Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global mapping of epigenetic modifications of histone H3 Lysine 4 di- and trimethylation in Rice

ABSTRACT: We present high-resolution maps of DNA methylation and H3K4 di- and tri-methylation of two entire chromosomes and two fully sequenced centromeres in rice shoots and cultured cells. Most transposable elements have highly methylated DNA but no H3K4 methylation whereas over half of protein-coding genes have both methylated DNA and di- and/or tri-methylated H3K4. Methylation of DNA but not H3K4 correlates with suppressed transcription. In contrast, if both DNA and H3K4 are methylated transcription is only slightly reduced. Transcriptional activity was positively correlated with H3K4Me3/H3K4Me2 within the gene body: genes with predominantly H3K4Me3 were actively transcribed whereas genes with predominantly H3K4Me2 were transcribed at moderate levels. Both H3K4Me2 and H3K4Me3 exhibited two peaks in long rice genes; a minor peak correlated with putative transcription start sites and a major peak downstream, implying possible roles in transcriptional initiation and elongation. Keywords: whole genome profiling, DNA methylation, ChIP

ORGANISM(S): Oryza sativa

PROVIDER: GSE9925 | GEO | 2008/01/04

SECONDARY ACCESSION(S): PRJNA103927

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps of chromatin state in pre-osteoblastic and lineage-committed cells.

Project description:Epigenetic mechanisms regulate osteogenic lineage differentiation of mesenchymal stromal cells. Histone methylation is an important step in controlling local chromatin structure and gene expression and it is controlled by multiple lysine demethylases. Although Lsd1 knockdown did not affect global H3K4 methylation levels, genome-wide ChIP-Seq analysis revealed high levels of Lsd1 at gene promoters and its binding was associated with di- and tri-methylation of histone 3 at lysine 4 (H3K4me2 and H3K4me3)

2021-10-30 | GSE186665 | GEO

Differential H3K4 methylation identifies developmentally poised hematopoietic genes

Project description:We assess the concordance of histone H3 lysine 4 dimethylation (H3K4me2) and trimethylation (H3K4me3) on a genome-wide scale in erythroid development by analyzing pluripotent, multipotential and unipotent cell types. Although H3K4me2 and H3K4me3 are concordant at most genes, multipotential hematopoietic cells have a subset of genes that are differentially methylated (H3K4me2+/me3-). These genes are transcriptionally silent, highly enriched in lineage-specific hematopoietic genes, and uniquely susceptible to differentiation-induced H3K4 demethylation. Self-renewing embryonic stem cells, which restrict H3K4 methylation to genes that contain CpG islands (CGIs), lack H3K4me2+/me3- genes. These data reveal distinct epigenetic regulation of CGI and non-CGI genes during development and indicate an interactive relationship between DNA sequence and differential H3K4 methylation in lineage-specific differentiation. Keywords: comparison of different cell lines Multipotential and erythroid-differentiated hematopoietic cells were compared. Expression was measured using Affymetrix microarrays. H3K4me2 and H3K4me3 enrichment was assessed using Agilent tiling arrays.

2008-04-29 | E-GEOD-11044 | biostudies-arrayexpress

Effect of LSD1 knockdown on histone H3K4 methylation in HEL human erythroleukemia cell line.

Project description:To understand the role of LSD1 in regulating histone H3K4 methylation status, ChIP-seq analyse of mono- and di-methylated H3K4 in LSD1-KD HEL cells were performed. The analyses revealed demethylation of H3K4me1 and H3K4me2 by LSD1 at regulatory regions including CEBPA gene enhancer.

2021-05-04 | GSE145399 | GEO

Differential H3K4 methylation identifies developmentally poised hematopoietic genes

2008-04-29 | GSE11044 | GEO

Histone H3 lysine 4 trimethylation regulates RNA polymerase II promoter-proximal pause-release

Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.

2023-03-14 | PXD028858 | Pride

H3K4me3 regulates RNA polymerase II promoter-proximal pause-release

Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, by using mouse embryonic stem cells (mESCs) as a model system, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Notably, we show that H3K4me3 is required for the recruitment of the Integrator Complex Subunit 11 (INTS11), which is essential for the eviction of paused RNAPII and transcriptional elongation. Thus, our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.

2023-02-10 | PXD039176 | Pride

H3K4me3 ChIP chips

Project description:In yeast and other eukaryotes, the histone methyltransferase Set1 mediates methylation of lysine 4 on histone H3 (H3K4me). This modification marks the 5' end of transcribed genes in a 5' to 3' tri- to di- to monomethyl gradient, and promotes association of chromatin remodeling enzymes that regulate transcription. In a screen to identify factors that control the distinct H3K4 methylation states, we identified Ctk1, the serine 2 C-terminal domain (CTD) kinase for RNA polymerase II (RNAP II). We found that CTK1 deletion nearly abolished H3K4 monomethylation, yet caused a significant increase in H3K4 di- and trimethylation. Both on individual genes and genome-wide, the loss of CTK1 disrupted the H3K4 methylation patterns normally observed. H3K4me2 and H3K4me3 spread 3' into the body of genes, while H3K4 monomethylation was diminished. These effects were dependent on the catalytic activity of Ctk1, but are independent of Set2-mediated H3K36 methylation. Furthermore, these effects are not due to spurious transcription initiation in the body of genes, changes in RNAP II occupancy, changes in serine 5 CTD phosphorylation patterns, or to ‘transcriptional stress’. These data show that Ctk1 acts to restrict the spread of H3K4 methylation through a mechanism that is independent of a general transcription defect. The evidence presented indicates that Ctk1 controls the maintenance of suppressive chromatin in the coding regions of genes by both promoting H3K36 methylation, which leads to histone hypoacetylation, and by preventing the 3' spread of H3K4 trimethylation, a mark associated with chromatin remodeling at the 5' end of genes. Keywords: ChIP-chip

2006-11-01 | GSE5572 | GEO

Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa (Nimblegen)

Project description:In higher eukaryotes, histone methylation is involved in the maintenance of cellular identity during somatic development. During spermatogenesis, most nucleosomes are replaced by protamines. Therefore, it is unclear if histone modifications function in paternal transmission of epigenetic information. Here we show that active H3K4 di-methylation (H3K4me2) and repressive H3K27 tri-methylation (H3K27me3), two modifications important for Trithorax and Polycomb-mediated gene regulation, are present in chromatin of human spermatozoa and show methylation-specific distributions at regulatory regions. H3K4me2-marked promoters control gene functions in spermatogenesis and cellular homeostasis suggesting that this mark reflects germline transcription. In contrast, H3K27me3 marks promoters of key developmental regulators in sperm as in soma. Many H3K27me3-marked genes are never expressed in the male and female germline, and in early “totipotent” embryos, suggesting a function for Polycomb in repressing somatic determinants across generations. Targets of H3K4me2 and H3K27me3 are also modified in mouse spermatozoa, implicating an evolutionary conserved role for histone methylation in chromatin inheritance via the male germline. Chromatin immuno precipitation (ChIP) was performed on sperm samples obtained from 9 normospermic donors. DNA associated with H3K4me2 or H3K27me3 was precipitated using specific antibodies. Input and precipitated DNA were amplified and hybridized to a tiling microarray (NimbleGen Systems Inc.) representing 18029 promoter regions (2200bp upstream to 500bp downstream of transcription start sites) of all RefSeq annotated human genes. For each modification 3 independent ChIP experiments were performed of which one was hybridized in a dye swap configuration.

2010-05-16 | E-GEOD-13863 | biostudies-arrayexpress

Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa (Nimblegen)

2010-05-16 | GSE13863 | GEO

Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa (Illumina)

Project description:In higher eukaryotes, histone methylation is involved in the maintenance of cellular identity during somatic development. During spermatogenesis, Since most nucleosomes are replaced by protamines during spermatogenesis . Iit is therefore unclear whether if histone modifications function in paternal transmission of epigenetic information. Here we show that H3K4 di-methylation (H3K4me2) and H3K27 tri-methylation (H3K27me3), two modifications important for Trithorax and Polycomb-mediated gene regulation, display methylation-specific distributions at regulatory regions in human spermatozoa. H3K4 dimethylation H3K4me2-marksed promoters of genes relevant control gene functions in spermatogenesis and cellular homeostasis suggesting that this mark reflects germline transcription. In contrast, H3K27 trimethylation (H3K27me3) marks promoters of key developmental regulators in sperm like in somatic cells. Promoters of orthologous genes are similarly modified in mouse spermatozoa. Further, particularly genes with extensive H3K27me3 coverage around transcriptional start sites are never expressed during male and female gametogenesis, nor in pre-implantation embryos. These data are compatible with a function for Polycomb in repressing somatic determinants across generations. Importantly, however, we observe only modest selective retention of nucleosomes at regulatory regions in human sperm suggesting that paternal transmission of H3K27me3-encoded epigenetic information may be subjected to variegation. Identification of nucleosome containing regions in 6 human sperm samples

2010-05-16 | E-GEOD-19889 | 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