Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE141067 | GEO | 2020/06/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Hist]

Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous).

2016-06-15 | GSE83255 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Hist]

Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous). Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.

2016-06-15 | E-GEOD-83255 | biostudies-arrayexpress

Mitotic H3K9 acetylation patterns are controlled by phase-specific activity of the histone deacetylases HDAC2, 3 and SIRT1

Project description:Histone acetylation play a fundamental role in many biological processes. H3K9ac is tightly linked to active transcription, and enriched in promoters, enhancers and insulators. During mitosis H3k9ac levels are reduced, and the mechanism of this reduction is not clear. Here, we used small molecules inhibitors of histone deacetylases and evaluated by immunofluorescence and western blots the involvement of each of the targeted enzymes in regulating H3K9ac during prophase, metaphase, anaphase, telophase and cytokinesis. We identified three histone deacetylases, HDAC2, HDAC3 and SIRT1, as modulators of H3K9ac mitotic levels. HDAC2 inhibition, increased global H3K9ac in prophase, whereas HDAC3 or SIRT1 inhibition, increased H3K9ac levels in metaphase. Next, we performed ChIP-seq in mitotic cells following specific inhibition of each of these histone deacetylases. While we observed a high concordance between the genomic areas impacted by HDAC2 and HDAC3, we detected a small set of loci that were unique to each condition, with HDAC3-specific targets being enriched for genes involved in mitosis regulation.

2022-08-14 | GSE168180 | GEO

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

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

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

2021-03-01 | GSE139064 | GEO

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

2021-03-01 | GSE138964 | GEO

Disease-Associated SNPs From non-Coding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells [ChIP-Seq]

Project description:We applied ChIP-Seq on two histone marks: H3K4me1 and H3K27ac in healthy human neutrophils. After peak calling, we obtained the peak regions enriched with H3K4me1 and H3K27ac histone marks and identifed aciive enhancers (H3K27ac+/H3K4me1+) and H3K27ac active enhancers (H3K27ac+/H3K4me1-) in human neutrophils and checked whether those enhancers are located in the LD blocks of 22 SNPs associtated with Juvenile Idiopathic Arthritis. Identification of active enhancers in human neutrohils

2015-06-12 | E-GEOD-66896 | biostudies-arrayexpress

Genome-wide analysis of Staufen1-bound mRNAs in prometaphase

Project description:The goal of this experiment was to identify Staufen1-bound mRNAs in prometaphase cells. Stau1 abundance fluctuates through the cell cycle: it is high in the G2 phase of the cell cycle and rapidly decreases as cells transit through mitosis. The importance of controlling Stau1 levels was underscored by the observation that its overexpression impairs mitosis as well as proliferation of transformed cell lines. As a major post-transcriptional regulator, Stau1 may exert its role(s) through the spatial and/or temporal regulation of its bound mRNAs. Therefore, to gather clues to support this possibility, we identified Stau1-bound mRNAs in prometaphase as a means to identify mRNAs that could be subjected to post-transcriptional modulation when Stau1 is partly degraded in mitosis. HEK293T cells were transfected with plasmids coding for Stau155-FLAG or the empty vector as control. Cells were synchronized in prometaphase with nocodazole. Stau1-bound mRNAs were isolated after immunoprecipitation using anti-FLAG antibody.

2014-07-03 | E-GEOD-51183 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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