Atrophin (Atro) ChIP-seq data from Drosophila S2 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE87471 | GEO | 2017/03/16
SECONDARY ACCESSION(S): PRJNA344879
REPOSITORIES: GEO
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Project description:We sought to determine the genomic binding profile of the Drosophila Hox protein AbdA in a homogenous cell system. S2-DRSC cells that have no Hox expression were stably transfected with HA-tagged AbdA under the control of a metallothionein promoter. Upon AbdA expression, we identified high enrichment of AbdA at a large number transcription start sites that colocalises with the GAGA and M1BP. Genes targeted by GAGA and M1BP contain paused RNA polymerase II and show enrichment of PcG proteins. Upon AbdA binding at M1BP-target sites, a significant reduction in PcG protein binding is observed with a concomitant reduction in RNA Pol II pausing. These data suggest that AbdA targets both GAGA- and M1BP-controlled genes, and at M1BP-controlled genes, AbdA binding is sufficient to release PcG-mediated RNA Pol II pausing to induce gene transcription.
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Project description:modENCODE_submission_710 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Early origins of replication were identified by treating cells with hydroxyurea (HU), a potent inhibitor of nucleotide synthesis, in the presence of the nucleotide analogue BrdU. Treatment of synchronized S2-DRSC cells with HU stalls replication forks and activates the intra S-phase checkpoint, thereby limiting BrdU incorporation to those sequences immediately adjacent to early activating replication origins. BrdU enriched sequences surrounding early origins of replication are then enriched by immunoprecipitation with an anti-BrdU antibody. Early origins are then detected by hybridization to Agilent genomic tiling arrays. Peaks are called using MA2C (http://liulab.dfci.harvard.edu/MA2C/MA2C.htm) Keywords: CHIP-chip For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Sex: Male NUMBER OF REPLICATES: 3; EXPERIMENTAL FACTORS: Cell Line S2-DRSC
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Project description:GAGA associated transcription factor (GAF) is a highly abundant and essential protein in Drosophila. GAF recognizes and binds arrays of GA dinucleotides via a zinc finger DNA binding domain to regulate transcription by binding to general TF machinery or recruit nucleosome remodeling factors. We performed GAF ChIP-seq to quantify the intensity of GAF binding at high resolution in S2 cells. In addition, we performed GAF ChIP-seq in S2 cells that were depleted of GAF by RNAi. By quantifying the degree to which all GAF binding sites are susceptible to GAF depletion, we found the cellular degree of depletion does not translate equally to the depletion of GAF at individual chromatin bound sites. For example, some high intensity GAF binding sites were completely unaffected by GAF depletion, while lower affinity binding sites were often ablated upon GAF depletion. These data sets will serve as a valuable resource to others who study the dynamic interplay between GAF and chromatin. We also compared the GAF binding sites to the full set of genomic ChIP data that is available for S2 cells and compared the intensity for each factor and histone modification/variant. Lastly, we investigated the influence that GAF had upon inducible transcription factor binding using the heat shock system.
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2013-08-01 | E-GEOD-40646 | biostudies-arrayexpress
Project description:Transcription activation involves RNA polymerase II (Pol II) recruitment and release from the promoter into productive elongation, but how specific chromatin regulators control these steps is not fully understood. Here we identify a novel activity of the co-regulator and histone acetyltransferase p300/CBP in positioning promoter-proximal paused Pol II. We find that CBP inhibition impedes transcription through the +1 nucleosome, causing âdribblingâ of Pol II from the canonical pause site genome-wide. We further discovered that promoters strongly occupied by Drosophila CBP and GAGA-factor have high levels of paused Pol II, a unique chromatin signature and strong expression regardless of cell type. Interestingly, CBP activity is rate-limiting for Pol II recruitment to these highly-paused promoters but for transit into elongation at other genes. Thus, we uncover a key role for CBP during transcription in directly controlling different rate-limiting steps depending on promoter features. Examination of transcriptional regulation with and without CBP inhibition for 10 minutes in Drosophila S2 cells. Two biological replicates for each condition.
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Project description:Purpose: The transcription fact Lola is identified as a conponent acting downstream of Hippo signaling to restrict ISC proliferation and regulate midgut homeostasis. To further elucidate the mechanism of Lola regulating ISC proliferation and midgut homeostasis,Chromatin immunoprecipitation assay followed by sequencing (ChIP-seq) was performed to identify genes suppressed directly by Lola. Methods: Chromatin lysates were clarified from homogenized and sonicated S2 cells; protein-DNA complexes were isolated with antibody. Genomic DNA fragments were purified with a DNA purification kit (QIAGEN) and subjected to high throughput sequencing using Illumina HiSeq2500. Process: After the genomic DNA segments were sequenced using Illumina HiSeq2500. After quality control with fastqc (version 0.11.8), we built genome index from Drosophila melanogaster genome(BDGP6)with bowtie2-build. Reads were aligned to Drosophila genome BDGP6 index with bowtie2. Then we converted sam files to bam files with samtools. Peaks were called from the aligned reads using MACS2 callpeak, and peaks annotation using R package ChIPseeker. Conclusion: Thousands of Lola-associated chromatin binding sites were identified in cultured S2 cells. Analysis of the Lola binding profiles revealed that Lola mainly binds to the regions around transcription start sites (TSS) and promoters.
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Project description:modENCODE_submission_710 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Early origins of replication were identified by treating cells with hydroxyurea (HU), a potent inhibitor of nucleotide synthesis, in the presence of the nucleotide analogue BrdU. Treatment of synchronized S2-DRSC cells with HU stalls replication forks and activates the intra S-phase checkpoint, thereby limiting BrdU incorporation to those sequences immediately adjacent to early activating replication origins. BrdU enriched sequences surrounding early origins of replication are then enriched by immunoprecipitation with an anti-BrdU antibody. Early origins are then detected by hybridization to Agilent genomic tiling arrays. Peaks are called using MA2C (http://liulab.dfci.harvard.edu/MA2C/MA2C.htm) Keywords: CHIP-chip For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
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