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

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

PROVIDER: PRJNA1014578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25918587.fastq.gz	Fastqsanger.gz
	SRR25918588.fastq.gz	Fastqsanger.gz
	SRR25918589.fastq.gz	Fastqsanger.gz
	SRR25918590.fastq.gz	Fastqsanger.gz
	SRR25918591.fastq.gz	Fastqsanger.gz

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PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity

Project description:PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity

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

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

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

2024-06-17 | GSE242383 | GEO

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

2024-09-12 | GSE242384 | GEO

PHF2 maintains neural progenitor genome stability by preserving pericentric heterochromatin integrity

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-17 | GSE242385 | 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

Silencing of pericentric heterochromatin associated with SIRT6-dependent H3K18 deacetylation protects against mitotic errors and cellular senescence

Project description:Pericentric heterochromatin silencing at mammalian centromeres is essential for mitotic fidelity and genomic stability. Defective pericentric silencing is observed in senescent cells, aging tissues, and mammalian tumors, but the underlying mechanisms and functional consequences of these defects are unclear. Here, we uncover a pivotal role of the human SIRT6 enzyme in pericentric transcriptional silencing, and this function protects against mitotic defects, genomic instability, and cellular senescence. At pericentric heterochromatin, SIRT6 promotes deacetylation of a new substrate, histone H3 lysine K18 (H3K18), and inactivation of SIRT6 in cells leads to H3K18 hyperacetylation and aberrant accumulation of pericentric transcripts. Strikingly, RNAi-depletion of these transcripts rescues the mitotic and senescence phenotypes of SIRT6-deficient cells. Together, our findings reveal a new function for SIRT6 and H3K18Ac regulation at heterochromatin, and demonstrate the pathogenic role of de-regulated pericentric transcription in aging- and cancer- related cellular dysfunction. H3K18ac, H3K9ac, H3K9me3, H3K56ac and Input ChIP-seq for U2OS cell

2016-04-04 | E-GEOD-69809 | biostudies-arrayexpress

Transcriptome analysis in PHf2 KO C2C12 cells

Project description:To evaluate the role of Phf2 in C2C12 myotube, we generated Phf2 KO C2C12 cells and analyzed the transcriptome by RNA-sequencing.

2024-02-29 | GSE226618 | GEO

Silencing of pericentric heterochromatin associated with SIRT6-dependent H3K18 deacetylation protects against mitotic errors and cellular senescence

2016-04-04 | GSE69809 | GEO

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

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