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Series GSE81795 Query DataSets for GSE81795
Status Public on Jul 26, 2016
Title An epigenetic mark of polycomb response elements implemented by Trx/MLL/COMPASS
Organisms Drosophila melanogaster; Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary In Drosophila, Polycomb Response Elements (PREs) are identified as genomic sequences allowing the maintenance of transcriptional repression in the absence of the initiating signal. Although PREs in Drosophila are well characterized, the existence of mammalian PRE-like elements remains debated. Accumulating evidence supports a model in which CpG islands function to recruit Polycomb-Group complexes (PcG), however, it is not evident which subclasses of CpG islands serve as PREs. Trithorax (Trx), which is required for positive regulation of gene expression in Drosophila, is known to co-bind Drosophila PREs where it is thought to antagonize polycomb-dependent silencing of nearby genes. Here, we demonstrate the existence of Trx-dependent H3K4 dimethylation loci that specifically mark Drosophila PREs and are required for the maintenance of expression of the nearby genes. Similarly, in human cells, we find ~ 3000 MLL1 (human Trx homologue)-dependent H3K4 dimethylation loci, which correlate strongly with CpG island density. In the absence of MLL1 and H3K4 dimethylation at these loci, there is an increase in H3K27 trimethylation levels, suggesting these sites can recruit Polycomb Repressive Complex 2 (PRC2). By inhibiting PRC2-dependent silencing in the absence of MLL1, we establish that a balance exists between MLL1 and PRC2, and their respective capacity to maintain or repress transcription. Thus, by investigating a conserved function between Trx and MLL1, we provide rules for the identification of CpG island subclasses serving as PRE-like sequences within the human genome.
Overall design To examine changes in histone-modification profiles and gene expression after depletion of Trx in Drosophila S2 cells, and MLL1 in human HCT116 cells. We also treated MLL1-NULL HCT116 cells with GSK126 (5uM) for 4 days and measured changes in gene expression.
Contributor(s) Rickels RA, Collings CK, Shilatifard A
Citation(s) 27447986
Submission date May 23, 2016
Last update date May 15, 2019
Contact name Ali Shilatifard
Organization name Northwestern University Feinberg School of Medicine
Department Department of Biochemistry and Molecular Genetics
Lab Shilatifard Lab
Street address 320 E Superior St
City Chicago
State/province IL
ZIP/Postal code 60611
Country USA
Platforms (3)
GPL13304 Illumina HiSeq 2000 (Drosophila melanogaster)
GPL18573 Illumina NextSeq 500 (Homo sapiens)
GPL19132 Illumina NextSeq 500 (Drosophila melanogaster)
Samples (87)
GSM2175500 dm3_dsLacZ_H3K27ac_140226_rep1
GSM2175501 dm3_dsLacZ_H3K27ac_151208_rep2
GSM2175502 dm3_dsLacZ_H3K27me3_140226_rep1
BioProject PRJNA322547
SRA SRP075582

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Supplementary file Size Download File type/resource
GSE81795_RAW.tar 89.7 Gb (http)(custom) TAR (of BW)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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