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Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency

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

ORGANISM(S): Mus musculus

PROVIDER: GSE122338 | GEO | 2019/05/09

REPOSITORIES: GEO

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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

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.

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Three Transcription Factor Functions Empower Progression from Naïve to Formative Pluripotency

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

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

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

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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]

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FoxO transcription factors actuate the formative pluripotency specific gene expression programme

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

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Glutamine Metabolism Regulates the Pluripotency Transcription Factor OCT4.

Project description:The molecular mechanisms underlying the regulation of pluripotency by cellular metabolism in human embryonic stem cells (hESCs) are not fully understood. We found that high levels of glutamine metabolism are essential to prevent degradation of OCT4, a key transcription factor regulating hESC pluripotency. Glutamine withdrawal depletes the endogenous antioxidant glutathione (GSH), which results in the oxidation of OCT4 cysteine residues required for its DNA binding and enhanced OCT4 degradation. The emergence of the OCT4(lo) cell population following glutamine withdrawal did not result in greater propensity for cell death. Instead, glutamine withdrawal during vascular differentiation of hESCs generated cells with greater angiogenic capacity, thus indicating that modulating glutamine metabolism enhances the differentiation and functional maturation of cells. These findings demonstrate that the pluripotency transcription factor OCT4 can serve as a metabolic-redox sensor in hESCs and that metabolic cues can act in concert with growth factor signaling to orchestrate stem cell differentiation.

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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.

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Cnot8 Eliminates Naïve Regulation Networks and Is Essential for Naïve-to-Formative Pluripotency Transition [scRNA-Seq]

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