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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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H3K4me3 chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

ABSTRACT: Purpose: To determine H3K4me3 chromatin profile in UBC9WT and UBC9KO BMDC before and after LPS stimulation. Methods: H3K4me3 chromatin profile was determined by sequencing UBC9 WT and UBC9 KO BMDC chromatin immunoprecipitated with antibody specific for H3K4me3. Results: We show differential chromatin profile for H3K4me3 on the ifnb1 locus between UBC9 KO cells and UBC9 WT. Conclusions: Loss of SUMOylation causes a deregulation of ifnb1 transcription activation mark. A study of H3K4me3 chromatin profile in UBC9 WT and UBC9 KO Bone Marrow derived Dendritic Cells.

ORGANISM(S): Mus musculus

SUBMITTER: Adrien Decque

PROVIDER: E-GEOD-66338 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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H3K4me3 chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

Project description:Purpose: To determine H3K4me3 chromatin profile in UBC9WT and UBC9KO BMDC before and after LPS stimulation. Methods: H3K4me3 chromatin profile was determined by sequencing UBC9 WT and UBC9 KO BMDC chromatin immunoprecipitated with antibody specific for H3K4me3. Results: We show differential chromatin profile for H3K4me3 on the ifnb1 locus between UBC9 KO cells and UBC9 WT. Conclusions: Loss of SUMOylation causes a deregulation of ifnb1 transcription activation mark.

2015-12-14 | GSE66338 | GEO

SUMO and RNAPolII chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

Project description:Purpose: To determine SUMO1 and SUMO2 chromatin profile in a static and dynamic manner in BMDC before and after LPS stimulation, and to determine RNAPolII chromatin occupancy in sumoylation-deficient BMDC compared to wild-type cells. Methods: SUMO1, SUMO2 and RNAPolII chromatin profiles were determined by sequencing BMDC chromatin immunoprecipitated with antibodies specific for SUMO1, SUMO2 and RNAPolII before and after LPS stimulation. Results: We show dynamic occupancy of three distal sites upstream of Ifnb1 gene by SUMO1 and SUMO2, as well as increased RNAPolII recruitment on selected genes. Conclusions: SUMO acts as a regulator of inflammatory and anti-viral gene programs. A study of SUMO and RNAPolII chromatin profile in Bone Marrow derived Dendritic Cells.

2015-12-14 | E-GEOD-66315 | biostudies-arrayexpress

Dynamics of TRIM33 binding in macrophages and effects of TRIM33 deletion on chromatin state during activation of primary macrophages.

Project description:To get insight into TRIM33 functions, TRIM33 ChIP-seq was carried out in murine macrophage cell line (RAW) and in bone marrow-derived macrophages (BMDM). The results showed that, in addition to its role in hematopoietic differentiation, TRIM33 may modulate PU.1 transcriptional activity during macrophage development and/or activation.To characterize the role of TRIM33 in macrophages, we bred TRIM33fl/fl mice with Lyz-Cre mice where the Cre recombinase gene is under the regulatory sequences of the Lyz gene that is expressed only in mature myeloid cells. Bone marrow cells from LyzCre/Trim33+/+ mice and LyzCre/Trim33flox/flox mice were differentiated in macrophages and treated during 0h, 4h, 12h and 24h with LPS. Using ChIP-seq, we provide a link between TRIM33 binding and H3K4me3 spreading on inflammatory genes in macrophages. Chromatin immunoprecipitations of TRIM33 and H3K4Me3 followed by multiparallel sequencing performed in murine bone marrow-derived macrophages (BMDM).

2015-11-23 | E-GEOD-43654 | biostudies-arrayexpress

BRG1 recruitment by transcription factors MITF and SOX10 defines a specific configuration of regulatory elements in the melanocyte lineage (RNA-seq)

Project description:Microphthalmia-associated transcription factor (MITF) is the master regulator of the melanocyte lineage. By tandem affinity purification and mass spectrometry, we present a comprehensive characterisation of the MITF interactome comprising multiple novel cofactors involved in transcription, DNA replication and repair and chromatin organisation, including a BRG1 chromatin remodelling complex comprising CHD7. BRG1 is essential for melanoma cell proliferation in vitro and for normal melanocyte development in vivo. MITF and SOX10 actively recruit BRG1 to a set of MITF-associated regulatory elements (MAREs) at active enhancers. MITF, SOX10 and YY1 bind between two BRG1-occupied nucleosomes thus defining both a combinatorial signature of transcription factors essential for the melanocyte lineage and a specific chromatin organisation of MAREs. Nevertheless, BRG1 silencing enhances MITF occupancy at MAREs showing that BRG1 acts to promote dynamic MITF interactions with chromatin. 19 samples corresponding to mRNA profiles of 501Mel and Hermes3A after MITF, BRG1 or control shRNA-mediated knockdown were generated by deep sequencing in triplicate (in duplicate for 501_shMITF and corresponding control 501_shSCR2), using HiSeq2500.

2015-04-02 | E-GEOD-61966 | biostudies-arrayexpress

Genome-wide analysis of RARÎ² transcriptional targets in mouse striatum links retinoic acid signaling with Huntingtonâs disease and other neurodegenerative disorders

Project description:The active vitamin A derivative retinoic acid (RA) is an important regulator of adult brain functions. How these regulations are achieved is poorly known, partly due to the paucity of information on RA molecular targets. The striatum, the region involved in control of motor, cognitive and affective functions, may be particularly prone to such regulation as it displays the highest levels of RA and its receptors (RARs). We report the first genome-wide analysis of RAR-binding sites in the brain. Using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), as well as transcriptomic analysis of RARÎ²-null mutant mice, we identified genomic transcriptional targets of RARÎ² in the striatum. Our data point to a strong contribution of RARÎ² in controlling neurotransmission, energy metabolism, and transcription, with a particular involvement of G-protein, cAMP and calcium signaling. Quantitative PCR analysis of striatal subregions revealed a higher sensitivity of ventral structures (nucleus accumbens) to lack of RARÎ² signaling. There is a high overlap of transcriptional targets of RARÎ² and genes affected in expression in Huntingtonâs disease (HD), and we observed a decrease of RARÎ² expression in the striatum of R6/2 transgenic mice, a murine model of HD. A large number of genes bearing RARÎ² binding sites have also been implicated in Alzheimerâs and Parkinsonâs diseases, raising the possibility that compromised RA signaling in striatum may be a mechanistic link explaining the similar affective and cognitive symptoms of these diseases. Globally, our data point to a possibility of a neuroprotective function of RARÎ² in the striatum. Genome-wide mapping of RARÎ² and H3K4me3 binding sites in mouse caudate putamen

2016-07-22 | E-GEOD-67829 | biostudies-arrayexpress

Single-cell chromatin accessibility data using scATAC-seq

Project description:A single hematopoietic stem cell can give rise to all blood cells with remarkable fidelity. Here, we define the chromatin accessibility and transcriptional landscape controlling this process in thirteen primary cell types that traverse the hematopoietic hierarchy. Exploiting the finding that enhancer landscapes better reflect cell identity than mRNA levels, we enable "enhancer cytometry" for accurate enumeration of pure cell types from complex populations. We further reveal the lineage ontogeny of genetic elements linked to diverse human diseases. In acute myeloid leukemia, chromatin accessibility reveals distinctive regulatory evolution in pre-leukemic HSCs (pHSCs), leukemia stem cells, and leukemic blasts. These leukemic cells demonstrate unique lineage infidelity, confirmed by single cell regulomes. We further show that pHSCs have a competitive advantage that is conferred by reduced chromatin accessibility at HOXA9 targets and is associated with adverse patient outcomes. Thus, regulome dynamics can provide diverse insights into human hematopoietic development and disease. Single-cell ATAC-seq of LMPPs, Monocytes, LSCs and Luekemic blast cells.

2016-06-01 | E-GEOD-74310 | biostudies-arrayexpress

mRNA sequencing of embryonic tails of sih mutants at 28 hours post fertilisation

Project description:We analysed the mRNA expression of embryos lacking blood flow at the onset of heart function. Examination of 3 WT and 3 sih mutants at 28 hpf

2015-12-31 | E-GEOD-59563 | biostudies-arrayexpress

SUMO and RNAPolII chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

2015-12-14 | GSE66315 | GEO

Genome-wide detection of DNase I hypersensitive sites in single cells and FFPE tissue samples

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

Large-scale epigenetic reprogramming is punctuated late during the evolution of pancreatic cancer progression [ChIP-Seq]

Project description:During pancreatic cancer progression, heterogeneous subclonal populations evolve in the primary tumor that possess differing capacities to metastasize and cause patient death. However, the genetics of metastasis reflects that of the primary tumor, and PDAC driver mutations arise early. This raises the possibility than an epigenetic process could be operative late. Using an exceptional resource of paired patient samples, we found that different metastatic subclones from the same patient possessed remarkably divergent malignant properties and global epigenetic programs. Global reprogramming was targeted to thousands of large chromatin domains across the genome that collectively specified malignant divergence. This was maintained by a metabolic shift within the pentose phosphate pathway, independent of KRAS driver mutations. Analysis of paired primary and metastatic tumors from multiple patients uncovered substantial epigenetic heterogeneity in primary tumors, which resolved into a terminally reprogrammed state in metastatic lesions. This supports a model whereby driver mutations accumulate early to initiate pancreatic tumorigenesis, followed by a period of subclonal evolution that generates sufficient intra-tumor heterogeneity for selection of epigenetic programs that may increase fitness during malignant progression and metastatic spread. To map the epigenomic landscape of pancreatic cancer progression as it evolves within patients. Chip-Seq (K27Me3, K36Me3, K9Me2/3, K4Me3 and K27Ac) of 2 patients (A13 and A38) and HPDE cell line. Patient A38 included local peritoneal metastasis and 2 distant metastsis (liver and lung mets), and 6AN treated and DMSO samples for lung matastasis. Patient A13 included 2 primary tumors and 1 distant lung metastasis. Each sample has been done with replicates.

2016-10-24 | E-GEOD-63125 | biostudies-arrayexpress

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