Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA95865 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The absent, small or homeotic discs 2 (ash2) gene, a member of the trithorax Group (trxG) of transcriptional regulators, is functionally related to ash1. However, ASH2 and ASH1 belong to distinct multimeric complexes of unknown composition and it is unclear how they act to regulate transcription. In this study, examination of gene expression profiles in wing imaginal discs from ash2 and ash1 mutants revealed their transcriptomes are very similar and correlate with wing phenotypes. Keywords: loss of function analysis
2007-07-31 | GSE4923 | GEO
Project description:Trithorax group (TrxG) proteins counteract Polycomb silencing by an as yet uncharacterized mechanism. A well-known member of the TrxG is the histone methyltransferase Absent, Small, or Homeotic discs 1 (ASH1). In Drosophila ASH1 is needed for the maintenance of Hox gene expression throughout development, which is tightly coupled to preservation of cell identity. In order to understand the molecular function of ASH1 in this process, we performed affinity purification of tandem-tagged ASH1 followed by mass spectrometry (AP-MS) and identified FSH, another member of the TrxG as interaction partner. Here we provide genome-wide chromatin maps of both proteins based on ChIP-seq.
2013-06-30 | GSE30820 | GEO
Project description:Trithorax group (TrxG) proteins counteract Polycomb silencing by an as yet uncharacterized mechanism. A well-known member of the TrxG is the histone methyltransferase Absent, Small, or Homeotic discs 1 (ASH1). In Drosophila ASH1 is needed for the maintenance of Hox gene expression throughout development, which is tightly coupled to preservation of cell identity. In order to understand the molecular function of ASH1 in this process, we performed affinity purification of tandem-tagged ASH1 followed by mass spectrometry (AP-MS) and identified FSH, another member of the TrxG as interaction partner. Here we provide genome-wide chromatin maps of both proteins based on ChIP-seq. Our Dataset comprises of 4 ChIP-seq samples using chromatin from S2 cells which was immunoprecipitated, using antibodies against Ash1, FSH-L and FSH-SL.
2013-06-30 | E-GEOD-30820 | biostudies-arrayexpress
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:We have carried out eukaryotic whole-genome Illumina RNA-seq of regenerating blastema cells and control undamaged wing imaginal disc cells to identify the differentially expressed genes during regeneration.
2017-07-25 | GSE101797 | GEO
Project description:Ash1 is a Trithorax Group (TrxG) protein with histone methyl transferase activity that is associated with gene activation. Here we use ChIP-chip to determine the occupancy of Ash1 at promoters in murine embryonic stem cells.
2010-02-28 | GSE20063 | GEO
Project description:Ash1 is a Trithorax Group (TrxG) protein with histone methyl transferase activity that is associated with gene activation. Here we use ChIP-chip to determine the occupancy of Ash1 at promoters in murine embryonic stem cells. This dataset includes singlet ChIP-chip data targeting Ash1 in murine Embryonic stem cells.
2010-05-14 | E-GEOD-20063 | biostudies-arrayexpress
Project description:Background: The question of how cells re-establish gene expression states after cell division is still poorly understood. Genetic and molecular analyses have indicated that Trithorax group (TrxG) proteins are critical for the long-term maintenance of active gene expression states in many organisms. A generally accepted model suggests that TrxG proteins contribute to maintenance of transcription by protecting genes from inappropriate Polycomb group (PcG)-mediated silencing, instead of directly promoting transcription. Results: Here we report a physical and functional interaction in Drosophila between two members of the TrxG, the histone methyltransferase ASH1 and the bromodomain and extraterminal family protein FSH. We investigated this interface at the genome level, uncovering a widespread colocalization of both proteins at promoters and PcG-bound intergenic elements. Our integrative analysis of chromatin maps and gene expression profiles revealed that the observed ASH1-FSH binding pattern at promoters is a hallmark of active genes. Inhibition of FSH-binding to chromatin resulted in global down-regulation of transcription. In addition, we found that genes displaying marks of robust PcG-mediated repression also have ASH1 and FSH bound to their promoters. Conclusions: Our data strongly favor a global coactivator function of ASH1 and FSH during transcription, as opposed to the notion that TrxG proteins impede inappropriate PcG-mediated silencing, but are dispensable elsewhere. Instead, our results suggest that PcG repression needs to overcome the transcription-promoting function of ASH1 and FSH in order to silence genes. Refer to individual Series
2013-02-06 | E-GEOD-36450 | biostudies-arrayexpress
Project description:Background: The question of how cells re-establish gene expression states after cell division is still poorly understood. Genetic and molecular analyses have indicated that Trithorax group (TrxG) proteins are critical for the long-term maintenance of active gene expression states in many organisms. A generally accepted model suggests that TrxG proteins contribute to maintenance of transcription by protecting genes from inappropriate Polycomb group (PcG)-mediated silencing, instead of directly promoting transcription. Results: Here we report a physical and functional interaction in Drosophila between two members of the TrxG, the histone methyltransferase ASH1 and the bromodomain and extraterminal family protein FSH. We investigated this interface at the genome level, uncovering a widespread colocalization of both proteins at promoters and PcG-bound intergenic elements. Our integrative analysis of chromatin maps and gene expression profiles revealed that the observed ASH1-FSH binding pattern at promoters is a hallmark of active genes. Inhibition of FSH-binding to chromatin resulted in global down-regulation of transcription. In addition, we found that genes displaying marks of robust PcG-mediated repression also have ASH1 and FSH bound to their promoters. Conclusions: Our data strongly favor a global coactivator function of ASH1 and FSH during transcription, as opposed to the notion that TrxG proteins impede inappropriate PcG-mediated silencing, but are dispensable elsewhere. Instead, our results suggest that PcG repression needs to overcome the transcription-promoting function of ASH1 and FSH in order to silence genes.
2013-02-06 | GSE36450 | GEO