Mouse liver DNase-seq identification of DNase hypersensitive sites (DHS) in male and female mouse liver for two mouse strains: C57BL/6J and CAST/EiJ.
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PROVIDER: PRJNA542218 | ENA |
REPOSITORIES: ENA
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Project description:Sequencing files provided here are mouse liver DNase-seq in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes RNA-seq and H3K27ac ChIP-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
2021-10-27 | GSE130912 | GEO
Project description:DNase I hypersensitive sites (DHSs) provide important information on the presence of transcriptional regulatory elements and the state of chromatin in mammalian cells1, 2, 3. Conventional DNase sequencing (DNase-seq) for genome-wide DHSs profiling is limited by the requirement of millions of cells4, 5. Here we report an ultrasensitive strategy, called single-cell DNase sequencing (scDNase-seq) for detection of genome-wide DHSs in single cells. We show that DHS patterns at the single-cell level are highly reproducible among individual cells. Among different single cells, highly expressed gene promoters and enhancers associated with multiple active histone modifications display constitutive DHS whereas chromatin regions with fewer histone modifications exhibit high variation of DHS. Furthermore, the single-cell DHSs predict enhancers that regulate cell-specific gene expression programs and the cell-to-cell variations of DHS are predictive of gene expression. Finally, we apply scDNase-seq to pools of tumour cells and pools of normal cells, dissected from formalin-fixed paraffin-embedded tissue slides from patients with thyroid cancer, and detect thousands of tumour-specific DHSs. Many of these DHSs are associated with promoters and enhancers critically involved in cancer development. Analysis of the DHS sequences uncovers one mutation (chr18: 52417839G>C) in the tumour cells of a patient with follicular thyroid carcinoma, which affects the binding of the tumour suppressor protein p53 and correlates with decreased expression of its target gene TXNL1. In conclusion, scDNase-seq can reliably detect DHSs in single cells, greatly extending the range of applications of DHS analysis both for basic and for translational research, and may provide critical information for personalized medicine. Exploring the landscape of chromatin accessibility in single cells and clinical samples
2015-11-25 | E-GEOD-61844 | biostudies-arrayexpress
Project description:Sequencing files provided here are mouse liver DNase-seq for male mouse livers collected at either a peak or trough of GH/STAT5 activity. This is part of a larger study that includes DNase-seq in mouse liver from hypophysectomized males, females, and hypox-male mice given a single dose of GH. DNase hypersensitivity site (DHS) analysis of these livers established that the naturally occurring, endogenous male rhythm of plasma GH pulse-stimulated liver STAT5 activation induces dynamic, repeated cycles of chromatin opening and closing at several thousand liver DHS and comprises a novel mechanism conferring male bias to liver chromatin accessibility.
2023-08-21 | GSE131848 | GEO
Project description:Mapping DNase I hypersensitive sites (DHSs) within nuclear chromatin is a traditional and powerful method of identifying genetic regulatory elements. DHSs have been mapped by capturing the ends of long DNase I-cut fragments (>100,000 bp), or 100-1200 bp DNase I-double cleavage fragments (also called double-hit fragments). But next generation sequencing requires a DNA library containing DNA fragments of 100-500bp. Therefore, we have modified the double-hit method and use short DNA fragments to generate DNA libraries for next generation sequencing. We call this method Short DHS Assay (Short DNAse I Hypersensitive Site assay). The short segments are 100-300bp and can be directly cloned and used for high-throughput sequencing. We identified 83,897 DHSs in 2,343,479 tags across the human genome. Our results indicate that the DHSs identified by the Short DHS assay are consistent with those identified by longer fragments in previous studies.
2015-06-19 | GSE38914 | GEO
Project description:Sequencing files provided here are mouse liver DNase-seq to identify DNase hypersensitive sites (DHS) in livers from intact and hypox female, hypox male, and hypox male mice given a single injection of GH and then euthanized 30, 90, or 240 minutes later. This is part of a larger study that includes DNase-seq in mouse liver from intact males determined to be STAT5-high or STAT5-low based on an endogenous pulse of GH/STAT5. This allows us to identify GH pulse-responsive DHS and better understand male-biased DHS regulation of sex-biased genes. Overall, our findings establish that pulsatile chromatin opening stimulated by endogenous, physiological hormone pulses is a novel mechanism for establishing widespread sex differences in chromatin accessibility and transcription factor binding, which are closely linked to sex-biased gene expression and the sexual dimorphism of liver function.
2023-08-21 | GSE131852 | GEO
Project description:DNase I hypersensitive sites (DHSs) provide important information on the presence of transcriptional regulatory elements and the state of chromatin in mammalian cells1, 2, 3. Conventional DNase sequencing (DNase-seq) for genome-wide DHSs profiling is limited by the requirement of millions of cells4, 5. Here we report an ultrasensitive strategy, called single-cell DNase sequencing (scDNase-seq) for detection of genome-wide DHSs in single cells. We show that DHS patterns at the single-cell level are highly reproducible among individual cells. Among different single cells, highly expressed gene promoters and enhancers associated with multiple active histone modifications display constitutive DHS whereas chromatin regions with fewer histone modifications exhibit high variation of DHS. Furthermore, the single-cell DHSs predict enhancers that regulate cell-specific gene expression programs and the cell-to-cell variations of DHS are predictive of gene expression. Finally, we apply scDNase-seq to pools of tumour cells and pools of normal cells, dissected from formalin-fixed paraffin-embedded tissue slides from patients with thyroid cancer, and detect thousands of tumour-specific DHSs. Many of these DHSs are associated with promoters and enhancers critically involved in cancer development. Analysis of the DHS sequences uncovers one mutation (chr18: 52417839G>C) in the tumour cells of a patient with follicular thyroid carcinoma, which affects the binding of the tumour suppressor protein p53 and correlates with decreased expression of its target gene TXNL1. In conclusion, scDNase-seq can reliably detect DHSs in single cells, greatly extending the range of applications of DHS analysis both for basic and for translational research, and may provide critical information for personalized medicine.
2015-11-25 | GSE61844 | GEO
Project description:This work is part of a larger study where we investigated activation of the nuclear receptor and transcription factor CAR (Nr1i3) by its specific agonist ligand TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene), which dysregulates hundreds of genes in mouse liver and is linked to male-biased hepatocarcinogenesis. We used DNase-seq and DNase hypersensitivity site (DHS) analysis to identify several thousand genomic regions (∆DHS) where short-term exposure to TCPOBOP induces localized changes (increases or decreases) in mouse liver chromatin accessibility, many of which cluster together with TCPOBOP-responsive genes. Sites of chromatin opening were highly enriched nearby genes induced by TCPOBOP and chromatin closing was highly enriched nearby genes repressed by TCPOBOP, consistent with TCPOBOP-responsive ∆DHS serving as enhancers and promoters that positively regulate CAR-responsive genes. Gene expression changes lagged behind chromatin opening or closing for a subset of TCPOBOP-responsive ∆DHS. DHS that were specifically responsive to TCPOBOP in male liver were significantly enriched for genomic regions with a basal male bias in chromatin accessibility; however, the male-biased response of hepatocellular carcinoma-related genes to TCPOBOP was not associated with a correspondingly male-biased ∆DHS response. These studies elucidate the genome-wide organization of CAR-responsive genes and of the thousands of associated genomic sites where TCPOBOP exposure induces both rapid and persistent changes in chromatin accessibility.
2018-04-09 | GSE104061 | GEO
Project description:Sequencing files provided here are mouse liver ChIP-seq for the activating histone mark H3K27ac in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes RNA-seq and DNase-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
2021-10-27 | GSE130909 | GEO
Project description:Sequencing files provided here are mouse liver RNA-seq in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes DNase-seq and H3K27ac ChIP-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
2021-10-27 | GSE130913 | GEO
Project description:The liver of DNase II-deficient embryos contains numerous macrophages carrying undigested DNA, and the embryos die in feto. Here, we examined the gene expression in the wild-type (GSM32833) and DNase II-/- (GSM32834) fetal liver, and found that a set of interferon (IFN)-inducible genes is strongly activated in the DNase II-/- fetal liver. When the DNase II-/- mice were crossed to IFN type I receptor (IFN-IR)-null mice, the mice deficient in both DNase II and IFN-IR genes were born apparently normally, indicating that the type I IFN and its inducible genes had the lethal effect on the mouse development. To examine which genes induced by IFN is responsible to kill the embryos, the gene expression of the fetal liver of DNase II-/- IRF-IR-/- embryos (GSM32835) was also examined. Keywords: other
2004-12-01 | GSE1859 | GEO