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Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist

ABSTRACT: Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist

PROVIDER: PRJNA546609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9203430.fastq.gz	Fastqsanger.gz
	SRR9203431.fastq.gz	Fastqsanger.gz
	SRR9203432.fastq.gz	Fastqsanger.gz
	SRR9203433.fastq.gz	Fastqsanger.gz
	SRR9203434_1.fastq.gz	Fastqsanger.gz

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Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist (ChIPseq, ATACseq)

Project description:Skeletal muscle possesses remarkable regenerative ability owing to the resident muscle stem cells (MuSCs). A prominent feature of quiescent MuSCs is a high content of heterochromatin. However, little is known about the mechanisms by which heterochromatin is maintained in MuSCs. We found that the mammalian Hairless (Hr) gene is expressed in quiescent MuSCs. Using a mouse model in which Hr can be specifically ablated in MuSCs, we demonstrate that Hr expression is critical for MuSC function and muscle regeneration. We show that Hr is a histone demethylase antagonist that preserves Histone 3 Lysine 9 trimethylation (H3K9me3) and maintains heterochromatin structure. Loss of Hr results in reduced H3K9me3 levels, reduced heterochromatin, increased susceptibility of MuSCs to genotoxic stress, and the accumulation of DNA damage. Our study not only elucidates the molecular mechanism by which Hr regulates histone demethylases, but also demonstrates the importance of heterochromatin maintenance in stem cell function.

2021-09-09 | GSE132220 | GEO

Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist [RNA-seq]

2021-09-09 | GSE132189 | GEO

Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist [RNA-seq]

Project description:Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist [RNA-seq]

| PRJNA546281 | ENA

Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist (ChIPseq, ATACseq)

Project description:Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist (ChIPseq, ATACseq)

| PRJNA546535 | ENA

Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist.

Project description:Skeletal muscle possesses remarkable regenerative ability because of the resident muscle stem cells (MuSCs). A prominent feature of quiescent MuSCs is a high content of heterochromatin. However, little is known about the mechanisms by which heterochromatin is maintained in MuSCs. By comparing gene-expression profiles from quiescent and activated MuSCs, we found that the mammalian Hairless (Hr) gene is expressed in quiescent MuSCs and rapidly down-regulated upon MuSC activation. Using a mouse model in which Hr can be specifically ablated in MuSCs, we demonstrate that Hr expression is critical for MuSC function and muscle regeneration. In MuSCs, loss of Hr results in reduced trimethylated Histone 3 Lysine 9 (H3K9me3) levels, reduced heterochromatin, increased susceptibility to genotoxic stress, and the accumulation of DNA damage. Deletion of Hr leads to an acceleration of the age-related decline in MuSC numbers. We have also demonstrated that despite the fact that Hr is homologous to a family of histone demethylases and binds to di- and trimethylated H3K9, the expression of Hr does not lead to H3K9 demethylation. In contrast, we show that the expression of Hr leads to the inhibition of the H3K9 demethylase Jmjd1a and an increase in H3K9 methylation. Taking these data together, our study has established that Hr is a H3K9 demethylase antagonist specifically expressed in quiescent MuSCs.

| S-EPMC8449361 | biostudies-literature

Hairless regulates heterochromatin maintenance and muscle stem cell function as a histone demethylase antagonist

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

2021-09-09 | GSE132256 | GEO

Dynamic evolution of the heterochromatin sensing histone demethylase IBM1

Project description:Heterochromatin constitutes a fundamental aspect of genomes that is crucial for maintaining genome stability. In flowering plants, maintenance of heterochromatin relies on a positive feedback loop involving the histone 3 lysine nine methyltransferase (H3K9), KRYPTONITE (KYP), and the DNA methyltransferase, CHROMOMETHYLASE3 (CMT3). An H3K9 demethylase, INCREASED IN BONSAI METHYLATION 1 (IBM1), has evolved to modulate the activity of KYP-CMT3 within transcribed genes. The absence of IBM1 activity results in aberrant methylation of gene bodies, which is deleterious. This study demonstrates extensive genetic and gene expression variations in KYP, CMT3, and IBM1 within and between flowering plant species. IBM1 activity in Arabidopsis thaliana is uniquely regulated by the abundance of H3K9me2 in a repetitive sequence within an intron preceding the histone demethylase domain. This mechanism enables IBM1 to monitor global levels of H3K9me2. We discovered that the methylated intron is prevalent across flowering plants, however, its underlying sequence exhibits dynamic evolution. Its absence in species lacking gene body DNA methylation suggests its primary role in sensing H3K9me2 and preventing its integration into these constitutively expressed genes. Furthermore, our investigation uncovered Arabidopsis thaliana accessions resembling weak ibm1 mutants, several Brassicaceae species with reduced IBM1 expression, and a potential IBM1 deletion. Evolution towards reduced IBM1 activity in some flowering plants could explain the frequent natural occurrence of diminished or lost CMT3 activity, as cmt3 mutants in A. thaliana mitigate the deleterious effects of IBM1.

2024-05-10 | GSE252913 | GEO

Dynamic evolution of the heterochromatin sensing histone demethylase IBM1

Project description:Dynamic evolution of the heterochromatin sensing histone demethylase IBM1

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LSD1 Prevents Aberrant Heterochromatin Formation in Neurospora crassa

Project description:Heterochromatin is a specialized form of chromatin that restricts access to DNA and inhibits genetic processes, including transcription and recombination. In Neurospora crassa, constitutive heterochromatin is characterized by trimethylation of lysine 9 on histone H3, hypoacetylation of histones, and DNA methylation. Here we explore whether the conserved histone demethylase, lysine-specific demethylase 1 (LSD1), regulates heterochromatin in Neurospora, and if so, how. Though LSD1 is implicated in heterochromatin regulation, its function is inconsistent across different systems; orthologs of LSD1 have been shown to either promote or antagonize heterochromatin expansion by removing H3K4me or H3K9me respectively. We identify three members of the Neurospora LSD complex (LSDC): LSD1, PHF1, and BDP-1, and strains deficient for any exhibit variable spreading of heterochromatin and establishment of new heterochromatin domains dispersed across the genome. Heterochromatin establishment outside of canonical domains in Neurospora share the unusual characteristic of DNA methylation-dependent H3K9me3; typically, H3K9me3 establishment is independent of DNA methylation. Consistent with this, the hyper-H3K9me3 phenotype of LSD1 knock-out strains is dependent on the presence of DNA methylation, as well as HCHC-mediated histone deacetylation, suggesting spreading is dependent on some feedback mechanism. Altogether, our results suggest LSD1 works in opposition to HCHC to maintain proper heterochromatin boundaries.

2021-07-21 | PXD017300 | Pride

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

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