Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment. [GRO-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE240508 | GEO | 2024/08/01
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate the function of H3K9me3 in constitutive heterochromatin formation in early embryo we have created embryos that are devoid of H3K9me3
2024-08-01 | GSE240507 | GEO
Project description:Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment. [GRO-seq]
| PRJNA1003942 | ENA
Project description:Germline inheritance of H3K9me3 and its function in constitutive heterochromatin establishment.[CUT&Tag]
| PRJNA1003940 | ENA
Project description:Heterochromatin is a key architectural feature of eukaryotic genomes crucial for silencing of repetitive elements. During Drosophila embryonic cellularization, heterochromatin rapidly appears over repetitive sequences, but the molecular details of how heterochromatin is established are poorly understood. Here, we map the genome-wide distribution of H3K9me3-dependent heterochromatin in individual embryos of Drosophila miranda at precisely staged developmental time points. We find that canonical H3K9me3 enrichment is established prior to cellularization and matures into stable and broad heterochromatin domains through development. Intriguingly, initial nucleation sites of H3K9me3 enrichment appear as early as embryonic stage 3 over transposable elements (TEs) and progressively broaden, consistent with spreading to neighboring nucleosomes. The earliest nucleation sites are limited to specific regions of a small number of recently active retrotransposon families and often appear over promoter and 5' regions of LTR retrotransposons, while late nucleation sites develop broadly across the entirety of most TEs. Interestingly, early nucleating TEs are strongly associated with abundant maternal piRNAs and show early zygotic transcription. These results support a model of piRNA-associated co-transcriptional silencing while also suggesting additional mechanisms for site-restricted H3K9me3 nucleation at TEs in pre-cellular Drosophila embryos.
| S-EPMC8285105 | biostudies-literature
Project description:H3K9me3-heterochromatin, compacted by HP1 proteins, restricts transcription factor binding and functions as a barrier to cell fate changes in development and reprogramming1,2. To investigate principles underlying H3K9me3-heterochromatin maintenance in mammalian cells, we applied degron engineering3,4 on mouse ESCs to conditionally deplete all three H3K9me3-methyltransferases within one hour and found an unexpectedly dynamic nature of heterochromatin maintenance. Following H3K9me3 methyltransferases degradation, HP1β dissociates from heterochromatin within three hours, and transcription factors quickly access the de-compacted heterochromatin, activating transcription of their targets, which then promotes H3K9me3 decay. Both passive dilution and active removal contribute to the H3K9me3 decay. Mathematical modeling reveals distinct H3K9me3 heterochromatin states with diverse chromatin features which influence initial H3K9me3 levels and the stability of H3K9me3 domains, thereby expanding our understanding of distinct heterochromatin domains. Rampant transposable element de-repression interferes with transcription of poised early developmental and signaling genes outside H3K9me3-domains, highlighting the intricate roles of dynamic H3K9me3-heterochromatin maintenance in safeguarding developmental programs. Our findings deconvolve the hierarchical relationships between H3K9me3 marks, methyltransferases, HP1 and transcription factors to reveal principles of H3K9me3-heterochromatin maintenance and how its remodeling enables transcription and cell fate change.
2024-09-19 | GSE233040 | GEO
Project description:H3K9me3-heterochromatin, compacted by HP1 proteins, restricts transcription factor binding and functions as a barrier to cell fate changes in development and reprogramming1,2. To investigate principles underlying H3K9me3-heterochromatin maintenance in mammalian cells, we applied degron engineering3,4 on mouse ESCs to conditionally deplete all three H3K9me3-methyltransferases within one hour and found an unexpectedly dynamic nature of heterochromatin maintenance. Following H3K9me3 methyltransferases degradation, HP1β dissociates from heterochromatin within three hours, and transcription factors quickly access the de-compacted heterochromatin, activating transcription of their targets, which then promotes H3K9me3 decay. Both passive dilution and active removal contribute to the H3K9me3 decay. Mathematical modeling reveals distinct H3K9me3 heterochromatin states with diverse chromatin features which influence initial H3K9me3 levels and the stability of H3K9me3 domains, thereby expanding our understanding of distinct heterochromatin domains. Rampant transposable element de-repression interferes with transcription of poised early developmental and signaling genes outside H3K9me3-domains, highlighting the intricate roles of dynamic H3K9me3-heterochromatin maintenance in safeguarding developmental programs. Our findings deconvolve the hierarchical relationships between H3K9me3 marks, methyltransferases, HP1 and transcription factors to reveal principles of H3K9me3-heterochromatin maintenance and how its remodeling enables transcription and cell fate change.
2024-09-19 | GSE233039 | GEO
Project description:H3K9me3-heterochromatin, compacted by HP1 proteins, restricts transcription factor binding and functions as a barrier to cell fate changes in development and reprogramming1,2. To investigate principles underlying H3K9me3-heterochromatin maintenance in mammalian cells, we applied degron engineering3,4 on mouse ESCs to conditionally deplete all three H3K9me3-methyltransferases within one hour and found an unexpectedly dynamic nature of heterochromatin maintenance. Following H3K9me3 methyltransferases degradation, HP1β dissociates from heterochromatin within three hours, and transcription factors quickly access the de-compacted heterochromatin, activating transcription of their targets, which then promotes H3K9me3 decay. Both passive dilution and active removal contribute to the H3K9me3 decay. Mathematical modeling reveals distinct H3K9me3 heterochromatin states with diverse chromatin features which influence initial H3K9me3 levels and the stability of H3K9me3 domains, thereby expanding our understanding of distinct heterochromatin domains. Rampant transposable element de-repression interferes with transcription of poised early developmental and signaling genes outside H3K9me3-domains, highlighting the intricate roles of dynamic H3K9me3-heterochromatin maintenance in safeguarding developmental programs. Our findings deconvolve the hierarchical relationships between H3K9me3 marks, methyltransferases, HP1 and transcription factors to reveal principles of H3K9me3-heterochromatin maintenance and how its remodeling enables transcription and cell fate change.
2024-09-19 | GSE231845 | GEO
Project description:H3K9me3-heterochromatin, compacted by HP1 proteins, restricts transcription factor binding and functions as a barrier to cell fate changes in development and reprogramming1,2. To investigate principles underlying H3K9me3-heterochromatin maintenance in mammalian cells, we applied degron engineering3,4 on mouse ESCs to conditionally deplete all three H3K9me3-methyltransferases within one hour and found an unexpectedly dynamic nature of heterochromatin maintenance. Following H3K9me3 methyltransferases degradation, HP1β dissociates from heterochromatin within three hours, and transcription factors quickly access the de-compacted heterochromatin, activating transcription of their targets, which then promotes H3K9me3 decay. Both passive dilution and active removal contribute to the H3K9me3 decay. Mathematical modeling reveals distinct H3K9me3 heterochromatin states with diverse chromatin features which influence initial H3K9me3 levels and the stability of H3K9me3 domains, thereby expanding our understanding of distinct heterochromatin domains. Rampant transposable element de-repression interferes with transcription of poised early developmental and signaling genes outside H3K9me3-domains, highlighting the intricate roles of dynamic H3K9me3-heterochromatin maintenance in safeguarding developmental programs. Our findings deconvolve the hierarchical relationships between H3K9me3 marks, methyltransferases, HP1 and transcription factors to reveal principles of H3K9me3-heterochromatin maintenance and how its remodeling enables transcription and cell fate change.
2024-09-19 | GSE270213 | GEO
Project description:Heterochromatin has important functions in the organization of nuclear structure, the maintenance of genome integrity, and the regulation of gene expression programs1-3. Here, we demonstrate that the genome of the early zebrafish embryo is packaged in an atypical chromatin state that lacks features characteristic of heterochromatin. The heterochromatic histone modification, histone H3 lysine 9 trimethyl (H3K9me3), is undetectable in embryonic chromatin and embryonic nuclei are devoid of condensed chromatin prior to activation of the zygotic genome. The BAF complex catalytic subunit Smarca2 is a guardian of this unique chromatin state, and miR-430 mediated degradation of maternal smarca2 RNA is required for heterochromatin establishment at the maternal to zygotic transition. Our results reveal a period of profound chromatin reorganization in the early zebrafish embryo and identify Smarca2 as an essential regulator of heterochromatin establishment during early development.
2019-02-26 | GSE113086 | GEO
Project description:H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development. This SuperSeries is composed of the SubSeries listed below.
2018-04-13 | GSE97778 | GEO