Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA124075 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gcn5/PCAF dobule knockout (dKO) in MEFs leads to loss of the global H3K9ac, but only affect expression of a small nubmer of genes according to RNA-Seq data. To examine the function of H3K9ac on gene activation, H3K9ac ChIP-Seq was performed. We found that H3K9ac at Transcriptional Start sites (TSSs) of no-changed, up-regulated and down-regulated genes are all dramatially decreased in Gcn5/PCAF dKO cells, suggesting that H3K9ac is largely not required for gene activation. PCAF-/-;Gcn5f/D MEFs were infected with retroviral Cre to delete Gcn5 to generate Gcn5/PCAF dKO cells, followed by H3K9ac ChIP-Seq analysis
2014-09-03 | E-GEOD-60967 | biostudies-arrayexpress
Project description:Histone acetyltransferases (HATs) GCN5/PCAF and CBP/p300 are transcription coactivators. However, how these HATs regulate ligand-induced nuclear receptor target gene expression remains unclear. Here we show in mouse embryonic fibroblasts (MEFs), deletion of GCN5/PCAF specifically eliminates acetylation on H3K9 (H3K9Ac) while deletion of CBP/p300 selectively reduces acetylation on H3K18 and H3K27 (H3K18/27Ac). Treating MEFs with a specific ligand for nuclear receptor PPARdelta induces sequential increases of H3K18/27Ac and H3K9Ac on the promoter of PPARdelta target gene Angptl4, which correlates with a robust ligand-induced Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9Ac but not H3K18/27Ac on Angptl4 promoter. Finally, we show CBP/p300 and their HAT activities are required, while GCN5/PCAF and H3K9Ac are dispensable, for ligand-induced PPARdelta target gene expression in MEFs. These results highlight the substrate and site specificities of HATs in cells, and suggest that GCN5/PCAF- and CBP/p300-mediated histone acetylations play distinct roles in regulating ligand-induced nuclear receptor target gene expression. PCAF and GCN5 have some redundant function. To identify PCAF/GCN5-regulated genes, immortalized MEFs with PCAF knockout and GCN5 conditional knockout were infected with retroviruses expressing either Cre recombinase or vector alone. We prepared duplicated RNAs from either vector or Cre infected cells (PCAF-/-;GCN5+/- or PCAF-/-;GCN5+/-) and RNAs from either Vector or Cre infected the other independently immortalized cells for 6 affymetrix microarray.
2013-12-31 | E-GEOD-20008 | biostudies-arrayexpress
Project description:Gcn5/PCAF dobule knockout (dKO) in MEFs leads to loss of the global H3K9ac, but only affect expression of a small nubmer of genes according to RNA-Seq data. To examine the function of H3K9ac on gene activation, H3K9ac ChIP-Seq was performed. We found that H3K9ac at Transcriptional Start sites (TSSs) of no-changed, up-regulated and down-regulated genes are all dramatially decreased in Gcn5/PCAF dKO cells, suggesting that H3K9ac is largely not required for gene activation.
2014-09-03 | GSE60967 | GEO
Project description:Gcn5/PCAF double knockout (dKO) leads to loss of the global H3K9ac. RNA-Seq was performed to define the changes of gene expression in response to Gcn5/PCAF deletion and H3K9ac loss PCAF-/-;Gcn5f/D MEFs were infected with retroviral Cre to delete Gcn5 to generate Gcn5/PCAF dKO cells, followed by RNA-Seq analysis using spike-in RNA as controls
2014-09-03 | E-GEOD-60968 | biostudies-arrayexpress
Project description:Histone acetyltransferases (HATs) GCN5/PCAF and CBP/p300 are transcription coactivators. However, how these HATs regulate ligand-induced nuclear receptor target gene expression remains unclear. Here we show in mouse embryonic fibroblasts (MEFs), deletion of GCN5/PCAF specifically eliminates acetylation on H3K9 (H3K9Ac) while deletion of CBP/p300 selectively reduces acetylation on H3K18 and H3K27 (H3K18/27Ac). Treating MEFs with a specific ligand for nuclear receptor PPARdelta induces sequential increases of H3K18/27Ac and H3K9Ac on the promoter of PPARdelta target gene Angptl4, which correlates with a robust ligand-induced Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9Ac but not H3K18/27Ac on Angptl4 promoter. Finally, we show CBP/p300 and their HAT activities are required, while GCN5/PCAF and H3K9Ac are dispensable, for ligand-induced PPARdelta target gene expression in MEFs. These results highlight the substrate and site specificities of HATs in cells, and suggest that GCN5/PCAF- and CBP/p300-mediated histone acetylations play distinct roles in regulating ligand-induced nuclear receptor target gene expression.
2013-12-31 | GSE20008 | GEO
Project description:Gcn5/PCAF double knockout (dKO) leads to loss of the global H3K9ac. RNA-Seq was performed to define the changes of gene expression in response to Gcn5/PCAF deletion and H3K9ac loss
2014-09-03 | GSE60968 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:PArtner and Localizer of BRCA2 (PALB2) is essential to maintain genome stability in human cells. Upon DNA damage by double DNA strand breaks, PALB2 is required to repair DNA by homologous recombination. In undamaged conditions, PALB2 protects coding regions, by preventing DNA stress due to collisions between transcription and replication machineries. PALB2 associates with chromatin, which is essential to fulfill its function in genome stability maintenance, however molecular mechanisms regulating PALB2 chromatin association remain unknown. In our previous published study describing the KAT2A/B(GCN5/PCAF)-acetylome (Fournier et al., Nat.Comm. 2016, doi: 10.1038/ncomms13227) we have identified PALB2 as an acetylated protein target of the acetyltransferases KAT2A (GCN5) and KAT2B (PCAF) in vivo. KAT2A/B-acetylated sites of PALB2 were mapped within its DNA/Chromatin association domain. In this current study, we have conducted in vitro acetyltransferase (AT) assays, by mixing purified recombinant GST-tagged PALB2 full-length (FL) and PALB2 fragment P2.2 which associates with DNA/chromatin (from residues 295-610), with Flag-PCAF, Flag-GCN5 and Flag-GCN5 catalytic mutant (mut), followed by proteomics analysis to map PALB2 acetylated lysines by KAT2A(GCN5) and KAT2B(PCAF) in vitro. PALB2 FL and P2.2 alone, or PALB2 FL and P2.2 mixed with GCN5 catalytic mutant, were used as negative controls.
2023-03-10 | PXD014681 | Pride
Project description:Differentially regulated genes in HtrA2 knockout MEFs upon rotenone treatment
| PRJNA114089 | ENA
Project description: Not available
| S-EPMC395764 | biostudies-literature