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  • This study describes the epigenetic profiling of the H3K9me2 in wt Drosophila larvae, as well as in Drosophila larvae for which the euchromatic catalytic enzyme depositing H3K9me2 (EHMT) is knocked out. ChIP-Seq profiling of H3K9me2 in wt and EHMT KO third instar Drosophila larvae
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  • Accession Number: GSE89459 Platform: GPL11203: Illumina Genome Analyzer IIx (Drosophila melanogaster) GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2017-08-25 Summary: trr ChIP-seq, trr RNA-seq, G9a RNA-seq Overall Design: trr ChIP-seq profiles on 0-5 day old fly heads in two replicates and mRNA profiles of trr- and G9a mutant 0-5 days old fly heads in two and three replicates respectively. Contact: Name: Tom Koemans Organization: Radboudumc Laboratory: van Bokhoven/ Schenck Deparment: Human genetics Address: Geert Grooteplein 10 Nijmegen Netherlands Email: tom.koemans@radboudumc.nl Organization: GEO Address: USA
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  • This is a dataset which comprises the following two different kinds of genomic data in Drosophila species: First, triplicate ChIP-seq data of CTCF (CCCTC binding factor) binding profiles in each of the four closely related Drosophila species : Drosophila melanogaster, Drosophila simulans, Drosophila yakuba and Drosophila pseudoobscura at white pre pupa stage; Second, triplicate RNA-seq data of white pre pupa whole animals of three Drosophila species: Drosophila melanogaster, Drosophila simulans and Drosophila yakub. The binding site/region/peaks are called using a modified method of QuEST( please see details in our related publication). The sequence read counts and RPKM values are calculated following the method in Mortazavi et al 2008 Nature Methods paper. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of CTCF binding in 4 Drosophila species and their correlation with gene expression levels in the same development stages
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  • ChIP-seq study analysing adult Drosophila melanogaster head, glial, neuronal and fat body, as well as embryonic RNA pol II and H2A.v binding by employing the GAL4-UAS system to generate GFP-fusion proteins and ChIP-seq
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  • Accession Number: GSE22447 Platform: GPL9061: Illumina Genome Analyzer II (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2011-01-05 Summary: This study describes the epigenetic profiling of the H3K9me2 in wt Drosophila larvae, as well as in Drosophila larvae for which the euchromatic catalytic enzyme depositing H3K9me2 (EHMT) is knocked out. Overall Design: ChIP-Seq profiling of H3K9me2 in wt and EHMT KO third instar Drosophila larvae Contact: Name: Hendrik Marks Organization: NCMLS Radboud University Nijmegen Deparment: Molecular Biology Address: Geert Grooteplein 26/28 Nijmegen Netherlands Email: h.marks@ncmls.ru.nl Organization: GEO Address: USA
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  • Accession Number: GSE87509 Platform: GPL16479: Illumina MiSeq (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2017-03-16 Summary: Drosophila Atro mutants have a large range of phenotypes, including neurodegeneration, segmentation, patterning and planar polarity defects. Although Atro mutants have diverse phenotypes, little is known about Atro’s binding partners and downstream targets. We present the first genomic analysis of Atro using ChIP-seq against endogenous Atro. These data sets will serve as a valuable resource for future studies on Atro. Overall Design: We performed three independent biological replicates of Atro ChIP-seq experiments in untreated S2 cells. A corresponding non-specific IgG control ChIP was performed with each Atro ChIP-seq and was used as a control. Contact: Name: Helen McNeill Organization: Lunenfeld Tanenbaum Research Institute Address: 600 University Ave. Toronto Ontario Canada Email: mcneill@lunenfeld.ca Organization: GEO Address: USA
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  • Accession Number: GSE42086 Platform: GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2012-11-15 Summary: ChIP-seq was performed using Drosophila Kc167 cells using antibodies against the two isoforms of Fs(1)h, the Brd4 homologue. Differences in binding patterns between the two isoforms are described. Overall Design: We examined the differences in Fs(1)h isoform binding across the genome and describe the short isoform to be correlated with transcription at enhancers and promoters. The long isoform is found predominately at insulator binding sites where multiple insulators are bound. Contact: Name: Wendy A Kellner Organization: Emory University Laboratory: Victor Corces Deparment: Biology Address: 1510 Clifton Road Atlanta GA 30322 USA Email: wkellne@emory.edu Phone: 404-727-4250 Organization: GEO Address: USA
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  • Accession Number: GSE59078 Platform: GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2015-02-13 Summary: Genomic enhancers regulate spatio-temporal gene expression by recruiting specific combinations of transcription factors (TFs). When TFs are bound to active regulatory regions, they displace canonical nucleosomes, making these regions biochemically detectable as nucleosome-depleted regions or accessible/open chromatin. Here we ask whether open chromatin profiling can be used to identify the entire repertoire of active promoters and enhancers underlying tissue-specific gene expression during normal development and oncogenesis in vivo. To this end, we first compare two different approaches to detect open chromatin in vivo using the Drosophila eye primordium as a model system: FAIRE-seq, based on physical separation of open versus closed chromatin; and ATAC-seq, based on preferential integration of a transposon into open chromatin. We find that both methods reproducibly capture the tissue-specific chromatin activity of regulatory regions, including promoters, enhancers, and insulators. Using both techniques, we screened for regulatory regions that become ectopically active during Ras-dependent oncogenesis, and identified 3778 regions that become (over-)activated during tumor development. Next, we applied motif discovery to search for candidate transcription factors that could bind these regions and identified AP-1 and Stat92E as key regulators. We validated the importance of Stat92E in the development of the tumors by introducing a loss of function Stat92E mutant, which was sufficient to rescue the tumor phenotype. Additionally we tested if the predicted Stat92E responsive regulatory regions are genuine, using ectopic induction of JAK/STAT signaling in developing eye discs, and observed that similar chromatin changes indeed occurred. Finally, we determine that these are functionally significant regulatory changes, as nearby target genes are up- or down-regulated. In conclusion, we show that FAIRE-seq and ATAC-seq based open chromatin profiling, combined with motif discovery, is a straightforward approach to identify functional genomic regulatory regions, master regulators, and gene regulatory networks controlling complex in vivo processes. Overall Design: FAIRE-Seq in Drosophila wild type eye-antennal imaginal discs (2 wt strains); ATAC-Seq in Drosophila wild type eye-antennal imaginal discs (3 wt strains) ; FAIRE-Seq in Drosophila Ras/Scrib induced eye disc tumors (1 early and 1 late); ATAC-Seq in Drosophila Ras/Scrib induced eye disc tumors (1 early and 1 late); ATAC-Seq in Drosophila eye discs with Unpaired over-expression (2 biological replicates); CTCF ChIP-seq in Drosophila eye discs; ChIP-seq input in Drosophila eye discs Contact: Name: Kristofer Davie Organization: KU Leuven Laboratory: Lab of Computational Biology Deparment: Center for Human Genetics / VIB Center for Brain and Disease Research Address: Herestraat 49 Bus 602 Leuven Flemish-Brabant Belgium Organization: GEO Address: USA
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  • Accession Number: GSE55932 Platform: GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2014-11-10 Summary: We analyzed gamma-H2Av ChIP-Seq from hand dissected salivary glands of wandering third instar larvae from wild-type (OrR) or suppressor of under-replication (SuUR) mutant Drosophila. Goals were to determine the DNA damage profile relative to underreplicated domains. We analyzed SUUR and Cdc45 ChIP-Seq from hand dissected early (stage 10) and late (stage 12/13) egg chambers from adult Drosophila ovaries. The goals was to determine the localization of SUUR relative to replication forks. Overall Design: ChIP-Seq of gamma-H2Av bound to third instar salivary gland DNA in WT and SuUR mutant Drosophila, analyzed by Illumina sequencing. One replicate is included for each of OrR (WT) or SuUR salivary glands.Rabbit IgG controls are included for OrR (WT). ChIP-Seq of SUUR and Cdc45 bound to egg chamber DNA from early and late stage egg chambers, analyzed by Illumina sequencing. One replicate is included for each ChIP reaction. Contact: Name: Terry L. Orr-Weaver Organization: Whitehead Institute for Biomedical Research Laboratory: Orr-Weaver Address: 9 Cambridge Center Cambridge MA 02142 USA Email: weaver@wi.mit.edu Phone: 617-258-5251 Organization: GEO Address: USA
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  • Accession Number: GSE56550 Platform: GPL9058: Illumina Genome Analyzer (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2015-07-23 Summary: We have analyzed ChIP-Seq of H3K9ac and H3K27me3 in wing imaginal discs and eye imaginal discs from Drosophila melanogaster. Overall Design: Examination of two histone modifications in wing/eye imaginal discs cells Contact: Name: Enrique Blanco Organization: Center for Genomic Regulation (CRG) Laboratory: Epigenetic Events in Cancer (L. Di Croce's lab) Deparment: Gene Regulation, Stem Cells and Cancer Address: Dr. Aiguader 88 Barcelona 08003 Spain Email: enrique.blanco@crg.eu Phone: +34 93 316 01 00 Organization: GEO Address: USA
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