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  • The Drosophila ubiquitin receptor dDsk2 associates to chromatin and stabilizes binding of the euchromatic dHP1c/WOC/ROW-complex (dHP1EU) to the transcription-start site (TSS) of active genes ChIP-Seq peak calling of WOC, ROW, Z4, HP1c and Dsk2 against Input sample in Drosophila melanogaster S2 cells
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  • ChiP-seq profiling of Drosophila melanogaster salivary glands to identify targets for NSL1 and MCRS2.
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  • Accession Number: GSE41440 Platform: GPL13112: Illumina HiSeq 2000 (Mus musculus) GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Mus musculus Published on 2012-12-01 Summary: Mono-methylation of histone H3 on lysine 4 (H3K4me1) and acetylation of histone H3 on lysine 27 (H3K27ac) are histone modifications that are highly enriched over the body of actively transcribed genes and enhancers. Although in yeast all H3K4 methylation patterns including H3K4me1 are implemented by Set1/COMPASS, there are three classes of COMPASS-like complexes in Drosophila that could carry out H3K4me1 on enhancers: dSet1, Trithorax and Trithorax-related (Trr). Here, we report that Trr, the Drosophila homolog of mammalian Mll3/4, can function as a major H3K4 mono-methyltransferase on enhancers in vivo. Loss of Trr results in a global decrease of H3K4me1 and H3K27ac in various tissues. Assays with the cut wing margin enhancer imply a functional role for Trr in enhancer-mediated processes. A genome-wide analysis demonstrates that Trr is required for H3K4me1 and H3K27ac on chromatin signatures that resemble the histone modification patterns described for enhancers. Since Trr and mammalian Mll3/4 complexes are distinguished by bearing a unique subunit, the H3K27 demethylase UTX, we propose a model in which the H3K4 mono-methyltransferase Trr, and the H3K27 demethylase, UTX, cooperate to regulate the transition from inactive/poised to active enhancers. Overall Design: ChIP-seq of Trr, LPT, UTX in Drosophila S2 Cells. ChIP-seq of H3K4me1, H3K4me3, H3K27ac, H3K27me3 in WT and Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1, H3K27me3 in LPT knock-down Drosophila S2 cells. ChIP-seq of LPT and UTX in Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1 and H3K27me3 in MLL1(+/+), MLL1(-/-), MLL3(+/+), and MLL3(-/-) Mouse Embryonic Fibroblasts (MEFs). Contact: Name: Alexander (Garrett) Garruss Organization: Stowers Institute for Medical Research Laboratory: Shilatifard Address: 1000 East 50th Street Kansas CIty Missouri 64110 USA Email: asg@stowers.org Organization: GEO Address: USA
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  • Accession Number: GSE103291 Platform: GPL11203: Illumina Genome Analyzer IIx (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2017-12-13 Summary: This analysis largely reflected the genomic distribution of dBigH1 in 0-2hpf early embryos. In these studies, we observed that dBigH1 was uniformely distributed across the genome. Overall Design: ChIP-Seq peak calling of dBigH1 against input sample in early embryos Contact: Name: Oscar Reina Garcia Organization: IRB Barcelona Deparment: Biostatistics and Bioinformatics Address: C/Baldiri Reixac 10 Barcelona Barcelona 08028 Spain Email: oscar.reina@irbbarcelona.org Organization: GEO Address: USA
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  • Accession Number: GSE40664 Platform: GPL11203: Illumina Genome Analyzer IIx (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2014-02-06 Summary: Genome-wide mapping of protein–DNA interactions is essential for a full understanding of transcriptional regulation. A precise map of binding sites for transcription factors, core transcriptional machinery is vital for deciphering the gene regulatory networks that underlie various biological processes. Chromatin immunoprecipitation followed by sequencing (ChIPseq) is a technique for genome-wide profiling of DNA-binding proteins. However, our conventional ChIPseq occasionally gives wider peaks which might be due to overlapping binding sites of two or more transcription factors. Therefore, to improve the resolution of our conventional ChIPseq which have DNA-protein footprint of ~100 bp, we decreased the size of DNA-protein footprint to ~ 50 bp by DNaseI digestion of whole cell extract (WCE). Overall Design: ChIP-seq for Twist transcription factor in Drosophila embryos Contact: Name: Samuel Richard Meier Organization: Stowers Institute for Medical Research Laboratory: Computational Biology Address: 1000 E 50th Street Kansas City MO 64110 USA Email: srm@stowers.org Phone: 816-926-4455 Organization: GEO Address: USA
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  • The genomic distribution of a novel transcription factor called M1BP was determined in Drosophila S2R+ cells Polyclonal antibody raised against M1BP was used to immunoprecipitate M1BP-DNA adducts generated by treating Drosophila cells with formaldehyde, lysing the cells, and shearing DNA by sonication. Immunoprecipitated DNA was sequenced using the AB SOLiD system.
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  • Accession Number: GSE39521 Platform: GPL9061: Illumina Genome Analyzer II (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2013-01-21 Summary: Myc is an important oncogene. It is considered as a transcription factor, but the function of Myc in normal or cancer cells have not been fully understood. In addition, Myc plays a role in cell proliferation and differentiation. It is also important for cell identity and stay on chromatin throughout the cell cycle. However, the inheritance of Myc is still a mystery. Here we study the function and inheritance of Myc in D. melanogaster by mapping the binding sites of Myc during interphase and mitosis using ChIP-seq. Overall Design: DNA sample of ChIP for Myc are collected from Kc cells in interphase or mitosis. Input sequences from previous study in the same cell type (GSM762848, GSM762849) are used as control. Contact: Name: Jingping Yang Organization: Emory Address: 1507 Clifton Rd Atlanta GA 30322 USA Email: idayang@hotmail.com Organization: GEO Address: USA
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  • ChIP-seq was performed to compare binding the genome-wide binding profile of the CLAMP transcription factor in two different Drosophila species. ChIP seq experiments compare the binding profile of CLAMP in female larvae to identify conservation of its binding sequence.
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  • This SuperSeries is composed of the following subset Series: GSE37027: Cell type-specific gene expression profiling of Drosophila neurons [RNA-Seq] GSE37032: Cell type-specific chromatin profiling of Drosophila neurons [ChIP-Seq] Refer to individual Series
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  • In order to idetify paused promoters in vivo, we performed tissue specific Pol II Chip-seq using mutant embryos for the dorsal gradient. We used two population of cells, either dorsal ectoderm cells (gd7 embryos) or mesodermal cells (Toll10b) embryos. ChIP-seq for Pol II in various Drosophila embryos
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