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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE218598 | GEO | 2024/08/09

REPOSITORIES: GEO

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

| PRJNA904381 | 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 [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 [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

Nuclear lamina integrity is required for proper spatial organization of chromatin in Drosophila.

Project description:How the nuclear lamina (NL) impacts on global chromatin architecture is poorly understood. Here, we show that NL disruption in Drosophila S2 cells leads to chromatin compaction and repositioning from the nuclear envelope. This increases the chromatin density in a fraction of topologically-associating domains (TADs) enriched in active chromatin and enhances interactions between active and inactive chromatin. Importantly, upon NL disruption the NL-associated TADs become more acetylated at histone H3 and less compact, while background transcription is derepressed. Two-colour FISH confirms that a TAD becomes less compact following its release from the NL. Finally, polymer simulations show that chromatin binding to the NL can per se compact attached TADs. Collectively, our findings demonstrate a dual function of the NL in shaping the 3D genome. Attachment of TADs to the NL makes them more condensed but decreases the overall chromatin density in the nucleus by stretching interphase chromosomes.

| S-EPMC6414625 | biostudies-literature

The nuclear lamina couples mechanical forces to cell fate in the preimplantation embryo via actin organization.

Project description:During preimplantation development, contractile forces generated at the apical cortex segregate cells into inner and outer positions of the embryo, establishing the inner cell mass (ICM) and trophectoderm. To which extent these forces influence ICM-trophectoderm fate remains unresolved. Here, we found that the nuclear lamina is coupled to the cortex via an F-actin meshwork in mouse and human embryos. Actomyosin contractility increases during development, upregulating Lamin-A levels, but upon internalization cells lose their apical cortex and downregulate Lamin-A. Low Lamin-A shifts the localization of actin nucleators from nucleus to cytoplasm increasing cytoplasmic F-actin abundance. This results in stabilization of Amot, Yap phosphorylation and acquisition of ICM over trophectoderm fate. By contrast, in outer cells, Lamin-A levels increase with contractility. This prevents Yap phosphorylation enabling Cdx2 to specify the trophectoderm. Thus, forces transmitted to the nuclear lamina control actin organization to differentially regulate the factors specifying lineage identity.

| S-EPMC10226985 | biostudies-literature

Genome-lamina interactions are established de novo in the early mouse embryo.

Project description:In mammals, the emergence of totipotency after fertilization involves extensive rearrangements of the spatial positioning of the genome1,2. However, the contribution of spatial genome organization to the regulation of developmental programs is unclear3. Here we generate high-resolution maps of genomic interactions with the nuclear lamina (a filamentous meshwork that lines the inner nuclear membrane) in mouse pre-implantation embryos. We reveal that nuclear organization is not inherited from the maternal germline but is instead established de novo shortly after fertilization. The two parental genomes establish lamina-associated domains (LADs)4 with different features that converge after the 8-cell stage. We find that the mechanism of LAD establishment is unrelated to DNA replication. Instead, we show that paternal LAD formation in zygotes is prevented by ectopic expression of Kdm5b, which suggests that LAD establishment may be dependent on remodelling of H3K4 methylation. Our data suggest a step-wise assembly model whereby early LAD formation precedes consolidation of topologically associating domains.

| S-EPMC6546605 | biostudies-literature

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