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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE167168 | GEO | 2021/08/01

REPOSITORIES: GEO

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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

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

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

| PRJNA703537 | ENA

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]

| PRJNA703543 | ENA

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

Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-01 | E-GEOD-81661 | biostudies-arrayexpress

Snail1 transcription factor controls telomere transcription and integrity.

Project description:Besides controlling epithelial-to-mesenchymal transition (EMT) and cell invasion, the Snail1 transcriptional factor also provides cells with cancer stem cell features. Since telomere maintenance is essential for stemness, we have examined the control of telomere integrity by Snail1. Fluorescence in situ hybridization (FISH) analysis indicates that Snail1-depleted mouse mesenchymal stem cells (MSC) have both a dramatic increase of telomere alterations and shorter telomeres. Remarkably, Snail1-deficient MSC present higher levels of both telomerase activity and the long non-coding RNA called telomeric repeat-containing RNA (TERRA), an RNA that controls telomere integrity. Accordingly, Snail1 expression downregulates expression of the telomerase gene (TERT) as well as of TERRA 2q, 11q and 18q. TERRA and TERT are transiently downregulated during TGFβ-induced EMT in NMuMG cells, correlating with Snail1 expression. Global transcriptome analysis indicates that ectopic expression of TERRA affects the transcription of some genes induced during EMT, such as fibronectin, whereas that of TERT does not modify those genes. We propose that Snail1 repression of TERRA is required not only for telomere maintenance but also for the expression of a subset of mesenchymal genes.

| S-EPMC5758914 | biostudies-literature

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