DNase I hypersensitivity with capture in mES cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA415942 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This dataset introduces a new protocol called DNase-capture, a method that focuses DNase-seq analysis on selected genomic regions, resulting in a substantial increase in region-specific sequencing coverage. DNase-seq takes advantage of the preferential cutting of DNase I. DNase-capture enhances the resolution of DNase-seq by mixing a DNase-seq library with biotin-tagged bait RNA sequences that are complementary to regions of interest. In a hybridization reaction, target DNA is captured away from background DNA through streptavidin bead binding, and the captured target DNA is sequenced.
2017-10-27 | GSE106217 | GEO
Project description:This dataset uses DNase-seq to profile the genome-wide DNase I hypersensitivity of mES and mES-derived cells along an early pancreatic lineage and provides the locations of putative Transcription Factor (TF) binding sites using the PIQ algorithm. DNase-seq takes advantage of the preferential cutting of DNase I in open chromatin and steric blockage of of DNase I by tightly bound TFs that protect associated genomic DNA sequences. After deep sequencing of DNase IM-bM-^@M-^Sdigested genomic DNA from intact nuclei, genome-wide data on chromatin accessibility as well as TF-specific DNase I protection profiles that reveal the genomic binding locations of a majority of TFs are obtained. Such TF signature M-bM-^@M-^XDNase profilesM-bM-^@M-^Y reflect the effect of the TF on DNA shape and local chromatin architecture, extending hundreds of base pairs from a TF binding site, and these profiles are centered on M-bM-^@M-^XDNase footprintsM-bM-^@M-^Y at the binding motif itself, which reflects the biophysics of protein-DNA binding. An algorithm, PIQ, is then applied that models the specific profile of each factor, and in combination with sequence information predicts the likely binding locations of over 700 TFs genome wide. This dataset includes DNase-seq hypersensitivity data from 6 mES-derived cell types: mESC, Mesendoderm, Mesoderm, Endoderm, Intestinal Endoderm, and Prepancreatic Endoderm. For each cell type, TF binding site predictions are made based on the identification TF-specific DNase-seq profiles over any of 1331 possible binding motifs. After significance thesholding, genome-wide binding site predictions for <700 TFs are included.
2014-01-19 | E-GEOD-53776 | biostudies-arrayexpress
Project description:This dataset uses DNase-seq to profile the genome-wide DNase I hypersensitivity of mES and mES-derived cells along an early pancreatic lineage and provides the locations of putative Transcription Factor (TF) binding sites using the PIQ algorithm. DNase-seq takes advantage of the preferential cutting of DNase I in open chromatin and steric blockage of of DNase I by tightly bound TFs that protect associated genomic DNA sequences. After deep sequencing of DNase I–digested genomic DNA from intact nuclei, genome-wide data on chromatin accessibility as well as TF-specific DNase I protection profiles that reveal the genomic binding locations of a majority of TFs are obtained. Such TF signature ‘DNase profiles’ reflect the effect of the TF on DNA shape and local chromatin architecture, extending hundreds of base pairs from a TF binding site, and these profiles are centered on ‘DNase footprints’ at the binding motif itself, which reflects the biophysics of protein-DNA binding. An algorithm, PIQ, is then applied that models the specific profile of each factor, and in combination with sequence information predicts the likely binding locations of over 700 TFs genome wide.
2014-01-19 | GSE53776 | GEO
Project description:Mapping DNaseI hypersensitive (HS) sites is an accurate method of identifying the location of genetic regulatory elements, including promoters, enhancers, silencers, insulators, and locus control regions. We employed whole genome tiled array strategies to identify DNaseI HS sites within human primary CD4+ T cells. Keywords: whole genome tiling array DNAse hypersensitivity from two biologic replicates of CD4+ T-cells were hybridized to a whole-genome tiling array set (38 arrays each) and compared to the input DNA from the same samples.
2007-11-19 | E-GEOD-8486 | biostudies-arrayexpress
Project description:DNase hypersensitivity using Nimblegen ENCODE arrays (DNase-chip) in primary human trachea epithelia (pHTE), normal human bronchial epithelia (NHBE), Caco2, HT29, human skin fibroblasts, primary human male epididymis. DNase hypersensitivity mapping is used to detect putative regulatory elements of the human genome. We digested chromatin from the above cell types with DNaseI using the DNase-chip protocol devised by Crawford et al. (Nat. Methods, 2006). Briefly, cells are lysed, chromatin is digested with increasing amounts of DNase I, digested ends are blunted in adequetely digested samples, ligated to biotinylated linkers, purified with streptavidin beads, amplified by LM-PCR. As control, randomly sonicated genomic DNA is used. LM-PCR material was labeled and hybridized to hg_17 ENCODE arrays at Nimblegen facility. DNaseI-digested chromatin was hybridized to Nimblegen ENCODE arrays (build hg17). Randomly sonicated genomic DNA was used as control. Three biological replicates on three arrays were performed for Caco2 cells, three replicates were done with skin fibroblasts (two digestions were pooled and hybridized to a single array [Sample: SkinFibro.sample2]), two replicates on two arrays were performed for pHTE, NHBE, and HT29, and a single experiment for primary male epididymis.
2009-10-31 | E-GEOD-18735 | biostudies-arrayexpress
Project description:DNase hypersensitivity using Nimblegen ENCODE arrays (DNase-chip) in primary human trachea epithelia (pHTE), normal human bronchial epithelia (NHBE), Caco2, HT29, human skin fibroblasts, primary human male epididymis. DNase hypersensitivity mapping is used to detect putative regulatory elements of the human genome. We digested chromatin from the above cell types with DNaseI using the DNase-chip protocol devised by Crawford et al. (Nat. Methods, 2006). Briefly, cells are lysed, chromatin is digested with increasing amounts of DNase I, digested ends are blunted in adequetely digested samples, ligated to biotinylated linkers, purified with streptavidin beads, amplified by LM-PCR. As control, randomly sonicated genomic DNA is used. LM-PCR material was labeled and hybridized to hg_17 ENCODE arrays at Nimblegen facility.
2009-11-01 | GSE18735 | GEO
Project description:We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes. Examination of histone modification marked nucleosomes and Dnase I hypersensitivity in prostate cancer and breast cancer cells with and without hormone treatment.
2012-03-25 | E-GEOD-33216 | biostudies-arrayexpress
Project description:We generated genome-wide maps of DNaseI hypersensitivity in mouse erythroid cells by DNase-Seq.
2012-01-30 | GSE27919 | GEO
Project description:We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes.
2012-03-25 | GSE33216 | GEO
Project description:We generated genome-wide maps of DNaseI hypersensitivity in mouse erythroid cells by DNase-Seq. Examination of DNaseI hypersensitivity in mouse erythroid cells.
2012-01-30 | E-GEOD-27919 | biostudies-arrayexpress