Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency [RNA-Seq]

ABSTRACT: Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency [RNA-Seq]

PROVIDER: PRJNA495847 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8034210_1.fastq.gz	Fastqsanger.gz
	SRR8034210_2.fastq.gz	Fastqsanger.gz
	SRR8034220_1.fastq.gz	Fastqsanger.gz
	SRR8034220_2.fastq.gz	Fastqsanger.gz
	SRR8034230_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 64

Similar Datasets

Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency

Project description:Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency

| PRJNA504653 | ENA

Three Transcription Factor Functions Empower Formative Transition from Naïve Pluripotency [ChIP-Seq]

Project description:The gene regulatory network in naïve mouse embryonic stem cells (ESC) is reconfigured to enable lineage commitment. Tcf3 sanctions rewiring to formative pluripotency by suppressing components of the ESC transcription factor circuitry. However, Tcf3 depletion only delays, and does not prevent transition. Here we delineate major contributions of Ets-family transcription factor Etv5 and the repressor Rbpj. ERK signalling triggers genome relocation of Etv5 to commission formative pluripotency enhancers. Concomitant up-regulation of Rbpj prevents reversion by repressing potent naïve factors, Nanog and Tbx3. Triple deletion of Etv5, Rbpj and Tcf3 disables naïve ESC, such that they remain undifferentiated and locked in self-renewal even in the presence of differentiation stimuli. Thus, pluripotency dynamics are driven by combined action of two repressors that respectively dissolve and extinguish the naive network, and an activator that initiates transcription of formative network genes. Similar tripartite modality might be a general requirement for robust cell state transitions.

2019-05-09 | GSE122239 | GEO

Three Transcription Factor Functions Empower Formative Transition from Naïve Pluripotency [ChIP-Seq]

Project description:Three Transcription Factor Functions Empower Formative Transition from Naïve Pluripotency [ChIP-Seq]

| PRJNA504298 | ENA

Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency [RNA-Seq]

Project description:The gene regulatory network in naïve mouse embryonic stem cells (ESCs) must be reconfigured for lineage competence. Tcf3 enables rewiring to formative pluripotency by repressing components of the ESC transcription factor circuitry. However, elimination of Tcf3 only delays, and does not prevent, state transition. Here we delineate distinct contributions of the Ets-family transcription factor Etv5 and the repressor Rbpj. Downstream of Erk1/2 signalling, Etv5 activates enhancers for formative pluripotency. Concomitant up-regulation of Rbpj ensures irreversible exit from the naïve state by extinguishing reversal factors, Nanog and Tbx3. Triple deletion of Etv5, Rbpj and Tcf3 incapacitates ESCs, such that they remain undifferentiated and locked in self-renewal even in the presence of differentiation stimuli. Thus, pluripotency progression is driven hierarchically by two repressors, that respectively dissolve and extinguish the naive network, and an initiator that commissions the formative network. Similar tripartite action may be a general mechanism for efficient cell transitions.

2019-05-09 | GSE121148 | GEO

Cooperative genetic networks drive embryonic stem cell transition from naïve to formative pluripotency

Project description:In the mammalian embryo, epiblast cells must exit the naïve state and acquire formative pluripotency. This cell state transition is recapitulated by mouse embryonic stem cells (ESCs), which undergo pluripotency progression in defined conditions in vitro. However, our understanding of the molecular cascades and gene networks involved in the exit from naïve pluripotency remains fragmentary. Here, we employed a combination of genetic screens in haploid ESCs, CRISPR/Cas9 gene disruption, large-scale transcriptomics and computational systems biology to delineate the regulatory circuits governing naïve state exit. Transcriptome profiles for 73 ESC lines deficient for regulators of the exit from naïve pluripotency predominantly manifest delays on the trajectory from naïve to formative epiblast. We find that gene networks operative in ESCs are also active during transition from pre- to post-implantation epiblast in utero. We identified 496 naïve state-associated genes tightly connected to the in vivo epiblast state transition and largely conserved in primate embryos. Integrated analysis of mutant transcriptomes revealed funnelling of multiple gene activities into discrete regulatory modules. Finally, we delineate how intersections with signalling pathways direct this pivotal mammalian cell state transition.

2020-12-22 | GSE145653 | GEO

FoxO transcription factors actuate the formative pluripotency specific gene expression programme [ChIP-Seq]

Project description:Naïve pluripotency is sustained by a self-reinforcing gene regulatory network (GRN) comprising core and naïve pluripotency-specific transcription factors (TFs). Upon exiting naïve pluripotency, ES cells transition through a formative post-implantation-like pluripotent state. However, the mechanisms underlying disengagement from the naïve GRN and initiation of the formative GRN remain unclear. Here, we demonstrate that phosphorylated AKT acts as a gatekeeper that prevents nuclear localization of FoxO TFs in naïve ESCs. PTEN-mediated reduction of AKT activity allows nuclear entry by FoxO TFs, enforcing a cell fate transition by binding and activating formative pluripotency-specific enhancers. Indeed, FoxO TFs are necessary and sufficient for transition from the naïve to the formative pluripotent state. Our work uncovers a pivotal role for FoxO TFs and AKT signalling in mechanisms underlying the exit from naïve pluripotency, a critical early embryonic cell fate transition.

2024-07-25 | GSE253479 | GEO

FoxO transcription factors actuate the formative pluripotency specific gene expression programme [RNA-Seq]

2024-07-25 | GSE253473 | GEO

FoxO transcription factors actuate the formative pluripotency specific gene expression programme [ATAC-Seq]

2024-07-25 | GSE253472 | GEO

Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-09 | GSE122338 | GEO

Cnot8 Eliminates Naïve Regulation Networks and Is Essential for Naïve-to-Formative Pluripotency Transition (RNA-Seq)

Project description:The transition of mammalian early epiblast at different phases is characterized by the differences of pluripotent states and developmental potential, involving extensive transcriptome changes. However, the role of post-transcriptional RNA degradation modulation in cell fate transition remains largely unexplored. Here, we report that deadenylase Cnot8 of Ccr4-Not complex specifically plays a role in naïve-to-formative transition of pluripotent stem cells (PSCs). Disruption of Cnot8 results in early embryonic lethality, accompanying with the increased expression levels of naïve transcription factors in mouse epiblasts. Cnot8 depletion leads to accumulated expression abundances and increased poly(A) tail lengths of massive transcripts including mRNAs of naïve regulation networks, impairing the naïve-to-formative pluripotency conversion. Mechanistically, Cnot8 interacts with Tob1 and Pabpc1 to guarantee the prompt mRNA deadenylation and degradation of naïve regulation networks at specific time. Together, these findings delineate the mechanism underlying PSC fate transition through global degradation of mRNAs for naïve regulation networks by Cnot8.

2022-05-11 | GSE174424 | 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