Project description:The cellular and nuclear states are constantly changing and closely linked to DNA replication and cell division, defining cell cycle phases. Pharmacological inhibition is a widely used strategy to enrich for specific phases to study them in isolation. However, it is important to understand how synchronization influences chromatin openness and gene expression compared to unperturbed cell cycle states. Here, we use an integrated approach to obtain G1, S and G2/M phases from mouse embryonic stem cells (mESC) and to profile their chromatin accessibility and marks as well as steady and nascent transcripts levels. We demonstrate that synchronization with thymidine and nocodazole leads to dramatic changes in chromatin compaction and gene expression, which only partially resemble bona fide cell cycle-dependent differences. Blocking with CDK1 inhibitor results in efficient synchronization and evokes moderate changes in chromatin accessibility, resembling G2/M phase. Correlative analysis suggests that cell cycle-specific variations in chromatin openness in unperturbed mESCs are mediated by CDK1 substrates and CTCF. This integrated strategy can be applied to most cultured cell lines under any conditions and holds the potential to further our understanding of cell cycle-dependent susceptibility to external cues and chromatin regulation.

2021-12-31 | GSE167963 | GEO

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