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Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo

ABSTRACT: Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo

PROVIDER: PRJNA904381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22215979.fastq.gz	Fastqsanger.gz
	SRR22215980.fastq.gz	Fastqsanger.gz
	SRR22215981.fastq.gz	Fastqsanger.gz
	SRR22215982.fastq.gz	Fastqsanger.gz
	SRR22215983.fastq.gz	Fastqsanger.gz

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Similar Datasets

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDamID]

Project description:Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDamID]

| PRJNA899049 | ENA

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [CELseq]

Project description:Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [CELseq]

| PRJNA1140248 | ENA

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDam&T-seq]

Project description:Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDam&T-seq]

| PRJNA904384 | ENA

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo.

Project description:In mammals, early embryonic development exhibits highly unusual spatial positioning of genomic regions at the nuclear lamina, but the mechanisms underpinning this atypical genome organization remain elusive. Here, we generated single-cell profiles of lamina-associated domains (LADs) coupled with transcriptomics, which revealed a striking overlap between preimplantation-specific LAD dissociation and noncanonical broad domains of H3K27me3. Loss of H3K27me3 resulted in a restoration of canonical LAD profiles, suggesting an antagonistic relationship between lamina association and H3K27me3. Tethering of H3K27me3 to the nuclear periphery showed that the resultant relocalization is partially dependent on the underlying DNA sequence. Collectively, our results suggest that the atypical organization of LADs in early developmental stages is the result of a tug-of-war between intrinsic affinity for the nuclear lamina and H3K27me3, constrained by the available space at the nuclear periphery. This study provides detailed insight into the molecular mechanisms regulating nuclear organization during early mammalian development.

| S-EPMC11525175 | biostudies-literature

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [CELseq]

Project description:In this study, we profiled genome-Nuclear Lamina (NL) contacts during the first stages of mouse embryonic development. We discovered a remarkable cell-to-cell variability in NL-contacts at the 2-cell stage, which is particularly strong on the paternal allele. We additionally obtained single-cell profiles for H3K27me3, H3K9me3 and DNA accessibility at this stage, but did not observe the same large-scale variability. The variability in NL-contacts did not appear to affect the trascription of underlying genes. Comparing NL-contact profiles with diverse histone modification profiles showed that large regions of typical NL-contacts are lost and instead are inriched for H3K27me3 during early development. To investigate the relationship between H3K27me3 and NL association, we used a conditional EED KO mouse model, which results in an absence of H3K27me3 during oocyte development and the early embryo. Profiling NL-contacts at the 2-cell stage in this syste revealed that regions enriched with H3K27me3 in WT regain NL association in the EED maternal KO. In addition, the loss of H3K27me3 resulted in more similar NL association profiles on the maternal and paternal allele. Together, these results suggest that H3K27me3 antagonizes NL association and that the non-canonical broad H3K27me3 domains present in the early embryo may be responsible for the early-embryo specific loss of NL associations in these regions.

2024-08-09 | GSE273151 | GEO

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDamID]

Project description:In this study, we profiled genome-Nuclear Lamina (NL) contacts during the first stages of mouse embryonic development. We discovered a remarkable cell-to-cell variability in NL-contacts at the 2-cell stage, which is particularly strong on the paternal allele. We additionally obtained single-cell profiles for H3K27me3, H3K9me3 and DNA accessibility at this stage, but did not observe the same large-scale variability. The variability in NL-contacts did not appear to affect the transcription of underlying genes. Comparing NL-contact profiles with diverse histone modification profiles showed that large regions of typical NL-contacts are lost and instead are enriched for H3K27me3 during early development. To investigate the relationship between H3K27me3 and NL association, we used a conditional EED KO mouse model, which results in an absence of H3K27me3 during oocyte development and the early embryo. Profiling NL-contacts at the 2-cell stage in this system revealed that regions enriched with H3K27me3 in WT regain NL association in the EED maternal KO. In addition, the loss of H3K27me3 resulted in more similar NL association profiles on the maternal and paternal allele. Together, these results suggest that H3K27me3 antagonizes NL association and that the non-canonical broad H3K27me3 domains present in the early embryo may be responsible for the early-embryo specific loss of NL associations in these regions.

2024-08-09 | GSE217462 | GEO

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo [scDam&T-seq]

Project description:In this study, we profiled genome-Nuclear Lamina (NL) contacts during the first stages of mouse embryonic development. We discovered a remarkable cell-to-cell variability in NL-contacts at the 2-cell stage, which is particularly strong on the paternal allele. We additionally obtained single-cell profiles for H3K27me3, H3K9me3 and DNA accessibility at this stage, but did not observe the same large-scale variability. The variability in NL-contacts did not appear to affect the transcription of underlying genes. Comparing NL-contact profiles with diverse histone modification profiles showed that large regions of typical NL-contacts are lost and instead are enriched for H3K27me3 during early development. To investigate the relationship between H3K27me3 and NL association, we used a conditional EED KO mouse model, which results in an absence of H3K27me3 during oocyte development and the early embryo. Profiling NL-contacts at the 2-cell stage in this system revealed that regions enriched with H3K27me3 in WT regain NL association in the EED maternal KO. In addition, the loss of H3K27me3 resulted in more similar NL association profiles on the maternal and paternal allele. Together, these results suggest that H3K27me3 antagonizes NL association and that the non-canonical broad H3K27me3 domains present in the early embryo may be responsible for the early-embryo specific loss of NL associations in these regions.

2024-08-09 | GSE218597 | GEO

Antagonism between H3K27me3 and genome-lamina association drives atypical spatial genome organization in the totipotent embryo

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

2024-08-09 | GSE218598 | GEO

Polycomb-lamina antagonism partitions heterochromatin at the nuclear periphery

Project description:Polycomb-lamina antagonism partitions heterochromatin at the nuclear periphery

| PRJNA747066 | ENA

Integrated genomic analyses of de novo pathways underlying atypical meningiomas [H3k27me3 ChIP-Seq]

Project description:Meningiomas are mostly benign brain tumors, with a potential for becoming atypical or malignant. Based on comprehensive genomic, transcriptomic and epigenomic analyses of meningiomas, we compared benign tumors to atypical ones. We show that the vast majority of primary (de novo) atypical meningiomas display loss of NF2, which co-occurs either with genomic instability or recurrent mutations in SMARCB1. These tumors harbor increased H3K27me3 repressive signal and a hypermethylated phenotype, mainly occupying the polycomb repressive complex 2 (PRC2) binding sites in human embryonic stem cells (hESCs), thereby phenocopying a more primitive cellular state. Consistent with this observation, and based on differential gene expression analysis as well as correlation of mRNA:miRNA regulatory networks, atypical meningiomas exhibit up-regulation of EZH2, the catalytic subunit of the PRC2 complex, well as the E2F2 and FOXM1 transcriptional networks that promote proliferation through activation of the cell cycle pathways. In addition, based on H3K27ac ChIP-seq analysis, we show atypical tumors to display an activated super-enhancer near the meningeal identity transcription factor ZIC1, leading to its transcriptional upregulation. Importantly, these primary atypical meningiomas do not harbor activating TERT promoter mutations, which have been reported in atypical tumors that progressed from benign ones. Our results establish the genomic landscape of primary atypical meningiomas, differentiating their profile from benign and progressed tumors and establishing novel therapeutic targets.

2016-12-20 | GSE92558 | GEO

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