Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stem cell plasticity, acetylation of H3K14 and de novo gene activation rely on KAT7

ABSTRACT: In the conventional model of transcriptional activation, transcription factors bind to response elements and recruit co-factors, including histone acetyltransferases. Contrary to this model, we show that the histone acetyltransferase KAT7 (HBO1/MYST2) is required genome-wide for histone H3 lysine 14 acetylation (H3K14ac). Examining neural stem cells, we found that KAT7 and H3K14ac were present not only at transcribed genes, but also at inactive genes, intergenic regions and in heterochromatin. KAT7 and H3K14ac were not required for the continued transcription of genes that were actively transcribed at the time of loss of KAT7, but indispensable for the activation of repressed genes. The absence of KAT7 abrogated neural stem cell plasticity, diverse differentiation pathways and cerebral cortex development. Reexpression of KAT7 restored stem cell developmental potential. Overexpression of KAT7 enhanced neuron and oligodendrocyte differentiation. Our data suggest that KAT7 prepares chromatin for transcriptional activation and is a prerequisite for gene activation.

ORGANISM(S): Mus musculus

PROVIDER: GSE220602 | GEO | 2022/12/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effects of loss of the histone lysine acetyltransferase KAT7 on mRNA levels in proliferating and differentiating mouse neural stem cells (neurosphere cells) [RNA-seq]

Project description:RNA-seq data of neural stem and progenitor cell (NSPC) isolates from Kat7lox/loxNesCreT/+ and Kat7+/+NesCreT/+ E14.5 foetuses for each, proliferating and differentiating conditions. KAT7 and H3K14ac were not required for the continued transcription of genes that were actively transcribed at the time of loss of KAT7, but indispensable for the activation of repressed genes.

2022-11-30 | GSE215970 | GEO

Chromatin immunoprecipitation and high-throughput sequencing (ChIP-seq) detection of histone H3 lysine 14 acetylation (H3K14ac) and KAT7 (HBO1) in E14.5 mouse neural stem and progenitor cells (NSPCs)

Project description:Tissue specific deletion of the gene encoding the histone acetyltransferase KAT7 (HBO1) in the developing mouse central nervous system using cre-recombinase expression driven by regulatory sequences of the nestin locus (NesCre transgene) resulted in defective cerebral cortex development, a complete failure of neural stem cells to give rise to neurons and oligodendrocytes during in vitro differentiation and a failure to express the neuronal differentiation program. KAT7 genome occupancy and histone H3 lysine 14 acetylation (H3K14ac) levels were assessed by ChIP-seq in proliferating Kat7 deleted vs. Kat7 intact neural stem and progenitor cells (NSPCs). KAT7 and H3K14ac were completely absent in the Kat7 deleted cells. IN KAT7 intact cells, KAT7 occupancy levels and H3K14ac levels within the body of genes correlated strongly and positively. Both were higher in genes that were expressed strongly than in genes with lower or no expression. However, KAT7 and H3K14ac were present in all genes including silent genes and in all other regions of the genome, including intergenic regions and regions decorated with histone H3 lysine 9 trimethylation (H3K9me3), an indicator of constitutive heterochromatin.

2022-11-30 | GSE216459 | GEO

Specific acetylase-deacetylase balance controls stress adaptation by modulating global histone H3K14 acetylation.

Project description:Histone acetylation and deacetylation is important for gene regulation. The histone acetyltransferase, Gcn5, is a known activator of transcriptional initiation that is recruited to gene promoters. Here we map genome-wide levels of Gcn5 occupancy and histone H3K14ac at high resolution. Gcn5 is predominantly localized to coding regions of highly transcribed genes where it antagonistically collaborates with the class II histone deacetylase, Clr3, to regulate histone H3K14ac levels. Regulation of histone H3k14ac levels is critical for regulation of many genes during stress adaptation. Our findings suggest a novel role for Gcn5 during transcriptional elongation in addition to its known role in transcriptional initiation. The data in this series showed Gcn5 occupancy and H3K14 acetylation levels in wild type, gcn5- and gcn5-/clr3- cells under KCl stress condition. Related expression data are GSE5227 and GSE13817 Keywords: Chip-chip

2009-08-01 | GSE13790 | GEO

Histone H3K9 and H3K14 acetylation mark active enhancers and promoters together with bivalent promoters in mouse embryonic stem cells

Project description:Transcription regulation in pluripotent embryonic stem (ES) cells is a complex process that involves multitude of regulatory layers, one of which is post-translational modification of histones. Here we have investigated the genome-wide occurrence of two histone marks, acetylation of histone H3K9 and K14 (H3K9ac and H3K14ac), in mouse ES cells. We demonstrate genome-wide that H3K9ac and H3K14ac show very high correlation. Examination of H3K9ac and H3K14ac in mES cells

2012-10-01 | E-GEOD-31284 | biostudies-arrayexpress

Stem cell plasticity, acetylation of H3K14 and de novo gene activation rely on KAT7

Project description:Stem cell plasticity, acetylation of H3K14 and de novo gene activation rely on KAT7

| PRJNA910515 | ENA

Histone H3K9 and H3K14 acetylation mark active enhancers and promoters together with bivalent promoters in mouse embryonic stem cells

2012-10-01 | GSE31284 | GEO

The histone lysine acetyltransferase HBO1 regulates hematopoietic stem cell quiescence and self-renewal

Project description:KAT7 (HBO1) is a histone acetyltransferase required for histone H3 lysine 14 acetylation (H3K14ac) and normal levels of gene expression in hematopoietic stem and progenitor cells (HSPCs). The loss of H3K14ac was detected by western blot in whole bone marrow and by flow cytometry in specific HSPC populations. In order to determine the normal distribution of H3K14ac in the HSPC population a CUT&Tag experiment was performed using lineage negative, cKit positive Sca1 positive cells (LSK) and lineage negative, cKit positive Sca1 negative cells (progenitor cells). HBO1 was deleted using the poly(I:C) inducible MX1-cre recombinase transgene and compared to Kat7 heterozygous control cells, in which the MX1-cre was likewise induced. Analysis was performed at a stage when H3K14ac was no longer detectable by western blot. In order to control for the effects of PCR amplification and normalisation of library size before sequencing, equal numbers of Drosophila Schneider 2 cells were added to each sorted mouse cell population (“spike in”). After sequencing-read quality control, reads were mapped to a combined Mus musculus (Mm10) and Drosophila melanogaster (DmelR635) genome. To each mouse sample a normalisation factor based on the recovery of Drosophila reads within the same sample was applied. Genomic distribution of KAT7 (HBO1) was determined in control progenitor cells by CUT&Tag.

2021-10-13 | GSE185820 | GEO

KAT7 promotes malignant phenotypes of colorectal cancer via MRAS-mediated activation of the MAPK/ERK pathway

Project description:Histone acetyltransferases (HATs) play a crucial role in transcriptional regulation by acetylating histones. Dysregulation of HAT activity is implicated in developmental disorders and cancer. In this study, we discovered an upregulated KAT7 signaling pathway in colorectal cancer (CRC) and its association with poor patient survival. Knockdown of KAT7 suppressed CRC cell viability, proliferation, migration, and invasion while promoting apoptosis. Conversely, KAT7 overexpression enhanced these cellular processes. In vivo experiments demonstrated that KAT7 knockdown inhibited CRC growth and lung metastasis. Mechanistically, KAT7 acetylated histone H3 at lysine 14 (H3K14) to enhance MRAS transcription, which activated the MAPK/ERK pathway and promoted tumorigenesis. Overexpression of MRAS or treatment with the ERK activator C6 Ceramide rescued the tumor inhibition caused by KAT7 silencing. The acetyltransferase activity of KAT7 is essential for CRC progression. Reexpression of KAT7, but not KAT7 acetyltransferase activity-deficient mutants, rescued MRAS expression, ERK phosphorylation, and CRC tumorigenesis in KAT7 knockdown CRC cells. Taken together, our results define the essential role of KAT7 in CRC tumorigenesis, rationalizing its potential as a therapeutic target for CRC treatment.

2024-06-27 | GSE270298 | GEO

Effect of knockdown of KAT7 on gene expression in HCT116 cell line.

Project description:Accurate centriole formation is critical for cell replication. However, the holistic transcriptional regulatory mechanisms involved in this process remain elusive.We report here that KAT7 histone acetyltransferase is a key regulatory molecule that regulates centriole replication. Knockdown of KAT7 leads to reduced levels of histone H3K14 acetylation and reduced enrichment of H3K14ac in the promoter region of centriole formation-related genes, resulting in blocked centriole formation. Our data provide a new insight for the role of histone modifying factors in centriole replication-related pathways.

2024-10-13 | GSE236701 | GEO

EIN2 mediates histone H3K14 and non-canonical histone H3K23 acetylation in the nucleus in ethylene response [ChIP-seq]

Project description:We report that ethylene specifically elevated acetylation of histone H3 at K14 and the non-canonical acetylation of histone H3 at K23. We perform Chip-sequencing of H3K14Ac, H3K23Ac and H3K9Ac using chromatins isolated from 3-day old etiolated Col-0 seedlings treated with ethylene or air gas. Results show that ethylene specifically elevates H3K14Ac and non-canonical H3K23Ac in EIN3 targeted genes that are regulated at the transcriptional level by ethylene.

2016-10-05 | GSE77394 | 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