The transcriptional and architectural resetting of pluripotent stem cell identity during G1 entry [RNA-Seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE149830 | GEO | 2021/03/01
REPOSITORIES: GEO
Similar Datasets
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 | GSE149831 | 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 | GSE138928 | 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.
2021-03-01 | GSE138964 | GEO
Project description:The identity of dividing cells is challenged during mitosis, as transcription is halted and chromatin architecture drastically altered. How cell type-specific gene expression and genomic organization are faithfully reset upon G1 entry in daughter cells remains elusive. To address this issue, we characterized at a genome-wide scale the dynamic transcriptional and architectural resetting of mouse pluripotent stem cells (PSCs) upon mitotic exit. This revealed distinct patterns of transcriptional reactivation with rapid induction of stem cell genes and their enhancers, a more gradual recovery of metabolic and cell cycle genes, and a weak and transient activation of lineage-specific genes only during G1. Topological reorganization at different hierarchical levels also occurred in an asynchronous manner and showed an overall weak coordination with transcriptional reactivation. Chromatin interactions around active promoters and enhancers, and particularly super enhancers, reformed at a faster rate than CTCF/Cohesin-bound structural loops. Interestingly, although regions with mitotic retention of the active histone mark H3K27ac associated both with faster transcriptional and architectural resetting, depletion of this mark specifically during mitosis perturbed transcriptional reactivation of H3K27ac-bookmarked genes without affecting chromatin topology. Our study provides an integrative map of the topological and transcriptional changes that lead to the resetting of pluripotent stem cell identity during mitotic exit, and reveals distinct patterns and features that balance the dual requirements for self-renewal and differentiation.
2021-03-01 | GSE164343 | GEO
Project description:The identity of dividing cells is challenged during mitosis, as transcription is halted and chromatin architecture drastically altered. How cell type-specific gene expression and genomic organization are faithfully reset upon G1 entry in daughter cells remains elusive. To address this issue, we characterized at a genome-wide scale the dynamic transcriptional and architectural resetting of mouse pluripotent stem cells (PSCs) upon mitotic exit. This revealed distinct patterns of transcriptional reactivation with rapid induction of stem cell genes and their enhancers, a more gradual recovery of metabolic and cell cycle genes, and a weak and transient activation of lineage-specific genes only during G1. Topological reorganization at different hierarchical levels also occurred in an asynchronous manner and showed an overall weak coordination with transcriptional reactivation. Chromatin interactions around active promoters and enhancers, and particularly super enhancers, reformed at a faster rate than CTCF/Cohesin-bound structural loops. Interestingly, although regions with mitotic retention of the active histone mark H3K27ac associated both with faster transcriptional and architectural resetting, depletion of this mark specifically during mitosis perturbed transcriptional reactivation of H3K27ac-bookmarked genes without affecting chromatin topology. Our study provides an integrative map of the topological and transcriptional changes that lead to the resetting of pluripotent stem cell identity during mitotic exit, and reveals distinct patterns and features that balance the dual requirements for self-renewal and differentiation.
2021-03-01 | GSE164341 | GEO
Project description:The identity of dividing cells is challenged during mitosis, as transcription is halted and chromatin architecture drastically altered. How cell type-specific gene expression and genomic organization are faithfully reset upon G1 entry in daughter cells remains elusive. To address this issue, we characterized at a genome-wide scale the dynamic transcriptional and architectural resetting of mouse pluripotent stem cells (PSCs) upon mitotic exit. This revealed distinct patterns of transcriptional reactivation with rapid induction of stem cell genes and their enhancers, a more gradual recovery of metabolic and cell cycle genes, and a weak and transient activation of lineage-specific genes only during G1. Topological reorganization at different hierarchical levels also occurred in an asynchronous manner and showed an overall weak coordination with transcriptional reactivation. Chromatin interactions around active promoters and enhancers, and particularly super enhancers, reformed at a faster rate than CTCF/Cohesin-bound structural loops. Interestingly, although regions with mitotic retention of the active histone mark H3K27ac associated both with faster transcriptional and architectural resetting, depletion of this mark specifically during mitosis perturbed transcriptional reactivation of H3K27ac-bookmarked genes without affecting chromatin topology. Our study provides an integrative map of the topological and transcriptional changes that lead to the resetting of pluripotent stem cell identity during mitotic exit, and reveals distinct patterns and features that balance the dual requirements for self-renewal and differentiation.
2021-03-01 | GSE164342 | GEO
Project description:The transcriptional and architectural resetting of stem cell identity during G1 entry
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Project description:The transcriptional and architectural resetting of stem cell identity during G1 entry [ATAC-Seq]
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Project description:The transcriptional and architectural resetting of stem cell identity during G1 entry [PRO-Seq]
| PRJNA577829 | ENA