lethal giant larvae, lgl, results in neoplastic transformation of imaginal disc epithelium - characterized by loss of their apico-basal polarity, unrestricted growth and invasion into neighboring tissues/organs. In genetic mosaics, however, lgl mutant clones are eliminated shortly after their initiation by cell competition. On the other hand, lgl mutant clones generated in Minute (M) genetic background, which compromises cell competition from the neighboring wild type cells, display clonal progression and tissue invasion. To gain insight into the molecular players of fly tumorigensis we undertook genome-wide transcriptional profiling of neoplastically transformed mosaic wing imaginal discs where lgl- clones were induced in M genetic background. Mosaic wing imaginal discs carrying wild type (lgl+) clones, also generated in M genetic background, served as controls. Transcriptional profile revealed up-regulation of a number of signaling pathways, such as Hippo, Wnt, TGF-beta or EGFR. Transcriptional profile of lgl- mosaic imaginal discs therefore provides a useful resource for identification of genes/pathways that are functionally relevant for carcinogenesis
2011-06-08 | E-MEXP-2753 | biostudies-arrayexpress
Project description:In Drosophila, homozygosity for neoplastic tumor suppressors, like lethal giant larvae, lgl results in malignant transformation of all larval imaginal discs. To gain insight into the molecular players involved in fly tumorigenesis we undertook genome-wide transcriptional profiling of neoplastically transformed wing imaginal discs of lgl mutants. Wild type (Canton S) wing imaginal discs served as control. The transcriptional profile, for instance, revealed the misregulation of JNK and JAK-STAT signaling which is implicated in epithelial transformation in Drosophila. These transcriptional profiles, therefore, provide a useful resource for identification of genes/pathways that are functionally relevant for carcinogenesis.
2011-09-21 | E-MEXP-2920 | biostudies-arrayexpress
Project description:Screening for binding partners of the splicing factor SmD3 and changes in interaction upon depletion of the protein Ecdysoneless (Ecd) in the nubbin domain of third-instar larval wing imaginal discs.
2021-09-09 | PXD019761 | Pride
Project description:Genome-wide identification of the binding sites of the Drosophila transcription factors Achaete, Asense, E(spl)m3-HLH and Senseless in wing imaginal cells using DamID profiling.
2014-01-01 | GSE53009 | GEO
Project description:Epithelial tumors can progress from a benign tissue overgrowth (hyperplasia) to a malignant neoplastic tumor, which is characterized by an increase in motility and invasiveness. The Cohen laboratory has developed an epithelial tumor model in which overexpression of the epidermal growth factor receptor gene (EGFR) leads to benign tissue hyperplasia. When combined with other cooperating factors, EGFR overexpression can lead to neoplasia and malignant metastasis. Microarray analysis were performed in normal epithelia, hyperplastic, and neoplastic tumors collected from Drosophila wing imaginal discs to identify genes whose misexpression correlates with tumor progression
2018-12-21 | GSE95613 | 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