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Distribution of TrxG, RNA Pol II and associated histone marks in Sg4 cells

ABSTRACT: PcG and TrxG are important epigenetic regulators of genome expression. Here we have determined genomic distributions of TRX, ASH1, RNA Pol II, H3K4me3, H3K27ac, H3K9ac in cultured Drosophila Sg4 cells by hybridization of ChIP products with tiling microarrays.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE18176 | GEO | 2010/01/08

SECONDARY ACCESSION(S): PRJNA119535

REPOSITORIES: GEO

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Distribution of PcG, TrxG, RNA Pol II and associated histone marks in ML-DmD23-c4 cells

Project description:PcG and TrxG are important epigenetic regulators of genome expression. Here we have determined genomic distributions of PC, E(Z), H3K27me3, TRX, ASH1, RNA Pol II, H3K4me3, H3K27ac in cultured Drosophila ML-DmD23-c4 cells by hybridization of ChIP products with tiling microarrays

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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

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The BET protein FSH functionally interacts with ASH1 to orchestrate global gene activity in Drosophila

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