Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE86818 | GEO | 2016/10/18

SECONDARY ACCESSION(S): PRJNA342617

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Nono, a Bivalent Domain Factor, Regulates Erk Signaling and Mouse Embryonic Stem Cell Pluripotency.

Project description: Not available

| S-EPMC5086807 | biostudies-literature

Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency [ChIP-Seq]

Project description:Here we report that NONO, a nuclear para-speckle component, instead functions as a chromatin regulator in mESCs acting in the ERK signaling pathway to regulate the balance between ground state versus mESCs primed for differentiation. NONO loss increases a \u201cground-like\u201d population of mESCs favoring self-renewal and more resist to differentiation, partially mimicking the effects of 2i. Mechanistically, NONO and ERK mainly co-binds a subset of development related, bivalent genes. Importantly, NONO and ERK reciprocally regulate one another, i.e. NONO regulates ERK activation while ERK controls NONO chromatin association, forming a self-reinforcing feedback loop. Our findings thus reveal a cell intrinsic mechanism involving NONO and ERK, which impact the balance between self-renewal and differentiation, respectively.

2016-10-18 | GSE73426 | GEO

Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency [RNA-Seq]

Project description:Here we report that Nono instead functions as a chromatin regulator cooperating with Erk to regulate mESC pluripotency. We demonstrate that Nono loss leads to robust self-renewing mESCs with enhanced expression of Nanog and Klf4, epigenome and transcriptome re-patterning to a “ground-like state” with global reduction of H3K27me3 and DNA methylation resembling the Erk inhibitor PD03 treated mESCs and 2i (both GSK and Erk kinase inhibitors)-induced “ground state”. Mechanistically, Nono and Erk co-bind at a subset of development-related, bivalent genes. Ablation of Nono compromises Erk activation and RNA polymerase II C-terminal Domain serine 5 phosphorylation, and while inactivation of Erk evicts Nono from chromatin, revealing reciprocal regulation. Furthermore, Nono loss results in a compromised activation of its target bivalent genes upon differentiation and the differentiation itself. These findings reveal an unanticipated role of Nono in collaborating with Erk signaling to regulate the integrity of bivalent domain and mESC pluripotency.

2016-10-18 | GSE86817 | GEO

Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency

Project description:Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency

| PRJNA342617 | ENA

CDK1-PDK1-PI3K/Akt signaling pathway regulates embryonic and induced pluripotency.

Project description: Not available

| S-EPMC5260505 | biostudies-literature

The pluripotency factor Nanog regulates pericentromeric heterochromatin organization in mouse embryonic stem cells.

Project description: Not available

| S-EPMC4863740 | biostudies-literature

Nodal signaling regulates the bone morphogenic protein pluripotency pathway in mouse embryonic stem cells.

Project description: Not available