Project description:We performed Pol II ChIP-seq experiments with 3rd instar larva salivary glands material from male, female and MSL2 RNAi D.melanogaster, as well as from S2 cell lines material. The antibody used recognizes the Rpb3 subunit of RNA Pol II irrespective of the phosphorylation state of the Rpb1 carboxy-terminal domain, therefore capturing Pol II during all stages of transcription. Corrected processed data has been made available following Vaquerizas et al (2013). [M-^SResponse to Comments on M-^SDrosophila Dosage Compensation Involves Enhanced Pol II Recruitment to Male X-Linked PromotersM-^T, Juan M. Vaquerizas, Florence M. G. Cavalli, Thomas Conrad, Asifa Akhtar, Nicholas M. Luscombe, Science 340 (6130): 273 (2013)]
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. This Series contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: PolII at 12 different time-points of Drosophila development. Note: 8wg16 is the name of PolII antibody for set2 datasets. Current Dataset: [GSM418514..GSM418522]: ChIP-chip of PolII in Drosophila pupae [GSM418549..GSM418557]: ChIP-chip of 8wg16 in Drosophila adult female [GSM418567..GSM418575]: ChIP-chip of 8wg16 in Drosophila embryos at 0-4 hours of development [GSM418580..GSM418588]: ChIP-chip of 8wg16 in Drosophila embryos at 4-8 hours of development [GSM418593..GSM418601]: ChIP-chip of 8wg16 in Drosophila L3 larvae [GSM442398..GSM442406]: ChIP-chip of PolII in L2 [GSM442407..GSM442415]: ChIP-chip of PolII in L3 [GSM442416..GSM442424]: ChIP-chip of 8wg16 in Drosophila embryos at 4-8 hours of development - Set2 [GSM443110..GSM443118]: ChIP-chip of 8wg16 in Drosophila embryos at 16-20 hours of development For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
Project description:To identify the presence of different chromatin states in homogeneous primary cells, Drosophila melanogaster plasmatocytes were isolated from 3rd instar larvae and subjected to cross-linked ChIP-seq using antibodies against a range of H3 histone modifications and PolII.
Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERM-NM-1 and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERM-NM-1 binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERM-NM-1, and that ERM-NM-1 binding is increased by E2. Approximately 15% of the uterine ERM-NM-1 binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERM-NM-1 binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERM-NM-1 binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERM-NM-1 to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERM-NM-1 bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERM-NM-1 binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERM-NM-1 and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues. one sample each, vehicle ER-alpha ChIP seq,1 hour estradiol ER-alpha ChIP seq, vehicle RNA polymerase II ChIP seq,1 hour estradiol RNA polymerase II ChIP seq, input DNA
Project description:Chromatin immunoprecipitation of Snt1, of PolII, and of H3K4me2, respectively, applied with tilling array chip (ChIP on chip of Snt1, of PolII, and of H3K4me2, respectively) analysis demonstrated that a compared genomic occupancy of Snt1, of PolII, and of H3K4me2 in Saccharomyces cerevisiae wild type cells compared anong those in Hst1 deleted, Hos2 deleted and Hst2 & Hos2 double deleted cells
Project description:Chromatin immunoprecipitation of Set3, of PolII, and of H3K4me2, respectively, applied with tilling array chip (ChIP on chip of Set3, of PolII, and of H3K4me2, respectively) analysis demonstrated that a compared genomic occupancy of Set3, of PolII, and of H3K4me2 in Saccharomyces cerevisiae wild type cells compared anong those in Hst1 deleted, Hos2 deleted and Hst2 & Hos2 double deleted cells
Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERα and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERα binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERα, and that ERα binding is increased by E2. Approximately 15% of the uterine ERα binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERα binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERα binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERα to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERα bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERα binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERα and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues.
Project description:modENCODE_submission_3251 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We will precisely identify sequence elements that direct DNA replication by using chromatin immunoprecipitation of known replication initiation complexes. These experiments will be conducted in multiple cell types and developmental tissues. 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-seq. BIOLOGICAL SOURCE: Developmental Stage: Mixed Embryos 0-24h; EXPERIMENTAL FACTORS: Developmental Stage Mixed Embryos 0-24h; Antibody (target is PolII); read length (read_length 36)