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H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity

ABSTRACT: H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity

PROVIDER: PRJNA703537 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13758000_1.fastq.gz	Fastqsanger.gz
	SRR13758000_2.fastq.gz	Fastqsanger.gz
	SRR13758001_1.fastq.gz	Fastqsanger.gz
	SRR13758001_2.fastq.gz	Fastqsanger.gz
	SRR13758002_1.fastq.gz	Fastqsanger.gz

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H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [ATAC-seq]

Project description:H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [ATAC-seq]

| PRJNA703542 | ENA

H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [RNA-seq]

Project description:H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [RNA-seq]

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H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [RNA-seq]

Project description:Development in multicellular organisms is governed by a carefully orchestrated program of gene expression controlled by both genetic and epigenetic factors1,2. Histone H3 lysine 9 methylation (H3K9me) is the defining modification of heterochromatin, which is thought to have two main functions. It silences satellite repeats and transposable elements to ensure genome stability3, and stabilizes differentiated states by repressing tissue-specific genes4,5. Not surprisingly, the loss of appropriately targeted heterochromatin is associated with cancer, loss of tissue integrity, and aging5-8. How H3K9me restricts transcription is unknown. Here we show that in C. elegans H3K9me2 is required to silence different sets of genes in embryos and differentiated post-mitotic cells. During nematode development H3K9me is lost from genes that define cell-type identity and is gained at genes expressed at prior stages or in alternative tissues. We found that a continuous deposition of H3K9me2 is necessary to maintain silencing in terminally differentiated cells. Its loss leads to DNA decompaction, but this is not sufficient to derepress H3K9me-marked genes. Instead, gene derepression in differentiated tissues requires distinct sets of transcription factors (TF) that aberrantly activate enhancers or promoters. Tissue-specific H3K9me distribution thus contributes critically to cell-type specific TF binding providing a rationale for how a limited set of TFs can control complex organismal development9,10.

2021-08-01 | GSE167167 | GEO

H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [ATAC-seq]

2021-08-01 | GSE167165 | GEO

H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [CUT&RUN; ChICseq]

2021-08-01 | GSE167166 | GEO

H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [CUT&RUN ChICseq]

Project description:H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity [CUT&RUN ChICseq]

| PRJNA703541 | ENA

H3K9me blocks transcription factor activity in differentiated cells to ensure tissue integrity

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

2021-08-01 | GSE167168 | GEO

H3K9me selectively blocks transcription factor activity and ensures differentiated tissue integrity.

Project description:The developmental role of histone H3K9 methylation (H3K9me), which typifies heterochromatin, remains unclear. In Caenorhabditis elegans, loss of H3K9me leads to a highly divergent upregulation of genes with tissue and developmental-stage specificity. During development H3K9me is lost from differentiated cell type-specific genes and gained at genes expressed in earlier developmental stages or other tissues. The continuous deposition of H3K9me2 by the SETDB1 homolog MET-2 after terminal differentiation is necessary to maintain repression. In differentiated tissues, H3K9me ensures silencing by restricting the activity of a defined set of transcription factors at promoters and enhancers. Increased chromatin accessibility following the loss of H3K9me is neither sufficient nor necessary to drive transcription. Increased ATAC-seq signal and gene expression correlate at a subset of loci positioned away from the nuclear envelope, while derepressed genes at the nuclear periphery remain poorly accessible despite being transcribed. In conclusion, H3K9me deposition can confer tissue-specific gene expression and maintain the integrity of terminally differentiated muscle by restricting transcription factor activity.

| S-EPMC8572725 | biostudies-literature

m6A-modified cenRNA stabilizes CENPA to ensure centromere integrity in cancer cells

Project description:m6A-modified cenRNA stabilizes CENPA to ensure centromere integrity in cancer cells

| PRJNA962900 | ENA

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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