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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [RNA-seq]

ABSTRACT: H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [RNA-seq]

PROVIDER: PRJNA818175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18395919_1.fastq.gz	Fastqsanger.gz
	SRR18395919_2.fastq.gz	Fastqsanger.gz
	SRR18395920_1.fastq.gz	Fastqsanger.gz
	SRR18395920_2.fastq.gz	Fastqsanger.gz
	SRR18395921_1.fastq.gz	Fastqsanger.gz

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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States

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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [RNA-seq]

Project description:A small subgroup of embryonic stem cells (ESCs) exhibit molecular features similar to those of two-cell embryos (2C). Multiple chromatin modifiers associated with H3K9 trimethylation (H3K9me3) have been implicated in the mediation of the 2C-like transition. However, it remains elusive how H3K9me3 is remodeled and its association with totipotent cells. Here, we analyze the genome-wide change in H3K9me3 in 2C-like transitions. We revealed that a large fraction of trophoblast-stem-cell specific enhancers undergoes loss of H3K9me3 exclusively in MERVL+/Zscan4+ cells during 2C-like transitions.

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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [ChIP-seq]

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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [ChIP-seq]

Project description:H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States [ChIP-seq]

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H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States

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

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SMARCAD1 and TOPBP1 contribute to heterochromatin maintenance at the transition from the 2C-like to the pluripotent state

Project description:Chromocenters are established after the 2-cell (2C) stage during mouse embryonic development, but the factors that mediate chromocenter formation remain largely unknown. To identify regulators of 2C heterochromatin establishment, we generated an inducible system to convert embryonic stem cells (ESCs) to 2C-like cells. This conversion is marked by a global reorganization and dispersion of H3K9me3-heterochromatin foci, which are then reversibly formed upon re-entry into pluripotency. Profiling the chromatin-bound proteome (chromatome) by genome capture of ESCs transitioning to 2C-like cells, we uncover chromatin regulators involved in de novo heterochromatin formation. We identified TOPBP1 and investigated its binding partner SMARCAD1. SMARCAD1 and TOPBP1 associate with H3K9me3-heterochromatin in ESCs. Interestingly, the nuclear localization of SMARCAD1 is lost in 2C-like cells. SMARCAD1 or TOPBP1 depletion in mouse embryos lead to developmental arrest, reduction of H3K9me3 and remodeling of heterochromatin foci. Collectively, our findings contribute to comprehending the maintenance of chromocenters during early development.

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Expression data from 2C::tomato+ vs 2C::tomato - ES cells

Project description:We compared gene expression from 2C::tomato+/- ES cells from Kdm1a wt and mutant ES cultures 2C::tomato- samples 1, 5, 9 2C::tomato+ samples 2, 6, 10 We collecteded 3 replicates of RNA from 2C::tomato+ and - ES cells

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A transcriptional roadmap for 2C-like to pluripotent state transition [single cells]

Project description:In mouse embryonic stem cell (ESC) culture, a small proportion of cells display totipotent features by expressing a set of genes that are only active in 2-cell-stage embryos. These 2-cell-like (2C-like) cells spontaneously transit back into pluripotent state. We previously dissected the transcriptional dynamics of pluripotent to 2C-like transition and identified factors that modulate the transition. However, how 2C-like cells transits back to the pluripotent state and what factors drive this process remains largely unknown. To address these questions, we examined the transcriptional dynamics during the reverse transition from the 2C-like state to ESCs and identified an intermediate state involved in the transition. Interestingly, we found that mESCs exit from the 2C-like state through a molecular path characterized by a two-wave upregulation of pluripotent genes different from the one observed during the 2C-like entry transition. We also showed that nonsense-mediated mRNA decay (NMD) targets Dux mRNA and affects 2C-like state maintenance, suggesting that Dux degradation contributes to the reversal of 2C-like state.

2020-03-20 | GSE133233 | GEO

A transcriptional roadmap for 2C-like to pluripotent state transition [bulk RNA]

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