Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide binding of trr (ChIP-seq) and expression analysis (RNA-seq) of trr- and G9a mutant fly heads

ABSTRACT: trr ChIP-seq, trr RNA-seq, G9a RNA-seq

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE89459 | GEO | 2017/08/25

SECONDARY ACCESSION(S): PRJNA352259

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

G9a

Project description:Drosophila melanogaster G9a, G9a, is expressed in 3 baseline experiment(s);

| FBgn0040372 | ExpressionAtlas

G9a

Project description:Drosophila melanogaster G9a, G9a, is differentially expressed in 11 experiment(s);

| FBgn0040372 | ExpressionAtlas

Gene expression profiling in Drosophila larvae in normal and Cmi or Trr depletion backgrounds

Project description:RNA seq analyses of gene expression in wild type and Cmi or Trr depletion blue gut and clear gut larvae

2020-04-20 | GSE143239 | GEO

trr

Project description:Drosophila melanogaster trr, trithorax-related, is differentially expressed in 9 experiment(s);

| FBgn0023518 | ExpressionAtlas

trr

Project description:Drosophila melanogaster trr, trithorax-related, is expressed in 3 baseline experiment(s);

| FBgn0023518 | ExpressionAtlas

HiSeq Chip-seq analysis of whole genomic landscape of G9a and H3K9me2-targeted in CCICs

Project description:Purpose: to demonstrate that G9a maintain CCICs functional triats is independent of its methyltransferase activity. Method: ChIP-seq was applied to CCICs to elucidate the nature of G9a and H3K9me2-regulated differential gene targets by Illumina/Soleza Genome analyzer Results: It was shown that ghe 4,902 G9a-and H3K9me2-targeted genes are broadly idstributed throughout the genome, and both are co-localized at most of the sites in CCICs. G9a and H3K9me2-targeted in CCICs

2016-08-10 | E-GEOD-82131 | biostudies-arrayexpress

Histone H3K4 monomethylation catalyzed by Trr and mammalian COMPASS-like proteins at enhancers is dispensable for development and viability

Project description:Histone H3 lysine 4 monomethylation (H3K4me1) is an evolutionarily conserved feature of enhancer chromatin catalyzed by the COMPASS-like methyltransferase family that includes Trr in Drosophila melanogaster and MLL3 (encoded by KMT2C) and MLL4 (encoded by KMT2D) in mammals. Here we demonstrate that Drosophila embryos expressing catalytically deficient Trr eclose and develop to productive adulthood. Parallel experiments with a trr allele that augments enzyme product specificity show that conversion of H3K4me1 at enhancers to H3K4me2 and H3K4me3 is also compatible with life and results in minimal changes in gene expression. Similarly, loss of the catalytic SET domains of MLL3 and MLL4 in mouse embryonic stem cells (mESCs) does not disrupt selfrenewal. Drosophila embryos with trr alleles encoding catalytic mutants manifest subtle developmental abnormalities when subjected to temperature stress or altered cohesin levels. Collectively, our findings suggest that animal development can occur in the context of Trr or mammalian COMPASS-like proteins deficient in H3K4 monomethylation activity and point to a possible role for H3K4me1 on cis-regulatory elements in specific settings to fine-tune transcriptional regulation in response to environmental stress.

2017-10-02 | GSE95781 | GEO

RNA-Seq from wt and G9A knockout ES cells

Project description:To measure gene expression difference between wt and g9A knockout ES cells G9A TT2 ES cells (Yokochi et al) were treated with Veh. Or 4OHT (to delete G9A)

2012-06-18 | E-GEOD-36896 | biostudies-arrayexpress

Transcription profiling of mouse embryonic fibroblasts deleted for G9a reconstituted with empty vector (delta), wild type FLAG-G9a (WT), FLAG-G9a K165A (K165A) or FLAG-G9a H1093K catalytic mutant reveasl methylation of hMTase G9a on a histone-like site regulates protein complex assembly

Project description:Gene expression in eukaryotes is tightly linked to the methylation state of specific lysine residues within the N-terminal region of the core histone proteins. While the mechanisms connecting histone lysine methylation to effector protein recruitment and control of gene activity are increasingly well understood, it remains unknown whether non-histone chromatin proteins are targets for similar modification-recognition systems. Here we show that histone H3 and the H3 methyltransferase G9a share a conserved methylation motif that is both necessary and sufficient to mediate in vivo interaction with the potent epigenetic regulator Heterochromatin Protein 1 (HP1). As with H3, G9a-HP1 interaction is dependent on lysine methylation and can be reversed by adjacent phosphorylation. NMR analysis demonstrates that the HP1 chromodomain recognizes methyl-G9a through a binding mode similar to that used in recognition of methyl-H3, and that adjacent phosphorylation directly antagonizes G9a-HP1 interaction. In addition to uncovering the chromodomain as a generalized methyl-lysine binding module, these data identify histone-like modification cassettes (or âhistone mimicsâ) as an entirely new class of non-histone methylation targets, and directly demonstrate the relevance of the principles underlying the histone code to the regulation of non-histone proteins. Experiment Overall Design: Two independent Affymetrix gene expression microarray analyses were performed on samples from G9a-deleted MEFs reconstituted with empty vector (delta), wild type FLAG-G9a (WT), FLAG-G9a K165A (K165A) or FLAG-G9a H1093K catalytic mutant (H1093K).

2008-06-15 | E-GEOD-8011 | biostudies-arrayexpress

The genomic distribution of G9a, H3K9me2, H3K27me3 and Mef2c in cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice

Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify the genomic regions bound to G9a in cardiomyocytes (CMs),we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on isolated G9a-KO and Cre CMs, and considered the best G9a-bound genomic regions as those that had a loss or decrease of G9a binding as well as a lower level of H3K9me2 in G9a-KO CMs. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether the loss of G9a had an effect on the distribution of this histone mark. To this end, we performed ChIP-seq for H3K27me3 in Cre CMs and G9a-KO CMs. Finally co-immunoprecipitation assays revealed that G9a interacts with Mef2c, thus to elucidate the function of the G9a–Mef2c interaction in adult cardiomyocytes, we used ChIP-seq to define the genomic distribution of Mef2c in Cre CMs and G9a-KO CMs.

2017-08-30 | GSE93690 | GEO

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