Ontology highlight
ABSTRACT:
PROVIDER: PRJNA544540 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9117150.fastq.gz | Fastqsanger.gz | |||
| SRR9117160.fastq.gz | Fastqsanger.gz | |||
| SRR9117151.fastq.gz | Fastqsanger.gz | |||
| SRR9117161.fastq.gz | Fastqsanger.gz | |||
| SRR9117152.fastq.gz | Fastqsanger.gz |
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Project description:Mouse embryonic stem cells (ESCs) show cell-to-cell heterogeneity. A small fraction of 2-cell-like cells (2CLCs) marked by endogenous retrovirus activation emerge spontaneously. The 2CLCs are instable and they transit back to the pluripotent state without extrinsic stimulus. To understand how this bidirectional transition takes place, we performed single-cell RNA-seq on isolated 2CLCs which underwent 2C-like state exit and re-entry, and revealed a novel circular transitional process between 2C-like and pluripotent states. Mechanistically, we found that the cell cycle played an important role in mediating these transitions by regulating assembly of nucleolus and peri-nucleolar heterochromatin to influence 2C gene Dux expression. Collectively, our findings provide a roadmap of the 2C-like state entry and exit in ESCs and also a causal role of the cell cycle in promoting these transitions.
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Project description:Mouse embryonic stem cells (ESCs) show cell-to-cell heterogeneity. A small fraction of 2-cell-like cells (2CLCs) marked by endogenous retrovirus activation emerge spontaneously. The 2CLCs are instable and they transit back to the pluripotent state without extrinsic stimulus. To understand how this bidirectional transition takes place, we performed single-cell RNA-seq on isolated 2CLCs which underwent 2C-like state exit and re-entry, and revealed a novel circular transitional process between 2C-like and pluripotent states. Mechanistically, we found that the cell cycle played an important role in mediating these transitions by regulating assembly of nucleolus and peri-nucleolar heterochromatin to influence 2C gene Dux expression. Collectively, our findings provide a roadmap of the 2C-like state entry and exit in ESCs and also a causal role of the cell cycle in promoting these transitions.
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Project description:Mammalian genomes are a battleground for genetic conflict between repetitive elements (REs) and KRAB-zinc finger proteins (KZFPs). We explored whether KZFPs can regulate cell fate by employing Zfp819, which targets a satellite DNA array, ZP3AR. ZP3AR coats a megabase region of chromosome 7 that encompasses genes encoding ZSCAN4, a master transcription factor of totipotency. Depleting Zfp819 in mouse embryonic stem cells (mESCs) causes them to transition to a 2-cell (2C)-like state, whereby the ZP3AR array switches from a poised to an active enhancer state. This is accompanied by a global eviction of heterochromatin roadblocks, which we link to decreased SETDB1 stability. These events result in transcription of active LINE-1 elements and a block in differentiation. In sum, ZFP819 and TRIM28 partner up to close chromatin across Zscan4, allowing exit from totipotency. We propose that satellite DNAs may control developmental fate transitions through the barcoding and switching off of master transcription factor genes.
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Project description:Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions. Although the signaling circuits and gene regulatory networks regulating pluripotent stem cell differentiation have been intensely studied, how these networks are integrated in space and time with morphological transitions and mechanical deformations that occur during state transitions remains a fundamental open question. Here, we discover that stem cell fate transitions are gated by two critical signals - nuclear envelope fluctuations and osmotic stress - that emanate from growth factor signaling-controlled changes in nuclear volume and nucleoplasm viscosity/density to subsequently trigger changes in nuclear architecture and transcription. We observe that fate transitions in the early human embryo and in an in vitro model of exit from pluripotency are associated with rapid changes in nuclear volume and nuclear envelope mechanics. These changes alter nuclear mechanosensitivity and trigger changes in nucleoplasmic viscosity and nuclear condensates to prime chromatin for a cell fate transition. However, while this mechanical priming accelerates fate transitions, sustained biochemical signals are required for efficient induction of differentiation. Our findings establish a critical mechanochemical feedback mechanism that integrates nuclear mechanics, shape and volume with biochemical signaling and chromatin state to control cell fate transition dynamics.
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Project description:H3K9me3 Impedes Cell Fate Transition between 2C-Like and Pluripotent States
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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.
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