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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

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

ORGANISM(S): Mus musculus

PROVIDER: GSE207565 | GEO | 2023/04/18

REPOSITORIES: GEO

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A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ATAC-Seq]

Project description:Cooperative DNA binding of transcription factors (TFs) integrates external stimuli and context across tissues and time. Naïve mouse embryonic stem cells (ESCs) are derived from early development and can sustain early embryonic pluripotent identity indefinitely. Here we ask whether TFs associated with pluripotency evolved to directly support this state or if it emerges from their combinatorial action? NANOG and ESRRB are key pluripotency factors that co-bind DNA. We find that when both factors are expressed at physiological levels, ESRRB supports pluripotency. However, when NANOG is not present, ESRRB supports a bistable culture of embryo-like primitive endoderm identity ancillary to pluripotency. The stochiometry between these factors quantitatively influences differentiation and in silico modelling of bipartite TF activity suggests ESRRB safeguards plasticity in differentiation. Thus the concerted activity of cooperative TFs transforms their effect to sustain intermediate cell identities that can be expanded ex vivo as highly stable stem cell models.

2023-04-18 | GSE207563 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

2023-04-18 | GSE207562 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [RNA-Seq]

2023-04-18 | GSE207560 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

2023-04-18 | GSE207564 | GEO

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation

| PRJNA856230 | ENA

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [scRNA-Seq]

| PRJNA856234 | ENA

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [RNA-Seq]

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [RNA-Seq]

| PRJNA856237 | ENA

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ChIP-Seq]

| PRJNA856236 | ENA

A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ATAC-Seq]

Project description:A Bipartate function of ESRRB integrates signaling over time to balance self-renewal and differentiation [ATAC-Seq]

| PRJNA856235 | ENA

Esrrb is a pivotal target of the Gsk3/Tcf3 axis regulating embryonic stem cell self-renewal.

Project description:Inhibition of glycogen synthase kinase-3 (Gsk3) supports mouse embryonic stem cells (ESCs) by modulating Tcf3, but the critical targets downstream of Tcf3 are unclear. We analyzed the intersection between genome localization and transcriptome data sets to identify genes repressed by Tcf3. Among these, manipulations of Esrrb gave distinctive phenotypes in functional assays. Knockdown and knockout eliminated response to Gsk3 inhibition, causing extinction of pluripotency markers and loss of colony forming capability. Conversely, forced expression phenocopied Gsk3 inhibition or Tcf3 deletion by suppressing differentiation and sustaining self-renewal. Thus the nuclear receptor Esrrb is necessary and sufficient to mediate self-renewal downstream of Gsk3 inhibition. Leukaemia inhibitory factor (LIF) regulates ESCs through Stat3, independently of Gsk3 inhibition. Consistent with parallel operation, ESCs in LIF accommodated Esrrb deletion and remained pluripotent. These findings highlight a key role for Esrrb in regulating the naive pluripotent state and illustrate compensation among the core pluripotency factors.

| S-EPMC3465555 | biostudies-literature

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