Project description:We report the application of DHS-Seq and digital genomic footprinting to study chromatin changes and transcription factor-DNA binding upon long-term Hsp90 depletion utilizing the temperature-sensitive allele G170D. By generating about 86 and 85.6 million reads for wild type and mutant, we were able to reconstitute the chromatin accessibility and the transcription factor-DNA binding maps under regular conditions and under conditions where Hsp90 was long-term inactivated. We find that there is a global reduction of transcription factor binding sites with concurrent loss of open chromatin upon Hsp90 inactivation. This data was used in conjunction with our previous work involving DHS-Seq studies and short-term Hsp90 depletion (GEO GSE88875) to distinguish the affected transcription factor networks and the chromatin changes upon short- and long-term Hsp90 depletion. We identified two different modes of Hsp90 operation on transcription factor activities – short-term inactivation of Hsp90 altered transcription factor DNA binding activities, whereas long-term Hsp90 inactivation affected the steady-state levels of transcription factors. Overall, this study shows that Hsp90 regulates multiple transcription factor protein families and modulates chromatin architecture on a genome-wide scale.
Project description:DNaseI sensitivity/hypersensitivity using DNase-array method (Sabo et al Nature Methods 3:511-18, 2006) on Affymetrix whole-genome tiling DNA microarrays. Background: Focal alteration in chromatin structure in vivo, detectable through hypersensitivity to DNaseI and other nucleases, is the sine qua non of diverse transcriptional regulatory elements including enhancers, promoters, insulators, and locus control regions. Keywords: genomic
Project description:DNaseI sensitivity/hypersensitivity using DNase-array method (Sabo et al Nature Methods 3:511-18, 2006) on Affymetrix whole-genome tiling DNA microarrays. Background: Focal alteration in chromatin structure in vivo, detectable through hypersensitivity to DNaseI and other nucleases, is the sine qua non of diverse transcriptional regulatory elements including enhancers, promoters, insulators, and locus control regions. Keywords: genomic
Project description:DNaseI hypersensitivity using DNase-array method on Affy platform overall design Per DNase-array method (Sabo et al Nature Methods 3:511,2006) PMID: 15782197 This study is part of an ongoing screening process designed to obtain high quality cell-lines/tissues for further high throughput sequencing analysis. Bed files based on hg17 genome build Keywords: genomic
Project description:DNaseI hypersensitivity using DNase-array method on Affy platform overall design Per DNase-array method (Sabo et al Nature Methods 3:511,2006) PMID: 15782197 Keywords: genomic
Project description:This track is produced as part of the mouse ENCODE Project. This track shows DNaseI sensitivity measured genome-wide in mouse tissues and cell lines using the Digital DNaseI methodology (see below), and DNaseI hypersensitive sites. DNaseI has long been used to map general chromatin accessibility and DNaseI hypersensitivity is a universal feature of active cis-regulatory sequences. The use of this method has led to the discovery of functional regulatory elements that include enhancers, insulators, promotors, locus control regions and novel elements. For each experiment (tissue/cell type) this track shows DNaseI sensitivity as a continuous function using sequencing tag density (Signal), and discrete loci of DNaseI sensitive zones (HotSpots) and hypersensitive sites (Peaks). 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:We generated genome-wide maps of DNaseI hypersensitivity in mouse erythroid cells by DNase-Seq. Examination of DNaseI hypersensitivity in mouse erythroid cells.
Project description:This data was generated by ENCODE. If you have questions about the data, contact the submitting laboratory directly (Richard Sandstrom mailto:sull@u.washington.edu). If you have questions about the Genome Browser track associated with this data, contact ENCODE (mailto:genome@soe.ucsc.edu). This track is produced as part of the ENCODE Project. This track shows DNaseI sensitivity measured genome-wide in different cell lines using the Digital DNaseI methodology (see below), and DNaseI hypersensitive sites. DNaseI has long been used to map general chromatin accessibility and DNaseI hypersensitivity is a universal feature of active cis-regulatory sequences. The use of this method has led to the discovery of functional regulatory elements that include enhancers, insulators, promotors, locus control regions and novel elements. For each experiment (cell type) this track shows DNaseI sensitivity as a continuous function using sequencing tag density (Raw Signal), and discrete loci of DNaseI sensitive zones (HotSpots) and hypersensitive sites (Peaks)." For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf