Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CTCF and transcription orchestrate chromatin structure re-configuration after mitosis [Hi-C]

ABSTRACT: During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. Here we exploited the M-phase to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to re-sculpting the genome in newborn nuclei. While CTCF appears to be dispensable for large scale post-mitotic compartmentalization, depletion of CTCF specifically during the M-phase to G1-phase transition alters the re-establishment of local short-range compartmentalization after mitosis. Without CTCF, structural loops fail to reform, leading to illegitimate contacts between cis-regulatory elements (CREs) and altered gene expression in G1-phase. Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF depleted cells. Boundary reformation is largely disrupted upon CTCF loss. Yet, a subset (~27%) of boundaries emerges normally in the absence of CTCF and is characterized by transitions in chromatin states. Reformation of gene domains can occur prior to the full onset of transcription and can be linked to tri-methylation at lysine 36 of histone 3 (H3K36me3), a mark stable throughout mitosis. The focus on the de novo formation of nuclear architecture during G1 entry yielded novel insights into how CTCF and the process of transcription contribute to the dynamic re-configuration of chromatin architecture during the mitosis to G1 phase progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE168176 | GEO | 2021/06/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

CTCF and transcription orchestrate chromatin structure re-configuration after mitosis [ChIP-seq]

Project description:During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. Here we exploited the M-phase to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to re-sculpting the genome in newborn nuclei. While CTCF appears to be dispensable for large scale post-mitotic compartmentalization, depletion of CTCF specifically during the M-phase to G1-phase transition alters the re-establishment of local short-range compartmentalization after mitosis. Without CTCF, structural loops fail to reform, leading to illegitimate contacts between cis-regulatory elements (CREs) and altered gene expression in G1-phase. Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF depleted cells. Boundary reformation is largely disrupted upon CTCF loss. Yet, a subset (~27%) of boundaries emerges normally in the absence of CTCF and is characterized by transitions in chromatin states. Reformation of gene domains can occur prior to the full onset of transcription and can be linked to tri-methylation at lysine 36 of histone 3 (H3K36me3), a mark stable throughout mitosis. The focus on the de novo formation of nuclear architecture during G1 entry yielded novel insights into how CTCF and the process of transcription contribute to the dynamic re-configuration of chromatin architecture during the mitosis to G1 phase progression.

2021-06-17 | GSE168168 | GEO

Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

Project description:Chromatin architecture is temporarily disrupted during mitosis. Yet, how chromatin architecture is reconfigured during M-G1 phase transition is unknown. To examine this, we performed Hi-C experiments on cell populations at defined cell cycle stages between mitosis and G1 phase.

2019-11-27 | GSE129997 | GEO

Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

Project description:Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

| PRJNA533460 | ENA

The transcriptional and architectural resetting of stem cell identity during G1 entry [Hi-C]

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

The transcriptional and architectural resetting of stem cell identity during G1 entry [ATAC-Seq]

2021-03-01 | GSE138964 | GEO

The transcriptional and architectural resetting of stem cell identity during G1 entry [PRO-Seq]

2021-03-01 | GSE138928 | GEO

Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [EU-RNA-seq]

Project description:During mitosis, transcription of genomic DNA is dramatically reduced, before its reactivation occurs during nuclear reformation in anaphase/telophase. Many aspects of the underlying principles that mediate transcriptional memory and reactivation in the daughter cells remain unclear. Here, we used ChIP-seq on synchronized cells at different stages after mitosis to generate genome-wide maps of histone modifications. In combination with EU-RNA-seq and Hi-C analyses, we show that, during prometaphase, promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, while losing H3K27ac. Enhancers harboring mitotic H3K4me1 are associated with cell type-specific transcription factor motifs and mitotic activation of cell identity genes. As cells exit mitosis, promoters regain H3K27ac, which correlates with transcriptional reactivation. Insulators also gain H3K27ac and CCCTC binding factors (CTCF) in anaphase/telophase. This increase may play a role in the establishment of topologically associating domains (TADs). Together, our results show that the genome is reorganized in sequential order, in which histone methylations occur first in prometaphase, histone acetylation and CTCF in anaphase/telophase, transcription in cytokinesis, and long-range chromatin interactions in early G1. Our results provide insights into the histone modification landscape that allows faithful reestablishment of the transcriptional program and TADs during cell division.

2020-06-11 | GSE141137 | GEO

Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [ChIP-seq]

2020-06-11 | GSE141081 | GEO

Dynamic regulation of histone modifications and long-range chromosomal interactions during post-mitotic transcriptional reactivation [Hi-C]

2020-06-11 | GSE141067 | GEO

Mapping of CTCF occupancy in interphase and mitosis cells

Project description:To address whether CTCF is involved in the transcription of early G1 genes immediately after mitotic exit, we carried out ChIP sequencing (ChIP-seq) experiments to evaluate CTCF binding to genomic DNA in asynchronous cells and nocodazole-arrested mitotic cells. Of the 62,996 peaks identified in the asynchronous cells, 41,397 peaks (65.71%) were lost in the mitotic cells. However, the 21,599 peaks (34.29%) were identified in the both conditions, indicating that the enrichment level of CTCF is decreased in the mitotic cells. It has been reported that expression profiles of the first 2 hours of G1 phase in HeLa cells. A scatter plot comparison of the genes expressed in the early G1 phase indicated the reduced CTCF binding level in the mitotic phase. These results indicate that CTCF was dissociated or CTCF bound to chromosomes was reduced in the mitotic chromatin and then may be re-associated to chromatin in the early G1 phase.

2019-06-18 | GSE83579 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data