Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq experiment of shControl and shPHF2 NSCs

ABSTRACT: Histone H3 lysine 9 methylation (H3K9me) is essential for cellular homeostasis; however, its contribution to development is not well established. Here, we demonstrate that the H3K9me2 demethylase PHF2 is essential for neural progenitor proliferation in vitro and for early neurogenesis in the chicken spinal cord. Using genome-wide analyses and biochemical assays we show that PHF2 controls the expression of critical cell cycle progression genes, particularly those related to DNA replication, by keeping low levels of H3K9me3 at promoters. Accordingly, PHF2 depletion induces R-loop accumulation that leads to extensive DNA damage and cell cycle arrest. These data reveal a role of PHF2 as a guarantor of genome stability that allows proper expansion of neural progenitors during development.

ORGANISM(S): Mus musculus

PROVIDER: GSE122264 | GEO | 2019/09/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIP-seq experiment of PHF2 and H3K9me2 in NSCs

Project description:Histone H3 lysine 9 methylation (H3K9me) is essential for cellular homeostasis; however, its contribution to development is not well established. Here, we demonstrate that the H3K9me2 demethylase PHF2 is essential for neural progenitor proliferation in vitro and for early neurogenesis in the chicken spinal cord. Using genome-wide analyses and biochemical assays we show that PHF2 controls the expression of critical cell cycle progression genes, particularly those related to DNA replication, by keeping low levels of H3K9me3 at promoters. Accordingly, PHF2 depletion induces R-loop accumulation that leads to extensive DNA damage and cell cycle arrest. These data reveal a role of PHF2 as a guarantor of genome stability that allows proper expansion of neural progenitors during development.

2019-09-10 | GSE122263 | GEO

PHF2-mediated H3K9me balance orchestrates heterochromatin stability and progenitor proliferation in early neurogenesisPHF2-mediated H3K9me balance orchestrates heterochromatin stability and progenitor proliferation in early neurogenesis

Project description:Heterochromatin stability is crucial for progenitor proliferation during early neurogenesis. It relays on the maintenance of local hubs of H3K9me. However, the current understanding of the processes involved in the formation of efficient localized levels of H3K9me remains limited. To address this intriguing question, we used a neural stem cell (NSC) to analyze the function of the H3K9me2 demethylase PHF2, which is crucial for progenitor proliferation. Through mass spectroscopy and genome-wide assays, we uncovered that PHF2 interacts with heterochromatin components and it is enriched at pericentromeric heterochromatin (PcH) boundaries. This binding is essential for maintaining silenced the satellite repeats thereby preventing DNA damage and genome instability. Depletion of PHF2 led to increased transcription of heterochromatic repeats, accompanied by a decrease in H3K9me3 levels and alterations in PcH organization. Further analysis revealed that PHF2's PHD and catalytic domains are crucial for maintaining PcH stability and preventing unscheduled repeat transcription, thereby safeguarding genome integrity. These results highlight the multifaceted nature of PHF2's functions in maintaining heterochromatin stability and regulating gene expression during neural development. Altogether, our study unravels the intricate relationship between heterochromatin stability and progenitor proliferation during mammalian neurogenesis, shedding light on its potential as a therapeutic target for neurodevelopmental disorders

2024-06-11 | PXD051336 | Pride

PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity (ATAC-Seq)

Project description:Heterochromatin stability is crucial for progenitor proliferation during development. It relays on the maintenance of local hubs of H3K9me. However, the mechanisms underlying the establishment of competent local levels of H3K9me remain poorly understood. To address this intriguing question, we used a neural stem cell (NSC) model to analyze the significance of the H3K9me2 demethylase PHF2, which is crucial for progenitor proliferation. Through mass spectroscopy and genome-wide assays, we uncovered that PHF2 interacts with heterochromatin components and it is enriched at pericentromeric heterochromatin (PcH) boundaries. This binding is essential for maintaining silenced the satellite repeats and to prevent DNA damage and genome instability. To do that, PHF2 balances H3K9me3 levels at these boundaries to ensure high H3K9me3 levels at satellite repeats. Mechanistically, we discover that while its catalytic and PHD domains are indispensable, the intrinsically disordered region within PHF2 is dispensable for stabilizing PcH. Altogether, our study sheds light on the intricate relationship between heterochromatin stability and progenitor proliferation during mammalian neurogenesis.

2024-09-12 | GSE242384 | GEO

PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity (ChIP-Seq)

2024-06-17 | GSE242383 | GEO

ChIP-seq experiment of PHF2 and H3K9me2 in NSCs

Project description:ChIP-seq experiment of PHF2 and H3K9me2 in NSCs

| PRJNA504430 | ENA

RNA-seq experiment of shControl and shPHF8 Astrocytes

Project description:In this study we analyzed the contribution of PHF8 histone demethylase to astrocytes differentiation from mouse neural stem cells. We found that PHF8 depletion affects astocytes differentiation. Moreover, PHF8 is crucial for synaptogenesis in neurons/astrocytes cocultures. Genome wide analysis demonstrated that PHF8 controls the expression of critical astrogenic and synaptogenic genes by keeping low levels of H4K20me1 at promoters. PHF8 depletion induces aberrant astrocytes phenotype and caused a significant decrease in miniature excitatory postsynaptic currents (mEPSC) frequency and amplitude in neurons/astrocytes coclutures. These data reveal a new role of PHF8 in astrocyte differentiation and function, modulating neuronal synapse. Thus, lack of histone demethylase activity associated to PHF8 mutations might led to synapse disfunction that could directly impact into X-linked intellectual disabilities.

2021-06-14 | GSE141970 | GEO

ChIP-seq experiment of PHF8 in Astrocytes differentiated from mouse NSCs

2021-06-14 | GSE141969 | GEO

H3K9 methylation regulates heterochromatin silencing through incoherent feedforward loops

Project description:Histone H3 lysine-9 methylation (H3K9me) is a hallmark of the condensed and transcriptionally silent heterochromatin. It remains unclear how H3K9me controls transcription silencing and how cells delimit H3K9me domains to avoid silencing essential genes. Here, using Arabidopsis genetic systems that induce H3K9me2 in genes and transposons de novo, we show that H3K9me2 accumulation paradoxically also causes the deposition of the euchromatic mark H3K36me3 by a SET domain methyltransferase, ASHH3. ASHH3-induced H3K36me3 confers anti-silencing by preventing the demethylation of H3K4me1 by LDL2, which mediates transcriptional silencing downstream of H3K9me2. These results demonstrate that H3K9me2 not only facilitates but orchestrates silencing by actuating antagonistic silencing and anti-silencing pathways, providing insights into the molecular basis underlying proper partitioning of chromatin domains and the creation of metastable epigenetic variation.

2024-06-27 | GSE246527 | GEO

RNA-seq experiment of shControl and shPHF2 NSCs

Project description:RNA-seq experiment of shControl and shPHF2 NSCs

| PRJNA504429 | ENA

Epigenetic inheritance uncoupled from sequence-specific recruitment

Project description:We used ChIP-seq to examine the requirements for inheritance of H3K9me at endogenous and ectopic loci. H3K9me2 and H3K9me3 ChIP-seq in multiple S. pombe strains

2014-11-26 | E-GEOD-63304 | 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