Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-Seq for Yrr1 protein on Saccharomyces cerevisiae cells carrying different YRR1 alleles in response to 4-nitroquinoline-N-oxide (4NQO)

ABSTRACT: In this study, we constructed three isogenic strains of S96 yrr1Î background (its native YRR1 gene was knocked out) carrying three different YRR1 alleles, YRR1_S96, YRR1_YJM789, YRR1_S96-I775E, respectively. We then conducted chromatin immuno-precipitation followed by high-throughput sequencing (ChIP-Seq) for Yrr1 protein on the three strains grown in Yeast Peptone Dextrose medium (YPD) and YPD + 4NQO. ChIP-Seq for Yrr1 protein was performed in biological triplicates on S96 cells carrying three different YRR1 alleles grown in YPD and YPD + 4NQO. Immune-precipitated DNA were sequenced for all the three cultures and input genomic DNA was sequenced for one culture.

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Xiaoqing Rong-Mullins

PROVIDER: E-GEOD-74700 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Pancreatic Beta-Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes [ChIP-seq]

Project description:The molecular clock is a transcriptional oscillator present in brain and peripheral cells that coordinates behavior and physiology with the solar cycle. Here we reveal that the clock gates insulin secretion through genome-wide transcriptional control of the pancreatic exocyst across species. Clock transcription factors bind to unique enhancer sites in cycling genes in beta cells that diverge from those in liver, revealing the dynamics of inter-tissue clock control of genomic and physiologic processes important in glucose homeostasis. ChIP-Seq in Beta-TC6 mouse beta cells

2015-11-10 | E-GEOD-70960 | biostudies-arrayexpress

Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [ChIP-Seq]

Project description:We report mapping of the PAX8 cistrome in three high grade serous ovarian cancer cell lines (KURAMOCHI, OVSAHO, and JHOS4) compared to three benign immortalized fallopian tube cell lines (FT33, FT194, and FT246). We identified a highly conserved PAX8 binding pattern common across benign fallopian tube cell lines that was distinct from the unique PAX8 binding patterns seen in each cancer cell line. Comparison of benign and malignant Mullerian cell lines.

2016-08-08 | E-GEOD-79893 | biostudies-arrayexpress

Mapping binding sites of SIN3 isoforms across the Drosophila genome.

Project description:SIN3 associates with RPD3 and other accessory proteins to form the SIN3 histone modifying complex. A single Sin3A gene encodes multiple SIN3 isoforms, of which SIN3 187 and SIN3 220 are predominant. Previous studies from our laboratory and others have indicated that SIN3 isoforms play non-redundant roles during fly development, however, the genes regulated by SIN3 isoforms are not known. We mapped the genome-wide binding sites of SIN3 isoforms in Drosophila. We established stable S2 cell lines that express either HA-tagged SIN3 187 or SIN3 220. The binding profiles revealed that the majority of the binding sites of SIN3 isoforms are overlapping. Our data revealed that SIN3 isoforms localize to euchromatic regions of the genome and enrichment of SIN3 isoforms are generally concentrated around the transcription start sites of genes. In addition, the extent of SIN3 binding confirmed previous findings indicating that SIN3 is a global transcriptional regulator. Genome-wide binding analysis of SIN3 187 and SIN3 220 in Drosophila. Using chromatin prepared from cell lines expressing either of the isoforms, we performed chromatin immunoprecipitation on chromatin prepared from cells that expresses either of the isoforms using an antibody against HA (ChIP). We coupled our ChIP with high resolution deep sequencing (ChIP-seq) to identify genomic targets of SIN3 isoforms.

2016-01-09 | E-GEOD-72171 | biostudies-arrayexpress

Mechanisms of Ikaros Tumor Suppression with HDAC1 through distinct histone markers in Pre-B ALL Leukemia

Project description:Ikaros functions as a master regulator of lymphocyte differentiation and a tumor suppressor. Ikaros binds DNA and regulates gene expression by chromatin remodeling. Mechanisms of Ikaros-mediated tumor suppression are unknown. Here we examined genome-wide occupancy of Ikaros and histone deacetylase 1 (HDAC1) and Histone midificaition markers in human leukemia, and found that the Ikaros and HDAC1 showed similar binding partern and HDAC1âDNA interactions are associated with the presence of bivalent chromatin, and the recruitment of HDAC1 by Ikaros is associated with bivalent chromatin at Ikaros target genes. Examine the genome-wide binding of Ikaros, HDAC1, H3K9me3, H3K9ac, H3K27me3, H3K4me3 and H3K36me3 in Nalm6 ALL leukemia cells.

2015-11-03 | E-GEOD-44217 | biostudies-arrayexpress

Conserved epigenomic signatures between mouse and human elucidate immune basis of Alzheimer's disease

Project description:Alzheimer’s disease (AD) is a severe1 age-related neurodegenerative disorder characterized by accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decline. Several genes have been implicated in AD, but chromatin state alterations during neurodegeneration remain uncharacterized. Here, we profile transcriptional and chromatin state dynamics across early and late pathology in the hippocampus of an inducible mouse model of AD-like neurodegeneration. We find a coordinated downregulation of synaptic plasticity genes and regulatory regions, and upregulation of immune response genes and regulatory regions, which are targeted by factors that belong to the ETS family of transcriptional regulators, including PU.1. Human regions orthologous to increasing-level enhancers show immune cell-specific enhancer signatures as well as immune cell expression quantitative trait loci (eQTL), while decreasing-level enhancer orthologs show fetal brain specific enhancer activity. Surprisingly, AD-associated genetic variants are specifically enriched in increasing-level enhancer orthologs implicating immune processes in AD predisposition. Indeed, increasing enhancers overlap known AD loci lacking protein-altering variants and implicate additional loci that do not reach genome-wide significance. Our results reveal new insights into the mechanisms of neurodegeneration and establish the mouse as a useful model for functional studies of AD regulatory regions. We profiled gene expression levels through RNA-Seq and histone mark levels through ChIP-Seq to compare control mice to the CK-p25 Alzheimer's disease model at 2 weeks and 6 weeks after induction of neurodegeneration.

2015-02-18 | E-GEOD-65159 | biostudies-arrayexpress

The PR/SET domain Zinc finger protein Prdm4 regulates gene expression in ES cells but plays a non-essential role in the developing mouse embryo.

Project description:ChIP-seq using anti-GFP antibody to map genomic binding of Prdm4-EGFP in stably transfected mouse embryonic stem cells Two independent ChIP-seq replicates for each of two independent Prdm4-EGFP expressing ES cell clones resulting in four anti-GFP ChIP-seq experiments. These samples have paired mouse IgG control.

2013-08-08 | E-GEOD-48372 | biostudies-arrayexpress

Genome wide identification of enhancer regions in the retrosplenial cortex of the prairie vole, Microtus ochrogaster.

Project description:We use ChIP-seq targeting histone 3 lysine 4 mono-methylation (H3K4me1) to identify putative enhancer sites genome-wide, in the retrosplenial cortex of adult prairie vole males. ChIP samples were generated by targeting a known enhancer mark (H3K4me1) in chromatin extracted from the retrosplenial cortex of 8 males. Illumina libraries were prepared from ChIP and INPUT DNA and sequenced on Illimuna HiSeq 2500 platform.

2015-12-11 | E-GEOD-73670 | biostudies-arrayexpress

Functional analysis of AEBP2, a PRC2 Polycomb protein, reveals a Trithorax phenotype in embryonic development and in ES cells

Project description:The Polycomb repressive complexes PRC1 and PRC2 are key mediators of heritable gene silencing in multicellular organisms. Here we characterize AEBP2, a known PRC2 cofactor which, in vitro, has been shown to stimulate PRC2 activity. We show that AEBP2 localises specifically to PRC2 target loci, including the inactive X chromosome. Proteomic analysis confirms that AEBP2 associates exclusively with PRC2 complexes. However, analysis of embryos homozygous for a targeted mutation of Aebp2 unexpectedly revealed a Trithorax phenotype, normally linked to antagonism of Polycomb function. Consistent with this we observe elevated levels of PRC2 mediated histone H3K27 methylation at target loci in Aebp2 mutant embryonic stem cells. We further demonstrate that mutant ES cells assemble atypical hybrid PRC2 sub-complexes, potentially accounting for enhancement of Polycomb activity, and suggesting that AEBP2 normally plays a role in defining the mutually exclusive composition of PRC2 sub-complexes. H3K27me3, SUZ12, and AEBP2 ChIP-Seq in wild-type and AEBP2 KO mouse ESCs, biological replicates, pre-cleared chromatin as input, additionally FS2 ChIP-Seq in cells with FS2 tagged AEBP2, HiSeq2000

2016-08-02 | E-GEOD-83082 | biostudies-arrayexpress

Genome-wide mapping of HIF-2Î± binding under normoxia in human bronchial epithelial cells (BEAS-2B)

Project description:Growing number of cancer (stem) cells and stem cells were described to accommodate constituent active HIF-2Î± under normoxia. Previous study of hypoxia effect may have obscured some of normoxic HIF-2Î± functions as hypoxia inducible features. Our interest in study of protective potential of HIFs in lung cells led us to discover pseudohypoxia functions of HIF-2Î± under normoxia in human bronchial epithelial cells which exhibit pluripotency related markers and features. Our study provided perspective to pseudohypoxia functions of HIF-2Î± via enrichment of de novo motifs. In addition to the C-TAD, the N-TAD of HIF-2Î± was found to contribute to targeting on these non-canonical loci. Further elucidation of pseudohypoxia mechanism could resolve its implication of malignancy or pluripotency. We report globally mapped binding of HIF-2Î± under normoxia by using high throughput sequencing

2016-07-06 | E-GEOD-81635 | biostudies-arrayexpress

Genome-wide epigenetic cross-talk between DNA methylation and H3K27me3 in zebrafish embryos

Project description:DNA methylation and histone modifications are epigenetic marks implicated in the complex regulation of vertebrate embryogenesis. The cross-talk between DNA methylation and Polycomb-dependent H3K27me3 histone mark has been reported in a number of organisms and both marks are known to be required for proper developmental progression. Here we provide genome-wide DNA methylation (MethylCap-seq) and H3K27me3 (ChIP-seq) maps for three stages (dome, 24hpf and 48hpf) of zebrafish (Danio rerio) embryogenesis, as well as all analytical and methodological details associated with the generation of this dataset. DNA methylation (MethylCap-seq) and H3K27me3 (ChIP-seq) profling of zebrafish embryogenesis

2015-07-22 | E-GEOD-70847 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data