LncRNA based TOBF1 chromatin recruitment in early G1 modulates mouse embryonic stem cell identity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA297949 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1799720.fastq.gz | Fastqsanger.gz | |||
| SRR1799721.fastq.gz | Fastqsanger.gz | |||
| SRR2570140.fastq.gz | Fastqsanger.gz | |||
| SRR2570142.fastq.gz | Fastqsanger.gz | |||
| SRR2570143.fastq.gz | Fastqsanger.gz |
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2017-02-01 | GSE73806 | GEO
Project description:The molecular identity of dividing cells is temporarily challenged during mitosis, as transcription is halted and chromatin architecture is drastically altered. The principles and key players that ensure faithful propagation of cell identity upon G1 entry in the daughter cells remain elusive. Here, we used rapidly dividing mouse pluripotent stem cell (PSC) as a study model to characterize for the first time the dynamic transcriptional and architectural resetting of cell identity during mitotic exit, and assess the role of mitotic bookmarking by the active histone mark H3K27 acetylation (H3K27ac). Globally, compartments and topologically associating domains (TADs) were quickly reformed and gradually gained strength and activity throughout G1, while long-range chromatin interactions were reestablished at a slower rate. Binding of PSC-specific transcription factors (TFs) and transcriptional machinery associated with faster boundary insulation and contact formation, while CTCF, Cohesin and Polycomb-bound regions were characterized by a slower architectural resetting. Similarly, transcriptional reactivation of both PSC enhancers and their target genes occurred in early G1, while enhancers and genes involved in housekeeping/cell cycle or differentiation processes were activated in a gradual or transient manner, respectively. Mitotic bookmarking by H3K27ac promoted faster compartmentalization, boundary insulation, and loop formation, as well as rapid transcriptional reactivation. Interestingly, we identified a group of developmental genes and enhancers that were transiently activated in G1 and were marked by H3K27ac specifically during mitosis. This study provides insights into the relative kinetics of transcriptional and architectural rewiring after mitosis and establishes a unique role for H3K27ac bookmarking in the resetting of stem cell identity.
2021-03-01 | GSE139064 | GEO
Project description:The molecular identity of dividing cells is temporarily challenged during mitosis, as transcription is halted and chromatin architecture is drastically altered. The principles and key players that ensure faithful propagation of cell identity upon G1 entry in the daughter cells remain elusive. Here, we used rapidly dividing mouse pluripotent stem cell (PSC) as a study model to characterize for the first time the dynamic transcriptional and architectural resetting of cell identity during mitotic exit, and assess the role of mitotic bookmarking by the active histone mark H3K27 acetylation (H3K27ac). Globally, compartments and topologically associating domains (TADs) were quickly reformed and gradually gained strength and activity throughout G1, while long-range chromatin interactions were reestablished at a slower rate. Binding of PSC-specific transcription factors (TFs) and transcriptional machinery associated with faster boundary insulation and contact formation, while CTCF, Cohesin and Polycomb-bound regions were characterized by a slower architectural resetting. Similarly, transcriptional reactivation of both PSC enhancers and their target genes occurred in early G1, while enhancers and genes involved in housekeeping/cell cycle or differentiation processes were activated in a gradual or transient manner, respectively. Mitotic bookmarking by H3K27ac promoted faster compartmentalization, boundary insulation, and loop formation, as well as rapid transcriptional reactivation. Interestingly, we identified a group of developmental genes and enhancers that were transiently activated in G1 and were marked by H3K27ac specifically during mitosis. This study provides insights into the relative kinetics of transcriptional and architectural rewiring after mitosis and establishes a unique role for H3K27ac bookmarking in the resetting of stem cell identity.
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Project description:The molecular identity of dividing cells is temporarily challenged during mitosis, as transcription is halted and chromatin architecture is drastically altered. The principles and key players that ensure faithful propagation of cell identity upon G1 entry in the daughter cells remain elusive. Here, we used rapidly dividing mouse pluripotent stem cell (PSC) as a study model to characterize for the first time the dynamic transcriptional and architectural resetting of cell identity during mitotic exit, and assess the role of mitotic bookmarking by the active histone mark H3K27 acetylation (H3K27ac). Globally, compartments and topologically associating domains (TADs) were quickly reformed and gradually gained strength and activity throughout G1, while long-range chromatin interactions were reestablished at a slower rate. Binding of PSC-specific transcription factors (TFs) and transcriptional machinery associated with faster boundary insulation and contact formation, while CTCF, Cohesin and Polycomb-bound regions were characterized by a slower architectural resetting. Similarly, transcriptional reactivation of both PSC enhancers and their target genes occurred in early G1, while enhancers and genes involved in housekeeping/cell cycle or differentiation processes were activated in a gradual or transient manner, respectively. Mitotic bookmarking by H3K27ac promoted faster compartmentalization, boundary insulation, and loop formation, as well as rapid transcriptional reactivation. Interestingly, we identified a group of developmental genes and enhancers that were transiently activated in G1 and were marked by H3K27ac specifically during mitosis. This study provides insights into the relative kinetics of transcriptional and architectural rewiring after mitosis and establishes a unique role for H3K27ac bookmarking in the resetting of stem cell identity.
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Project description:The molecular identity of dividing cells is temporarily challenged during mitosis, as transcription is halted and chromatin architecture is drastically altered. The principles and key players that ensure faithful propagation of cell identity upon G1 entry in daughter cells remain elusive. Here, we characterized at a genome-wide scale the dynamic transcriptional and architectural resetting of mouse pluripotent stem cells upon mitotic exit.
2021-03-01 | GSE149830 | GEO
Project description:EPR is a long non-coding RNA (lncRNA) that controls cell proliferation in mammary gland cells by regulating gene transcription. Here, we report on Mettl7a1 as a direct target of EPR. We show that EPR induces Mettl7a1 transcription by rewiring three-dimensional chromatin interactions at the Mettl7a1 locus. Our data indicate that METTL7A1 contributes to EPR-dependent inhibition of TGF-β signaling. METTL7A1 is absent in tumorigenic murine mammary gland cells and its human ortholog (METTL7A) is downregulated in breast cancers. Importantly, re-expression of METTL7A1 in 4T1 tumorigenic cells attenuates their transformation potential, with the putative methyltransferase activity of METTL7A1 being dispensable for its biological functions. We found that METTL7A1 localizes in the cytoplasm whereby it interacts with factors implicated in the early steps of mRNA translation, associates with ribosomes, and affects the levels of target proteins without altering mRNA abundance. Overall, our data indicates that METTL7A1 —a transcriptional target of EPR— modulates translation of select transcripts.
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