Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

57 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pol II and its associated epigenetic marks are present at pol III-transcribed non-coding RNA genes (I)

ABSTRACT: Epigenetic control is an important aspect of gene regulation. Despite detailed understanding of many examples, the transcription of non-coding RNA genes by RNA polymerase (pol) III is less well characterized. Here we profile the epigenetic features of pol III target genes throughout the human genome. This reveals that the chromatin landscape of pol III-transcribed genes resembles that of pol II templates in many ways, although there are also clear differences. Our analysis also discovered an entirely unexpected phenomenon, namely that pol II co-localizes with the majority of genomic loci that are bound by pol III. Chip-Seq experiments for six samples: Pol III, TFIIIB, TFIIIC, H3K4me3 in HeLa cells and Pol III, S2 phos Pol II in CD4+ cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Iouri Chepelev

PROVIDER: E-GEOD-20040 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Pol II and its associated epigenetic marks are present at Pol III-transcribed noncoding RNA genes.

Barski Artem A Chepelev Iouri I Liko Dritan D Cuddapah Suresh S Fleming Alastair B AB Birch Joanna J Cui Kairong K White Robert J RJ Zhao Keji K

Nature structural & molecular biology 20100425 5

Epigenetic control is an important aspect of gene regulation. Despite detailed understanding of protein-coding gene expression, the transcription of noncoding RNA genes by RNA polymerase III (Pol III) is less well characterized. Here we profile the epigenetic features of Pol III target genes throughout the human genome. This reveals that the chromatin landscape of Pol III-transcribed genes resembles that of Pol II templates in many ways, although there are also clear differences. Our analysis al ...[more]

PMID: 20418881

Similar Datasets

CTCF demarcates chromatin domains

Project description:Insulators are DNA elements, which prevent inappropriate interactions between the neighboring regions of the genome. They can be functionally classified as either enhancer blockers or domain barriers. CTCF (CCCTC binding factor) is the only known major insulator binding protein in the vertebrates and has been shown to bind many enhancer-blocking elements. However, it is not clear whether it plays a role in chromatin domain barriers between active and repressive domains. Here, we used ChIP-Seq to map the genome-wide binding sites of CTCF in three cell types and identified significant binding of CTCF to the boundaries of repressive chromatin domains marked by H3K27me3. Although we find an extensive overlapping of CTCF binding sites across the three cell types, its association with the domain boundaries is cell type-specific. We further show that the nucleosomes flanking CTCF binding sites are well positioned and associated with histone H2AK5 acetylation (H2AK5ac). Interestingly, we found a complementary pattern between the repressive H3K27me3 and the active H2AK5ac regions, which are separated by CTCF. Our findings indicate that CTCF may play important roles in the barrier activity of insulators and provide a resource for further investigation of the CTCF function in organizing chromatin in the human genome. Examination of the role of CTCF in chromatin domain barrier function In addition to the ChIP-seq analysis, two replicates of HeLa expression data were studied.

2008-10-20 | E-GEOD-12889 | biostudies-arrayexpress

Genome wide uH2A localization analysis highlights Bmi1-dependent deposition of the mark at repressed genes.

Project description:Polycomb group (PcG) proteins control organism development by regulating the expression of developmental genes. Transcriptional regulation by PcG proteins is achieved at least partly through the PRC2-mediated methylation on lysine 27 of histone H3 (H3K27) and PRC1-mediated ubiquitylation on lysine 119 of histone H2A (uH2A). As an integral component of PRC1, Bmi1 has been demonstrated to be critical for H2A ubiquitylation. Here we report genome wide localization of the Bmi1-dependent uH2A mark in MEF cells. Gene promoter averaging analysis indicates a peak of uH2A just inside the transcription start site (TSS) of well annotated genes. This peak is enriched at promoters containing the H3K27me3 mark and represents the least expressed genes in WT MEF cells. In addition, peak finding reveals regions of local uH2A enrichment throughout the mouse genome, including almost 700 gene promoters. Genes with promoter peaks of uH2A exhibit lower level expression when compared to genes that do not contain promoter peaks of uH2A. Moreover, we demonstrate that genes with uH2A peaks have increased expression upon Bmi1 knockout. Importantly, local enrichment of uH2A is not limited to regions containing the H3K27me3 mark. We describe the enrichment of H2A ubiquitylation at high density CpG promoters and provide evidence to suggest that DNA methylation may be linked to uH2A at these regions. Thus, our work not only reveals Bmi1-dependent H2A ubiquitylation but also suggests that uH2A targeting in differentiated cells may employ a different mechanism from that in ES cells. Keywords: Epigenetics Examination of uH2A binding in WT and Bmi1 null MEF cells.

2009-05-20 | E-GEOD-15896 | biostudies-arrayexpress

Mapping Epigenomic Type-Specific Differences Occurring During Hematopoiesis

Project description:Formation of the blood from self-renewing hematopoietic stem cells to terminal lineages necessarily involves epigenomic modifications of the genome to control regulator and signature gene expression. By analysing the global expression profiles of hematopoietic stem cells (HSCs), in vivo differentiated CD4+ T cells and CD19+ B cells as well as in vitro differentiated erythrocyte precursor cells, we identified hundreds of transcripts showing type-specific expression in these cell types. To understand the epigenomic changes related to tissue-specific expression during HSC differentiation, we examined the genome-wide distribution of H3K4me1, H3K4me3, H3K27me1, H3K27me3, histone variant H2A.Z, chromatin remodeler BRG1, and RNA Polymerase II in the same four cell types, as well as embryonic stem cells. Analysis of these datasets revealed that numerous key differentiation genes are primed for expression by Brg1 and Pol II binding, as well as bivalent modifications in the HSCs prior to their expression in downstream differentiated cell types. Much of this bivalency in HSC is retained from embryonic stem cells. After differentiation, these modified regions resolve to active chromatin modification configuration in the specific lineage, while in parallel differentiated lineages the bivalent modification remains; Pol II and Brg1 are lost in closer lineages but bivalency resolves to silent monovalency in more distant lineages. Correlation of tissue-specific gene expression with the epigenomic changes predicts tens of thousands of potential common enhancers and tissue-specific enhancers, which may critically contribute to the expression patterns. We provide a valuable dataset for further understanding the regulatory mechanisms of differentiation and function of blood lineages. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.

2013-03-25 | E-GEOD-39229 | biostudies-arrayexpress

Mapping Epigenomic Type-Specific Differences Occurring During Hematopoiesis [ChIP-Seq]

Project description:Formation of the blood from self-renewing hematopoietic stem cells to terminal lineages necessarily involves epigenomic modifications of the genome to control regulator and signature gene expression. By analysing the global expression profiles of hematopoietic stem cells (HSCs), in vivo differentiated CD4+ T cells and CD19+ B cells as well as in vitro differentiated erythrocyte precursor cells, we identified hundreds of transcripts showing type-specific expression in these cell types. To understand the epigenomic changes related to tissue-specific expression during HSC differentiation, we examined the genome-wide distribution of H3K4me1, H3K4me3, H3K27me1, H3K27me3, histone variant H2A.Z, chromatin remodeler BRG1, and RNA Polymerase II in the same four cell types, as well as embryonic stem cells. Analysis of these datasets revealed that numerous key differentiation genes are primed for expression by Brg1 and Pol II binding, as well as bivalent modifications in the HSCs prior to their expression in downstream differentiated cell types. Much of this bivalency in HSC is retained from embryonic stem cells. After differentiation, these modified regions resolve to active chromatin modification configuration in the specific lineage, while in parallel differentiated lineages the bivalent modification remains; Pol II and Brg1 are lost in closer lineages but bivalency resolves to silent monovalency in more distant lineages. Correlation of tissue-specific gene expression with the epigenomic changes predicts tens of thousands of potential common enhancers and tissue-specific enhancers, which may critically contribute to the expression patterns. We provide a valuable dataset for further understanding the regulatory mechanisms of differentiation and function of blood lineages. ChIP-Seq: profiling of DNA-associated proteins in blood cell subsets.

2013-03-25 | E-GEOD-39538 | biostudies-arrayexpress

esBAF is an essential component of the core pluripotency transcriptional network

Project description:Distinctive SWI/SNF-like ATP-dependent chromatin remodeling esBAF complexes are indispensable for the maintenance and pluripotency of mouse embryonic stem (ES) cells. To understand the mechanism underlying the roles of these complexes in ES cells, we performed high-resolution genome-wide mapping of the core ATPase subunit, Brg, using ChIP-Seq technology. We find that that esBAF, as represented by Brg, binds to genes encoding components of the core ES transcriptional circuitry, including Polycomb group proteins. esBAF colocalizes extensively with Oct4, Sox2 and Nanog genome-wide, and shows distinct functional interactions with Oct4 and Sox2 at its target genes. Surprisingly, no significant colocalization of esBAF with PRC2 complexes, represented by Suz12, is observed. Lastly, esBAF co-binds with Stat3 and Smad1 genome-wide, consistent with a direct and critical role in LIF and BMP signaling essential to maintain pluripotency. Taken together, our studies indicate that esBAF is both an essential component of the core pluripotency transcriptional network, and might also be a critical component of the LIF and BMP signaling pathways essential for maintenance of self-renewal and pluripotency. Brg knockdown effect on expression, Brg ChIP-Seq

2009-01-20 | E-GEOD-14344 | biostudies-arrayexpress

Genomic Profiling of HMGN1 Reveals an Association with Chromatin at Regulatory Regions

Project description:High mobility group (HMG) proteins interact with other architectural proteins to regulate chromatin structure. We performed genome-wide mapping experiments to examine the distribution of HMGN1 across the human genome. We discovered that HMGN1 proteins are enriched at regulatory regions such as DNase I HS sites, distal transcription factor binding sites and promoters of actively transcribed genes. YY1, the Yin Yang 1 transcription factor, is a ubiquitous transcription factor that functions either as a transcriptional activator or a repressor, depending on its interacting partner. To test the preferential localization of HMGN1 with active regulatory regions, we examined the association of transcription factor YY1 and HMGN1 in CD4+ T cells. Examination of the genomic profile of HMGN1 and the relationship with regulatory elements in CD4+ T cells.

2010-11-30 | E-GEOD-25674 | biostudies-arrayexpress

Characterization of genome-wide enhancer-promoter interactions reveals co-expression of interacting genes and modes of higher order chromatin organization

Project description:Recent epigenomic studies have predicted thousands of potential enhancers in the human genome. However, there has not been systematic characterization of target promoters for these potential enhancers. Using H3K4me2 as a mark for active enhancers, we identified genome-wide enhancer-promoter interactions in human CD4+ T cells. Among the 6,520 long-distance chromatin interactions, we identify 2,067 enhancers that interact with 1,619 promoters and enhance their expression. These enhancers exist in accessible chromatin regions and are associated with various histone modifications and Pol II binding. The promoters with interacting enhancers are expressed at higher levels than those without interacting enhancers and their expression levels are positively correlated with the number of interacting enhancers. Interestingly, interacting promoters are co-expressed in a tissue-specific manner. We also find that chromosomes are organized into multiple levels of interacting domains. Our results define a global view of enhancer-promoter interactions and provide a dataset to further understand mechanisms of enhancer targeting and long-range chromatin organization. Two biological replicates of ChIA-PET (Chromatin Interaction Analysis by Paired-End Tag Sequencing) experiment in CD4+ T cells

2012-01-24 | E-GEOD-32677 | biostudies-arrayexpress

Mapping of INS promoter interactions reveals its role in long-range regulation of SYT8 transcription

Project description:Insulin (INS) synthesis and secretion from pancreatic M-NM-2 cells are tightly regulated; their deregulation causes diabetes. Here we map INS-associated loci in human pancreatic islets by 4C and 3C techniques and show that the INS gene physically interacts with the SYT8 gene, located over 300 kb away. This interaction is elevated by glucose and accompanied by increases in SYT8 expression. Inactivation of the INS promoter by promoter-targeting siRNA reduces SYT8 gene expression. SYT8-INS interaction and SYT8 transcription are attenuated by CTCF depletion. Furthermore, SYT8 knockdown decreases insulin secretion in islets. These results reveal a non-redundant role for SYT8 in insulin secretion and indicate that the INS promoter acts from a distance to stimulate SYT8 transcription. This suggests a function for the INS promoter in coordinating insulin transcription and secretion through long-range regulation of SYT8 expression in human islets. Circular Chromosome Conformation Capture (4C)-Seq experiments to profile interactions of INS promoter in human pancreatic islets isolated from two donors: donor 1 and donor 2.

2011-02-22 | E-GEOD-25862 | biostudies-arrayexpress

Genome-wide distribution of RNA-DNA hybrids identifies RNase H targets in tRNA genes, retrotransposons and mitochondria

Project description:During transcription the nascent RNA can invade the DNA template, forming extended RNA-DNA duplexes (R-loops). Here we employ ChIP-seq in strains expressing or lacking RNase H to map targets of RNase H activity throughout budding yeast genome. In wild-type strains, R-loops were readily detected over the 35S rDNA region transcribed by Pol I and over the 5S rDNA transcribed by Pol III. In strains lacking RNase H activity, R-loops were elevated over other Pol III genes notably tRNAs, SCR1 and U6 snRNA, and were also associated with the cDNAs of endogenous TY1 retrotransposons, which showed increased rates of mobility to the 5?-flanking regions of tRNA genes. Unexpectedly, R-loops were also associated with mitochondrial genes in the absence of RNase H1, but not of RNase H2. Finally, R-loops were detected on highly expressed protein-coding genes in the wild-type, notably over the second exon of spliced ribosomal protein genes. ChIP-seq of RNA-DNA hybrids using antibody S9.6

2014-11-03 | E-GEOD-53420 | biostudies-arrayexpress

Pol II and its associated epigenetic marks are present at pol III-transcribed non-coding RNA genes (II)

Project description:Epigenetic control is an important aspect of gene regulation. Despite detailed understanding of many examples, the transcription of non-coding RNA genes by RNA polymerase (pol) III is less well characterized. Here we profile the epigenetic features of pol III target genes throughout the human genome. This reveals that the chromatin landscape of pol III-transcribed genes resembles that of pol II templates in many ways, although there are also clear differences. Our analysis also discovered an entirely unexpected phenomenon, namely that pol II co-localizes with the majority of genomic loci that are bound by pol III. RNA-seq experiment for total RNA in CD4+ cells.

2010-04-25 | E-GEOD-20071 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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