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The goal of this experiment was to identify genomic dCAP-D3 binding sites in Drosophila S2R+ cells dCAP-D3 was immunoprecipitated in two separate experiments with antibody YZ834 which was developed in the Longworth lab. IgG immunoprecipiation was performed alongside the dCAP-D3 immunoprecipitation to serve as controls for each experiment. Input chromatin was also harvested from each of the two experiments.
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The patterning of Drosophila retina occurs both very fast and with high precision. This process is driven by the dynamic changes in signalling activity of the conserved Hedgehog (Hh) pathway, which coordinates cell fate determination, cell cycle and tissue morphogenesis. Here we show that during Drosophila retinogenesis, the retinal determination gene dachshund (dac) is not only a target of the Hh signaling pathway, but is also a modulator of its activity. Using developmental genetics techniques, we demonstrate that dac enhances Hh signaling by promoting the accumulation of the Gli transcription factor Cubitus interruptus (Ci) parallel to or downstream of fused. In the absence of dac, all Hh-mediated events associated to the morphogenetic furrow are delayed. One of the consequences is that, posterior to the furrow, dac- cells cannot activate a Roadkill-Cullin3 negative feedback loop that attenuates Hh signaling and which is necessary for retinal cells to continue normal differentiation. Therefore, dac is part of an essential positive feedback loop in the Hh pathway, guaranteeing the speed and the accuracy of Drosophila retinogenesis. ChIP-seq against Dachshund vs input ChIP-seq. Eye-antennal imaginal discs are dissected from Grh-GFP (Bloomington stock 42269) 3rd instar larvae and fixed with formaldehyde. Chromatin is prepared and sonicated until fragments reach an average size of 500 bp. Chromatin is immunoprecipitated with an anti-GFP Ab (ab290, Abcam) and the immunocomplexes are recovered with protein A/G magnetic beads (Millipore).
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This SuperSeries is composed of the following subset Series: GSE26895: Drosophila LID RNAi gene expression profiling GSE27078: LID ChIP-Seq in wild type, and H3K4me3 ChIP-Seq in wild type and lid RNAi Drosophila melanogaster GSE40599: POLIISER5 and POLIISER2 ChIP-Seq in mutant RNAi LID Drosophila Melanogaster Refer to individual Series
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dLint1 (CG1908) was ChIPseq`d in Drosophila melanogaster KC cells and S2 cells
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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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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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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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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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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 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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