Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [Illumina BeadArray]

ABSTRACT: Histone modifications regulate chromatin-dependent processes, yet the mechanisms by which they contribute to specific outcomes remain unclear. H3K4me3 is a prominent histone mark that is associated with active genes and promotes transcription through interactions with effector proteins that include initiation factor TFIID. We demonstrate that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53 targets. Further analyses show that (i) H3K4me3 enhances p53-dependent transcription by stimulating preinitiation complex (PIC) formation; (ii) H3K4me3, through TAF3 interactions, can act either independently or cooperatively with the TATA box to direct PIC formation and transcription; and (iii) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of p53 in response to genotoxic stress. Our findings indicate a mechanism by which H3K4me3 directs PIC assembly for the rapid induction of specific p53 target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43541 | GEO | 2013/03/02

SECONDARY ACCESSION(S): PRJNA186695

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [Illumina BeadArray]

Project description:Histone modifications regulate chromatin-dependent processes, yet the mechanisms by which they contribute to specific outcomes remain unclear. H3K4me3 is a prominent histone mark that is associated with active genes and promotes transcription through interactions with effector proteins that include initiation factor TFIID. We demonstrate that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53 targets. Further analyses show that (i) H3K4me3 enhances p53-dependent transcription by stimulating preinitiation complex (PIC) formation; (ii) H3K4me3, through TAF3 interactions, can act either independently or cooperatively with the TATA box to direct PIC formation and transcription; and (iii) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of p53 in response to genotoxic stress. Our findings indicate a mechanism by which H3K4me3 directs PIC assembly for the rapid induction of specific p53 target genes. Total RNAs from control or TAF3 knockdown cells before and after doxorubicin treatment were subjected to Illumina microarray analyses.

2013-03-02 | E-GEOD-43541 | biostudies-arrayexpress

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [ChIP-Seq]

Project description:Histone modifications regulate chromatin-dependent processes, yet the mechanisms by which they contribute to specific outcomes remain unclear. H3K4me3 is a prominent histone mark that is associated with active genes and promotes transcription through interactions with effector proteins that include initiation factor TFIID. We demonstrate that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53 targets. Further analyses show that (i) H3K4me3 enhances p53-dependent transcription by stimulating preinitiation complex (PIC) formation; (ii) H3K4me3, through TAF3 interactions, can act either independently or cooperatively with the TATA box to direct PIC formation and transcription; and (iii) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of p53 in response to genotoxic stress. Our findings indicate a mechanism by which H3K4me3 directs PIC assembly for the rapid induction of specific p53 target genes Examination of TAF3, RNAPII, and H3K4me3 distribution in HCT116 cells.

2013-03-02 | E-GEOD-43539 | biostudies-arrayexpress

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [HIT-Seq]

Project description:Histone modifications regulate chromatin-dependent processes, yet the mechanisms by which they contribute to specific outcomes remain unclear. H3K4me3 is a prominent histone mark that is associated with active genes and promotes transcription through interactions with effector proteins that include initiation factor TFIID. We demonstrate that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53 targets. Further analyses show that (i) H3K4me3 enhances p53-dependent transcription by stimulating preinitiation complex (PIC) formation; (ii) H3K4me3, through TAF3 interactions, can act either independently or cooperatively with the TATA box to direct PIC formation and transcription; and (iii) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of p53 in response to genotoxic stress. Our findings indicate a mechanism by which H3K4me3 directs PIC assembly for the rapid induction of specific p53 target genes Examination of genome wide binding sites of TAF3 full length protein vs TAF3 PHD domain alone (Full vs PHD), with or without M880A mutation (WT vs mut) in mouse MEF cells using HITseq method (PNAS 2010, 107:3135-3140, PMID: 20133638)

2013-03-02 | E-GEOD-43540 | biostudies-arrayexpress

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [HIT-Seq]

2013-03-02 | GSE43540 | GEO

H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation [ChIP-Seq]

2013-03-02 | GSE43539 | GEO

Control of Embryonic Stem Cell Lineage Commitment by Core Promoter Factor, TAF3 (RNA-Seq data)

2011-09-02 | GSE31271 | GEO

Control of Embryonic Stem Cell Lineage Commitment by Core Promoter Factor, TAF3 (ChIP-Seq data)

2011-09-02 | GSE31270 | GEO

Control of Embryonic Stem Cell Lineage Commitment by Core Promoter Factor, TAF3 (ChIP-Seq data)

2011-09-02 | E-GEOD-31270 | biostudies-arrayexpress

Control of Embryonic Stem Cell Lineage Commitment by Core Promoter Factor, TAF3 (RNA-Seq data)

Project description:We report that TAF3, a TBP-associated core promoter factor, is highly enriched in ES cells. In addition to its role in the core promoter recognition complex TFIID, genome-wide binding studies reveal that TAF3 localizes to chromosomal regions bound by CTCF and cohesin. Enrichment for TAF3/CTCF/cohesin bound regions distinguishes TAF3-activated from TAF3-repressed genes. Our findings support a new role of TAF3 in mediating long-range chromatin regulatory interactions to safeguard the finely-balanced transcriptional programs that give rise to pluripotency. Comparison of genome-wide expression patterns between TAF3-knockdown and WT embryonic stem cells using mRNA-Seq. Significantly differentially expressed protein-coding genes were identified by comparing control and knock-down samples at each timepoint (ES, embryoid body day 3 (EB3), EB6). Single and paired-end samples were combined at each timepoint, resulting in 3 tests for each gene (based on 8, 4, 4 independent measurements at ES ,EB3, EB6, respectively).

2011-09-02 | E-GEOD-31271 | biostudies-arrayexpress

The basal transcription complex component TAF3 transduces changes in nuclear phosphoinositides into transcriptional output

Project description:The aim of the experiment was to determine if changes in nuclear phosphoinositides induced by depletion of PIP4K2B impacts on gene expression through a specific phosphoinositide interaction site on TAF3. TAF3 is a core promoter complex protein that contains a PHD finger that interacts with H3K4me3. We determined that The TAF3 PHD finger also interacted with phosphoinositides and generated mutants of TAF3 that were unable to interact with phosphoinositides but still were capable of interacting with H3K4me3. PIP4K2B depletion enhances C2C12 myoblast differentiation. We depleted the endogenous TAF3 from C2C12 myoblast cells and rescued the cells with either a wild type TAF3 or a mutant unable to interact with PI (KK-TAF3). These cells were then maintained as controls or depeleted of PIP4K2B. The cells were then differentiated for two days or were treated wtih a etoposide. We aimed to identify genes that were reguated by PIP4K2B that required an intact phosphoinositide binding site.

2015-02-28 | GSE66353 | 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