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

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

PROVIDER: PRJNA1140248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29997502_1.fastq.gz	Fastqsanger.gz
	SRR29997502_2.fastq.gz	Fastqsanger.gz

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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 [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

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

Project description: Not available

| 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

IntS11 is a totipotent regulator that controls zygotic genome activation

Project description:As the first transcriptional milestone in life, zygotic genome activation (ZGA) driven by pioneer factors is a hallmark of totipotency, enabling embryos to transition from maternal to zygotic control. Yet, the mechanisms governing the totipotent state of embryonic chromatin remain a central unresolved question in developmental biology. Here we identified IntS11, a Pol II-associated protein, as a critical totipotency factor in Drosophila. We demonstrate that maternal IntS11 controls totipotent state of chromatin, ensuring proper ZGA by coordinating the transcription machinery assembly. Specifically, IntS11 mediates de novo Pol II recruitment and directs pioneer factors Zelda and GAF to zygotic gene regulatory regions. Our findings unveil a fundamental principle linking IntS11, pioneer factor binding, and Pol II engagement, providing novel insights into orchestration of ZGA.

| PXD064852 |

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