Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA380129 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5366720_1.fastq.gz | Fastqsanger.gz | |||
| SRR5366720_2.fastq.gz | Fastqsanger.gz | |||
| SRR5366721_1.fastq.gz | Fastqsanger.gz | |||
| SRR5366721_2.fastq.gz | Fastqsanger.gz | |||
| SRR5366722_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:H3K27me3 deposition over sarcomeric and cytoskeletal promoters is required for cardiomyocyte cytokinesis and wound invasion during zebrafish heart regeneration [ChIP-seq]
| PRJNA380130 | ENA
Project description:We identify the global transcriptional changes that occur between homeostatic and proliferative cardiomyocytes in the zebrafish heart and uncover an essential role for H3K27me3 deposition in facilitating successful myocardial regeneration. Specifically, we learned that cardiomyocyte proliferation is accompanied by downregulation of sarcomeric and cytoskeletal components and upregulation of the polycomb methylase Ezh2. Using ChIPseq, we demonstrate that this transcriptional repression is associated with deposition of new H3K27me3 modifications over the promoters. Using new genetic zebrafish lines that allow for inducible and cardiomyocyte-specific expression of a mutant form of histone 3 that is unable to be tri-methylated on lysine 27 (H3.3K27M), we discovered that addition of H3K27me3 marks is essential for cardiac regeneration in vivo. Earlier in the regenerative window, we found that H3.3K27M–expressing wound edge cardiomyocytes aberrantly maintain homeostatic levels of sarcomeric and actomyosin gene expression and show significant retention of sarcomere structure. While DNA replication occurs normally in these H3.3K27M cardiomyocytes, we observed significant increases in cardiomyocyte nucleation, a phenotype indicative of cytokinesis failures. In addition, nuclear density at the wound edge increases as new cardiomyocytes fail to colonize the injured area. Together, our study reveals that production of new cardiomyocytes and their infiltration into the injured region relies on H3K27me3-mediated sarcomeric and actomyosin cytoskeletal gene repression.
2019-09-17 | GSE96929 | GEO
Project description:Deciphering the genetic and epigenetic regulation of cardiomyocyte proliferation in organisms capable of robust cardiac renewal represents an attractive inroad towards regenerating the human heart. In the highly regenerative zebrafish heart, cardiomyocytes near the wound edge undergo dramatic changes in gene expression concomitant with sarcomere disassembly, loss of cell-cell adhesion, and detachment from the extracellular matrix (ECM), which leaves them poised to divide and give rise to new muscle cells that colonize the wound. Using integrated highthroughput transcriptional and chromatin analyses, we identified correlations between gene expression changes and activating H3K4me3 and/or repressive H3K27me3 dynamics8 in cardiomyocytes following injury. Within the category of downregulated genes that gain H3K27me3, transcripts encoding sarcomere and cytoskeletal components were significantly overrepresented. To investigate a functional requirement for H3K27me3-mediated gene silencing during zebrafish heart regeneration, we generated an inducible transgenic strain expressing a mutant version of histone 3, H3.3K27M, which allowed us to inhibit H3K27me3 catalysis in cardiomyocytes during the regenerative window. Hearts composed of H3.3K27M-expressing cardiomyocytes fail to regenerate with wound edge myocardium showing heightened expression of structural genes and prominent sarcomere structures. Although cell cycle re-entry was unperturbed, cytokinesis and wound invasion were significantly compromised. Collectively, our study identifies a requirement for H3K27me3-mediated silencing of structural genes during zebrafish heart regeneration and suggests that repression of similar structural components in the border zone of the infarcted human heart might improve its regenerative capacity.
2019-09-17 | GSE96930 | GEO
Project description:Deciphering the genetic and epigenetic regulation of injury-induced heart regeneration in organisms capable of robust cardiac renewal represents an attractive inroad towards regenerating the human heart. In the highly regenerative zebrafish heart, cardiomyocytes near the wound edge undergo dramatic gene expression changes concomitant with sarcomere disassembly, loss of cell-cell adhesion, and detachment from the extracellular matrix (ECM), which leaves them poised to divide and give rise to new muscle cells that colonize the wound. Using integrated high-throughput transcriptional and chromatin analyses, we identified correlations between gene expression changes and activating H3K4me3 and/or repressive H3K27me3 dynamics in cardiomyocytes following injury. Within the category of downregulated genes that gain H3K27me3, transcripts encoding sarcomere and cytoskeletal components were significantly overrepresented. To investigate a functional requirement for H3K27me3-mediated gene silencing during zebrafish heart regeneration, we generated an inducible transgenic strain expressing a mutant version of histone 3, H3.3K27M, which allowed us to inhibit H3K27me3 catalysis in cardiomyocytes during the regenerative window. Hearts composed of H3.3K27M-expressing cardiomyocytes fail to regenerate with wound edge myocardium showing heightened expression of structural genes and prominent sarcomere structures. Although cell cycle re-entry was unperturbed, cytokinesis and wound invasion were significantly compromised. Collectively, our study identifies a requirement for H3K27me3-mediated silencing of structural genes during zebrafish heart regeneration and suggests that repression of similar structural components in the border zone of the infarcted human heart might improve its regenerative capacity.
2019-09-17 | GSE96928 | GEO
Project description:Histone modifications are associated with distinct transcriptional states, but it is unclear whether they instruct gene expression. To investigate this, we mutated histone H3.3 K9 and K27 residues in mouse embryonic stem cells (mESCs). Here, we find that H3.3K9 is essential for controlling specific distal intergenic regions and for proper H3K27me3 deposition at promoters. The H3.3K9A mutation resulted in decreased H3K9me3 at regions encompassing endogenous retroviruses and induced a gain of H3K27ac and nascent transcription. These changes in the chromatin environment unleashed cryptic enhancers, resulting in the activation of distinctive transcriptional programs and culminating in protein expression normally restricted to specialized immune cell types. The H3.3K27A mutant disrupted deposition and spreading of the repressive H3K27me3 mark, particularly impacting bivalent genes with higher basal level of H3.3 at promoters. Therefore, H3.3K9 and K27 crucially orchestrate repressive chromatin states at cis-regulatory elements and bivalent promoters, respectively, and instruct proper transcription in mESCs.
2024-06-24 | MSV000095134 | MassIVE
Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
2023-09-10 | GSE190825 | GEO
Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
2023-09-10 | GSE160413 | GEO
Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
2023-09-10 | GSE160412 | GEO
Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
2023-09-10 | GSE160411 | GEO
Project description:Chromatin architecture relies on histone H1 whose central globular domain (GH1) sits on the nucleosome dyad and carboxy-terminal domain associates with linker DNA. We report that Arabidopsis H1 positively influences H3K27me3 chromatin enrichment over protein-coding genes but oppositely prevents its accumulation on telomeres and heterochromatic Interstitial Telomeric Repeats (ITRs). Contrasting with their neighboring heterochromatic environment, pericentromeric ITR regions remain highly compacted and are more prone to long-distance interactions with telomeres in H1 mutant plants. The switch from H1-rich to H3K27me3-rich ITR chromatin is further accompanied by an invasion of GH1-Myb Telomeric Repeat Binding protein 1 (TRB1), a structural component of telomeres capable to trigger H3K27me3 deposition over protein-coding genes displaying short telomeric motifs. This dual effect led us to propose a competition mechanism between H1 and TRB that prevents massive H3K27me3 deposition over large blocks of repeated motifs, thereby contributing to regulate H3K27me3 homeostasis over the genome.
2023-09-10 | GSE160410 | GEO