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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIPseq profile of RNA polymerase (pol II), the p65 subunit of NFkB, STAT1 and STAT2 in bone marrow derived macrophages after treatment with IFNb, heat-killed Listeria monocytogenes (hkL), or both.

ABSTRACT: Using ChIP-Seq analysis we define genes induced in macrophages through synergistic transcriptional activation by NFkB and the IFNb-activated transcription factor ISGF3.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Sebastian Wienerroither

PROVIDER: E-MTAB-2972 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Response to interferons and antibacterial innate immunity in the absence of tyrosine-phosphorylated STAT1.

Majoros Andrea A Platanitis Ekaterini E Szappanos Daniel D Cheon HyeonJoo H Vogl Claus C Shukla Priyank P Stark George R GR Sexl Veronika V Schreiber Robert R Schindler Christian C Müller Mathias M Decker Thomas T

EMBO reports 20160212 3

Signal transducer and activator of transcription 1 (STAT1) plays a pivotal role in the innate immune system by directing the transcriptional response to interferons (IFNs). STAT1 is activated by Janus kinase (JAK)-mediated phosphorylation of Y701. To determine whether STAT1 contributes to cellular responses without this phosphorylation event, we generated mice with Y701 mutated to a phenylalanine (Stat1(Y701F)). We show that heterozygous mice do not exhibit a dominant-negative phenotype. Homozyg ...[more]

PMID: 26882544

Publication: 1/2

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ChIPseq profile of STAT1 binding after 2h of IFNβ treatment, in bone marrow derived macrophages isolated from WT, Stat1Y701F and Stat1-/- mice.

Project description:Using ChIP-Seq analysis we define genes induced in macrophages through transcriptional activation by STAT1 and search for the gain of function in mutant Stat1Y701F compared to the Stat1-/- mice.

2016-01-25 | E-MTAB-3597 | biostudies-arrayexpress

Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

Project description:Reverse transcription-derived sequences account for at least half of the human genome. Although these retroelements are formidable motors of evolution, they can occasionally cause disease, and accordingly are inactivated during early embryogenesis through epigenetic mechanisms. In the mouse, at least for endogenous retroviruses, important mediators of this process are the tetrapod-specific KRAB-containing zinc finger proteins (KRAB-ZFPs) and their cofactor TRIM28. The present study demonstrates that KRAB/TRIM28-mediated regulation is responsible for controlling a very broad range of human-specific endogenous retroelements (EREs) in human embryonic stem (ES) cells and that it exerts, as a consequence, a marked effect on the transcriptional dynamics of these cells. It further reveals reciprocal dependence between TRIM28 recruitment at specific families of EREs and DNA methylation. It finally points to the importance of persistent TRIM28-mediated control of ERE transcriptional impact beyond their presumed inactivation by DNA methylation. Analyses of epigentic effectors and marks in KAP1 WT and KD human embryonic stem cells

2014-05-29 | E-GEOD-57989 | biostudies-arrayexpress

Histone Demethylase Lsd1 is Required to Repress Hematopoietic Stem and Progenitor Cell Signatures During Blood Cell Maturation

Project description:Here we describe that lysine-specific demethylase 1 (Lsd1/KDM1a), which demethylates histone H3 on LysM-bM-^@M-^I4 or LysM-bM-^@M-^I9 (H3K4/K9), is an indispensible epigenetic governor of hematopoietic differentiation. Integrative genomic analysis in primary hematopoietic cells, combining global occupancy of Lsd1, genome-wide analysis of its histone substrates H3K4 mono- and di-methylation and gene expression profiling, reveals that Lsd1 represses hematopoietic stem and progenitor cell (HSPC) gene expression programs during hematopoietic differentiation. We found that Lsd1 function was not restricted to transcription start sites, but is also critical at enhancers. Loss of Lsd1 at these sites was associated with increased H3K4me1 and H3K4me2 methylation levels on HSPC genes and their derepression. Failure to fully silence HSPC genes compromised differentiation of hematopoietic stem cells and mature blood cell lineages. Our data indicate that Lsd1-mediated concurrent repression of enhancer and promoter activity of stem and progenitor cell genes is a pivotal epigenetic mechanism required for proper hematopoietic maturation. To identify direct target genes of Lsd1 in myeloid cells we mapped global occupancy of Lsd1 in 32D granuolocytic progenitor cells and compared H3K4me1/me2/me3 and H3K27ac histone modifications in Lsd1fl/fl (wild type) vs. Lsd1fl/f Mx1Cre (knockout) Gr1dim Mac1 granuolocytic progenitor cells.

2013-06-25 | E-GEOD-40440 | biostudies-arrayexpress

Long-range chromosome interactions mediated by cohesin shape circadian gene expression [ChIP-Seq]

Project description:Mammalian circadian rhythm is established by the negative feedback loops consisting of a set of clock genes, which lead to the circadian expression of thousands of downstream genes. As genome-wide transcription is organized under the high-order chromosome structure, it is unclear how circadian gene expression is influenced by chromosome structure. In this study, we focus on the function of chromatin structure proteins cohesin as well as CTCF (CCCTC-binding factor) in circadian rhythm. We analyzed the interactome of a Bmal1-bound enhancer upstream of a clock gene, Nr1d1, by 4C-seq and observed that cohesin binding sites are enriched in the interactome. Integrating circadian transcriptome data and cistrome data, we found that cohesin-CTCF co-binding sites tend to insulate the phases of circadian oscillating genes while cohesin-non-CTCF sites facilitate the interaction between circadian enhancer and promoter. A coarse-grained model integrating the long-range effect of cohesin and CTCF markedly improved our mechanistic understanding of circadian gene expression. This model is subsequently supported by our RNA-seq data from cohesin knockout cells. Cohesin is required at least in part for driving the circadian gene expression by facilitating the enhancer-promoter looping. Taken together, our study provided a novel insight into the relationship between circadian transcriptome and the high-order chromosome structure. Bmal1 ChIP-Seq in WT mouse embryonic fibroblast cells

2016-04-04 | E-GEOD-77162 | biostudies-arrayexpress

Systematic Identification of Factors Crucial for Provirus Silencing in Embryonic Stem Cells (ChIP-seq)

Project description:Our study reports the first genome-wide atlas of functional nodes that mediate proviral silencing in ESCs. It provides evidences for the comprehensive, interconnected and multi-layered genetic/epigenetic machineries by which ESCs maintain the repressive state of provirus and ERVs. ChIP-seq analysis of Chaf1a, Trim28, Sumo2 and Zfp809 to demonstrate the mechanism of the silencing of Endogenous retroviruses

2015-09-14 | E-GEOD-70799 | biostudies-arrayexpress

Transcriptome analysis in macrophages treated with type I interferon, heat-killed Listeria monocytogenes, or both.

Project description:To define the group of genes which is synergistically induced by cooperative activity of the type I interferon - activated Jak/STAT pathway and other pathways, we treated bone marrow-derived macrophages (BMDM) with heat-killed Listeria (hkL; non-STAT pathways activated), type I interferon alone (only STAT pathway activated), or both stimuli together.

2015-06-15 | E-MTAB-3015 | biostudies-arrayexpress

Transcription factor binding dynamics during human ES cell differentiation

Project description:Pluripotent stem cells provide a powerful system to dissect the underlying molecular dynamics that regulate cell fate changes during mammalian development. Here we report the integrative analysis of genome wide binding data for 38 transcription factors with extensive epigenome and transcriptional data across the differentiation of human embryonic stem cells to the three germ layers. We describe core regulatory dynamics and show the lineage specific behavior of selected factors. In addition to the orchestrated remodeling of the chromatin landscape, we find that the binding of several transcription factors is strongly associated with specific loss of DNA methylation in one germ layer and in many cases a reciprocal gain in the other layers. Taken together, our work shows context-dependent rewiring of transcription factor binding, downstream signaling effectors, and the epigenome during human embryonic stem cell differentiation. 200 ChIP-seq experiments profiling 38 transcription factors (TFs) and several chromatin marks in 5 cell types--male human ES cell line HUES64 and directed differentiation of HUES64 towards mesendoderm (dMS, 12 hours), endoderm (dEN, 120 hours), mesoderm (dME, 120 hours), and ectoderm (dEC, 120 hours). In addition, three ES cell lines were derived with shRNA mediated knockdown of GATA4 and differention toward endoderm (dEN_shGATA4) and mesoderm (dME_shGATA4). These cell lines were used for MNChIP-seq of GATA4, SMAD1, and H3K27Ac and for 4 RRBS experiments in GATA4 knockdown and control cell lines.

2015-02-19 | E-GEOD-61475 | biostudies-arrayexpress

Evollutionally dynamic L1 regulation in embryonic stem cells

Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected. HA-tagged Gm6871 ChIP-seq in mES cells, RNA-seq in control and Gm6871 KD mES cells, KAP1 ChIP-seq in WT mES cells, RNA-seq in control and DNMTs KD hES cells.

2014-06-09 | E-GEOD-58323 | biostudies-arrayexpress

Systematic Identification of Factors Crucial for Provirus Silencing in Embryonic Stem Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-14 | E-GEOD-70865 | biostudies-arrayexpress

Transcription profiling of Lbeta T2 cells treated with either vehicle or activin A for different length of time to characterize the upregulation of gene expression by activin A.

Project description:The primary response of Lbeta T 2cells upon activin treatment at 1hr, 2hr, and 6hr is the significant up-regulation of FSHbeta subunit. Affymetrix genearray missed this important information due to cross-hybridization of its probes with other genes and chromosome segments. Activin modulates a network of genes and signaling pathways to exert a variety of functions. Experiment Overall Design: Subconfluent Lbeta T2 cells were seeded in cell culture flasks for 16 hours in phenol-free, serum-free medium, and then treated with either vehicle or activin A (30ng/ml). At 1hr, 2hr, or 6hr after treatment, total RNA was isolated using RNeasy Mini Kit. Integrity of RNA was evaluated with an Agilent 2100 Bioanalyzer, and purity/concentration was determined using a GeneSpec III before target preparationi and hybridizations.

2007-11-27 | E-GEOD-5232 | biostudies-arrayexpress

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