Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H4K16ac modification profile difference between Peg3-WT and KO MEF cells

ABSTRACT: PEG3 (Paternally Expressed Gene 3) is an imprinted gene encoding a DNA-binding protein. Two components of the mammalian MSL (Male-Specific Lethal) complex, Msl1 and Msl3, are known to be the genomic targets of PEG3. In this report, we performed genome-wide ChIP-seq experiments profiling H4K16ac levels using a set of MEF cells (Mouse Embryonic Fibroblast), the WT and KO of Peg3. The results indicated that about 10% of the mouse gene catalog showed high levels of H4K16ac levels in Peg3-KO MEFs than in Peg3-WT MEFs. This further suggests that mammalian Peg3 may control its downstream genes through the MSL complex.

ORGANISM(S): Mus musculus

PROVIDER: GSE97459 | GEO | 2017/08/15

SECONDARY ACCESSION(S): PRJNA381884

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIP-Seq profiles of MSL1, MSL2, MSl3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 in Drosophila S2 cells

Project description:ChIP-Seq profiles of MSL1, MSL2, MSl3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 in Drosophila S2 cells MSL1, MSL2, MSL3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 ChIP in Drosophila S2 cells. 1-3 biological replicates per experiment. Performed in single-read and paired-end read mode.

2012-12-11 | E-GEOD-37864 | biostudies-arrayexpress

ChIP-Seq profiles of MSL1, MSL2, MSl3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 in Drosophila S2 cells

Project description:ChIP-Seq profiles of MSL1, MSL2, MSl3, MOF, MLE, H4K16ac and RNA Polymerase II phosphorlyated on Serine 5 in Drosophila S2 cells

2012-12-11 | GSE37864 | GEO

Chromatin immunoprecipitation to determine MSL1, MSL3, MOF and H4K16Ac binding in Drosophila SL2 and Kc cells reveals MOF as a key regulator of dosage compensation and gene expression in Drosophila

Project description:Genome-wide binding profiles of MSL1, MSL3, MOF and H4K16Ac in Drosophila SL2 and Kc cells.

2008-06-12 | E-MEXP-1508 | biostudies-arrayexpress

Global examination of H3K9me3 levels and PEG3 binding sites between WT and KO

Project description:PEG3 (Paternally Expressed Gene 3) is an imprinted gene encoding a DNA-binding protein. In this study, we used MEF cells (Mouse Embryonic Fibroblast). We performed genome-wide ChIP-seq experiments profiling H3K9me3 levels as well as examine the set of genomic targets and also redefines the DNA-binding motif for the imprinted transcription factor, PEG3 in the WT and KO of Peg3. The results suggested high levels of H3K9 levels in Peg3-KO MEFs than in Peg3-WT MEFs, whereas several different genes involved several biochemical pathways seems to be have potential binding site for PEG3 protein, which tend to have a distinct profile of binding motif to its binding region. This further suggests that mammalian Peg3 may control its downstream genes in regulating several biological functions and regulate the H3K9 methylation levels.

2021-07-31 | GSE181069 | GEO

De novo mutations of MSL3 cause a novel X-linked syndrome due to impaired histone H4 lysine 16 acetylation

Project description:Epigenetic regulation by histone acetylation plays a key role in cellular homeostasis and its misregulation is associated with human disease. The Male Specific Lethal (MSL) complex associated MOF/KAT8 histone acetyl-transferase is responsible for bulk Histone 4 Lysine 16 acetylation (H4K16ac) in flies and mammals. H4K16ac is a peculiar case amongst the many histone tail modifications in directly affecting higher order chromatin compaction. Yet, its importance during human development and a potential involvement in human pathologies remains largely unknown. Here, we uncover that pathogenic variants in MSL3, a component of the MSL complex, are causative for a new recognizable X-linked syndrome affecting both male and female individuals. Common clinical features of the syndrome include a global delay in developmental milestones and speech, a progressive gait disturbance and recognizable dysmorphism. Using skin biopsies and patient-derived primary fibroblasts, we demonstrate that de novo variants or deletions of MSL3 affect the assembly and enzymatic activity of the MSL complex, hence globally impacting H4K16ac levels in vivo. Transcriptome analysis from patient cells showed misregulation of cellular pathways involved in morphogenesis, cellular shape and cell migration. Using RNAi and MSL3 reintroduction experiments, we phenocopy acute responses occurring on H4K16ac-sensitive MSL target genes, supporting that this syndrome is caused by the loss of MSL3. Finally, we use HDAC inhibitors to rebalance acetylation levels and are able to alleviate both molecular and cellular phenotypes of MSL3 patients cells. Taken together, we characterize a novel syndrome, which is caused by mutations of an epigenetic regulator, allowing us for the first time to unravel the crucial role of H4K16ac during human development.

2018-08-06 | GSE102250 | GEO

De novo mutations of MSL3 cause a novel X-linked syndrome due to impaired histone H4 lysine 16 acetylation

Project description:Epigenetic regulation by histone acetylation plays a key role in cellular homeostasis and its misregulation is associated with human disease. Histone 4 Lysine 16 acetylation (H4K16ac) serves a unique role amongst the many histone modifications as it directly affects chromatin structure1. The Male Specific Lethal (MSL) complex associated MOF/KAT8 histone acetyl transferase is responsible for bulk H4K16ac in flies and mammals. Yet, its importance during human development and a potential involvement in human pathologies remains largely unknown. Here, we uncover that pathogenic variants in MSL3, a component of the MSL complex, are causative for a new recognizable X-linked syndrome affecting Histone 4 Lysine 16 acetylation (H4K16ac) in both male and female individuals. Common clinical features of the syndrome include global developmental delay comprising profound speech delay, delayed ability to walk and craniofacial dysmorphism. Using patient-derived primary fibroblasts, we demonstrate that de novo variants or deletions of MSL3 affect the assembly and enzymatic activity of the MSL complex, hence impacting on global H4K16ac levels. Transcriptome analysis from patient cells showed misregulation of cellular pathways involved in serotonergic signaling, morphogenesis, axon guidance and cell structure. Finally, using HDAC inhibitor treatment, we can rescue expression of downregulated target genes, offering potential therapeutic avenues for MSL3-mutated patients. Taken together, we characterize a novel syndrome, named ILyADe (Impaired Lysine 16 acetylation associated disorder), which is caused by mutations of an epigenetic regulator, allowing us for the first time to unravel the crucial role of H4K16ac during human development. ILyaDe thus constitutes a new class of syndromes associated with misregulation of a single epigenetic modification caused by a genetic alteration.

2018-09-18 | PXD009317 | Pride

H4K16ac activates retrotransposons and contributes to their cis regulatory function [ATAC-seq]

Project description:Mammalian genomes harbour a large number of transposable elements (TEs) and their remnants. Most TEs are incapable of retrotransposition, however, they have evolved as cis-regulatory elements (CREs), enabling them to recruit host-encoded factors. Understanding the contribution of TEs in the regulation of the mammalian genome is an active area of research. Here we show that the male-specific lethal (MSL) complex-mediated acetylation of histone H4 lysine 16 (H4K16ac) regulates the transcription of TEs. Furthermore, H4K16ac marked TEs function as a rich source of cis regulatory elements in the human genome, wherein H4K16ac acts by maintaining the permissive chromatin structure and promoting the transcription of these TEs.

2023-04-13 | GSE200767 | GEO

H4K16ac activates retrotransposons and contributes to their cis regulatory function [RNA-seq]

2023-04-13 | GSE200769 | GEO

H4K16ac activates retrotransposons and contributes to their cis regulatory function [CUT&TAG]

2023-04-13 | GSE200768 | GEO

MOF-associated complexes have overlapping and unique roles in regulating pluripotency in embryonic stem cells and during differentiation [array]

Project description:The histone acetyltransferase (HAT) Mof is essential for mouse embryonic stem cells (mESC) pluripotency and early development. Mof is the enzymatic subunit of two different HAT complexes, MSL (Male-Specific Lethal) and NSL (Non-specific lethal). The individual contribution of MSL and NSL complexes to transcription regulation in mESCs is not well understood. Our genome-wide analysis of MSL and NSL localization show that i) MSL and NSL bind to specific and common sets of expressed genes, ii) NSL binds at promoters, iii) while MSL binds in gene bodies. Knockdown of Msl1 leads to a global loss of histone H4K16ac indicating that MSL is the main HAT acetylating H4K16 in mESCs. MSL was enriched at many mESC-specific genes, but also at bivalent domains. Thus, NSL and MSL HAT complexes differentially regulate specific sets of expressed genes in mESCs. Furthermore, MSL is essential for the regulation of key mESC-specific and bivalent developmental genes. Gene expression was analysed through microarrays in mESCs infected with shRNA vectors expressing either a non-target control, shRNA against Nsl1 or Msl1 to knockdown Nsl1 or Msl1.

2014-06-04 | E-GEOD-56646 | 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