Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144203 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR315119.fastq.gz | Fastqsanger.gz | |||
| SRR315120.fastq.gz | Fastqsanger.gz | |||
| SRR315121.fastq.gz | Fastqsanger.gz | |||
| SRR315122.fastq.gz | Fastqsanger.gz |
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Similar Datasets
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: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: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
Project description:Generation of chromatin maps for ASH1 and FSH applying ChIP-seq
| PRJNA155531 | ENA
Project description:The Drosophila Trithorax group (TrxG) protein ASH1 remains associated with mitotic chromatin through mechanisms that are poorly understood. ASH1 dimethylates histone H3 at lysine 36 via its SET domain. Here we identify domains of the TrxG protein ASH1 that are required for mitotic chromatin attachment in living Drosophila. Quantitative live imaging demonstrates that ASH1 requires AT hooks and the BAH domain but not the SET domain for full chromatin binding in metaphase, and that none of these domains are essential for interphase binding. Genetic experiments show that disruptions of the AT hooks and the BAH domain together, but not deletion of the SET domain alone, are lethal. Transcriptional profiling demonstrates that intact ASH1 AT hooks and the BAH domain are required to maintain expression levels of a specific set of genes, including several involved in cell identity and survival. This study identifies in vivo roles for specific ASH1 domains in mitotic binding, gene regulation and survival that are distinct from its functions as a histone methyltransferase.
2021-07-31 | GSE95226 | GEO
Project description:Mrg15 allosterically activates Ash1’s H3K36 methyltransferase activity and facilitates Ash1’s trithorax group protein function in Drosophila
| PRJNA360011 | ENA
Project description:see Super Series Summary Cross-linked chromatin derived from Drosophila S2-DRSC cells was immunoprecipitated using antibodies targeting ASH1 and FSH. Precipitated chromatin was sequenced applying Illumina sequencing.
2013-02-06 | E-GEOD-36404 | biostudies-arrayexpress
Project description:Chromatin accessibility in populations of Drosophila melanogaster
| PRJNA400650 | ENA
Project description:Analysis of the trithorax Group (trxG) genes ash2 and ash1 wing imaginal disc transcriptomes.
| PRJNA95865 | ENA