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  • ChIP-seq for Drosophila Insensitive, together with IgG control. Chromatin extracted from 2.5-6h w[1118] embryos and 6.5-12h w[1118] embryos. Samples from two time points were analyzed: 2.5-6h embryos and 6.5-12h embryos. In each time point there is one Insv ChIP sample and one IgG control sample.
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  • This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for 6 Histone modifications (H3K9me3, H3K27me3, H3K4me3, H3K4me1, H3K27Ac, H3K9Ac), PolII and CBP/p300. Each factor has been studied for 12 different time-points of Drosophila development. This SuperSeries is composed of the following subset Series: GSE15422: ChIP-chip of H3K9me3 in Drosophila at different time points of development GSE15423: ChIP-chip of H3K27me3 in Drosophila at different time points of development GSE15424: ChIP-chip of H3K4me3 in Drosophila at different time points of development GSE15425: ChIP-chip of H3K4me1 in Drosophila at different time points of development GSE15426: ChIP-chip of H3K9Ac in Drosophila at different time points of development GSE15427: ChIP-chip of CBP/p300 in Drosophila at different time points of development GSE15430: ChIP-chip of H3K27Ac in Drosophila at different time points of development GSE16013: Genome-wide maps of chromatin state in staged Drosophila embryos, ChIP-seq GSE16702: ChIP-chip of PolII in Drosophila at different time points of development GSE18068: Genome-wide maps of chromatin state in staged Drosophila embryos, RNA-seq For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf ChIP-chip: For each combination of time-point and antibody, triplicate ChIP experiments have been performed and hybridized on Agilent 244K arrays. 3 arrays per genome have been used so that each time-point is a set of 9 tiling arrays. ChIP-seq: For each combination of time-point and antibody, triplicate ChIP experiments have been performed and hybridized on Agilent 244K arrays. The hybridizations have been verified by sequencing one replicate of IP and one replicate of Input following Solexa sequencing procedure. RNA-seq: For each time-point (E-0-4h, E-4-8h, E-8-12h, E-12-16h, E-16-20h, E20-24h, L1, L2, L3, Pupae, Adult Males and Adult Females) a total RNA extraction has been performed. After conversion into double stranded DNA, the samples have been sequenced in duplicate on Solexa Genome Analyzer following Solexa sequencing procedure.
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  • This data consists of RNA-seq data of whole animal white pre pupa of four Drosophila species: Drosophila melanogaster, Drosophila simulans, Drosophila yakuba, and Drosophila pseudoobscura. The processed RPKM values are calculated following the method in Garber et al 2011 Nature Methods paper. Examination of H3K27me3 in 4 Drosophila species and its correlation with gene expression levels in the same development stage relevant ChIP-seq data can be found in GSE25663, GSE25668
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  • CREB-binding protein (CBP, also known as nejire) is a transcriptional co-activator that is conserved in metazoans. We have generated CBP ChIP-seq data from Drosophila S2 cells and compared it to modENCODE data. This shows that CBP is bound at genomic sites with a wide range of functions. As expected, we find that CBP is bound at active promoters and enhancers. In addition, we find that the strongest CBP sites in the genome are found at Polycomb Response Elements embedded in histone H3 lysine 27 trimethylated (H3K27me3) chromatin, where they correlate with binding of the Pho repressive complex. Interestingly, we find that CBP also binds to most insulators in the genome. At a subset of these, CBP may regulate insulating activity, measured as the ability to prevent repressive H3K27 methylation from spreading into adjacent chromatin. ChIP seq in Drosophila S2 cells using two different antibodies against CBP (nejire), one raised in rabbit against amino acids 2540-3190 (CBP rb), and one raised in guinea-pig against amino acids 1-178 (CBP gp)
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  • dLint1 (CG1908) was ChIPseq`d in Drosophila melanogaster KC cells and S2 cells
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  • ChIP-Seq peak calling of CP190 in wild-type and Ibf2 mutant Drosophila melanogaster third instar larvae Two wild-type and two Ibf2 mutant Drosophila melanogaster third instar larvae were sequenced.
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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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  • 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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  • 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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  • 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. 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
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