Project description:To formally assess how 5mC shapes the H3K27me3 landscape, we profiled the epigenome of naive and differentiated cells in the presence and absence of the DNA methylation machinery.

2024-07-16 | GSE242201 | GEO

Gain of chromatin loops marks the exit from naive pluripotency - ChIP seq for CTCF and Rad21

Project description:ChIP-seq to map the binding sites for CTCF and cohesin subunit Rad21 in the naive mES cells (46C cell line grown in the 2i/LIF condition) and in the neural stem cells (derived from the 46C ES cells using the mono-layer differentiation protocol, grown in the N2B27 medium these cells are Nestin+). The naive mES cells were grown in two different media (fetal bovine serum, FBS and 2i/LIF culture - naive pluripotency conditions) as detailed in the growth protocols.

2018-11-08 | E-MTAB-5732 | biostudies-arrayexpress

Gain of chromatin loops marks the exit from naive pluripotency - ChIP seq for CTCF and Rad21

Project description:Gain of chromatin loops marks the exit from naive pluripotency - ChIP seq for CTCF and Rad21

| PRJEB20728 | ENA

CpG island reconfiguration for the establishment and synchronization of polycomb functions upon exit from naive pluripotency

Project description:CpG island reconfiguration for the establishment and synchronization of polycomb functions upon exit from naive pluripotency

| PRJEB44207 | ENA

Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection

Project description:Stem cells intrinsically express a subset of genes which are normally associated with interferon stimulation and the innate immune response. However, expression of these interferon stimulated genes (ISG) in stem cells is independent from external stimuli such as viral infection. Here, we show that the interferon regulatory factor 1, Irf1, is directly controlled by the murine formative pluripotency gene regulatory network and transiently upregulated during the transition from naive to formative pluripotency. IRF1 binds to regulatory regions of a conserved set of ISGs and is required for their faithful expression upon exit from naive pluripotency. We show that in the absence of IRF1, cells exiting the naive pluripotent stem cell state are more susceptible to viral infection. Irf1 therefore acts as a link between the formative pluripotency network, regulation of innate immunity genes and defense against viral infections during formative pluripotency.

| S-SCDT-EMBOR-2022-55375V1 | biostudies-other

KLF4 Nuclear Export Requires ERK Activation and Initiates Exit from Naive Pluripotency.

Project description:Cooperative action of a transcription factor complex containing OCT4, SOX2, NANOG, and KLF4 maintains the naive pluripotent state; however, less is known about the mechanisms that disrupt this complex, initiating exit from pluripotency. We show that, as embryonic stem cells (ESCs) exit pluripotency, KLF4 protein is exported from the nucleus causing rapid decline in Nanog and Klf4 transcription; as a result, KLF4 is the first pluripotency transcription factor removed from transcription-associated complexes during differentiation. KLF4 nuclear export requires ERK activation, and phosphorylation of KLF4 by ERK initiates interaction of KLF4 with nuclear export factor XPO1, leading to KLF4 export. Mutation of the ERK phosphorylation site in KLF4 (S132) blocks KLF4 nuclear export, the decline in Nanog, Klf4, and Sox2 mRNA, and differentiation. These findings demonstrate that relocalization of KLF4 to the cytoplasm is a critical first step in exit from the naive pluripotent state and initiation of ESC differentiation.

| S-EPMC6000723 | biostudies-literature

Gain of CTCF-Anchored Chromatin Loops Marks the Exit from Naive Pluripotency.

Project description:The genome of pluripotent stem cells adopts a unique three-dimensional architecture featuring weakly condensed heterochromatin and large nucleosome-free regions. Yet, it is unknown whether structural loops and contact domains display characteristics that distinguish embryonic stem cells (ESCs) from differentiated cell types. We used genome-wide chromosome conformation capture and super-resolution imaging to determine nuclear organization in mouse ESC and neural stem cell (NSC) derivatives. We found that loss of pluripotency is accompanied by widespread gain of structural loops. This general architectural change correlates with enhanced binding of CTCF and cohesins and more pronounced insulation of contacts across chromatin boundaries in lineage-committed cells. Reprogramming NSCs to pluripotency restores the unique features of ESC domain topology. Domains defined by the anchors of loops established upon differentiation are enriched for developmental genes. Chromatin loop formation is a pervasive structural alteration to the genome that accompanies exit from pluripotency and delineates the spatial segregation of developmentally regulated genes.

| S-EPMC6327227 | biostudies-literature

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