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N6-methyladenosine modulate second cell fate decision by enhancing mRNA stability of pivotal transcription factors during primitive endoderm development [mESC_RNA-seq]

ABSTRACT: Transcription factors (TFs) have key roles in cell fate determination, and are rapidly upregulated to fulfill developmental functions. During second cell fate decisions in pre-implantation embryonic development, upregulated key TFs, including GATA6 and NANOG, drive the differentiation and functional establishment of primitive endoderm (PrE) and epiblast (EPI) cells. However, how the embryo achieves this swift TF upregulation and the precise molecular mechanisms underlying specific TF initiation remain unclear. In this study, we showed how N6-methyladenosine (m6A) affected embryo and embryoid differentiation. Using two types of extended pluripotent mouse embryonic stem cells with in vivo embryonic and extraembryonic potency-extended pluripotent stem cells (EPSCs) and totipotent blastomere-like cells (TBLCs) alongside mouse embryos, we observed that the m6A writers METTL3 and VIRMA were essential for PrE development. Mechanistically, globally increased mRNA stability occurred during embryo development - mediated by m6A modification. Specifically, m6A enhanced key regulator stability during PrE differentiation, such as Gata6, by interacting with the m6A reader IGF2BP3, thereby promoting protein production and ultimately impacting on cell fate decisions. Our results suggest that post-transcriptional mRNA regulation is a pioneering mechanism governing second cell fate decisions, and highlights the molecular mechanisms underlying mouse embryogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE325527 | GEO | 2026/03/23

REPOSITORIES: GEO

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N6-methyladenosine modulate second cell fate decision by enhancing mRNA stability of pivotal transcription factors during primitive endoderm development [TBLC_RNAseq]

Project description:Transcription factors (TFs) have key roles in cell fate determination, and are rapidly upregulated to fulfill developmental functions. During second cell fate decisions in pre-implantation embryonic development, upregulated key TFs, including GATA6 and NANOG, drive the differentiation and functional establishment of primitive endoderm (PrE) and epiblast (EPI) cells. However, how the embryo achieves this swift TF upregulation and the precise molecular mechanisms underlying specific TF initiation remain unclear. In this study, we showed how N6-methyladenosine (m6A) affected embryo and embryoid differentiation. Using two types of extended pluripotent mouse embryonic stem cells with in vivo embryonic and extraembryonic potency-extended pluripotent stem cells (EPSCs) and totipotent blastomere-like cells (TBLCs) alongside mouse embryos, we observed that the m6A writers METTL3 and VIRMA were essential for PrE development. Mechanistically, globally increased mRNA stability occurred during embryo development - mediated by m6A modification. Specifically, m6A enhanced key regulator stability during PrE differentiation, such as Gata6, by interacting with the m6A reader IGF2BP3, thereby promoting protein production and ultimately impacting on cell fate decisions. Our results suggest that post-transcriptional mRNA regulation is a pioneering mechanism governing second cell fate decisions, and highlights the molecular mechanisms underlying mouse embryogenesis.

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Rapid redistribution and extensive co-binding of NANOG and GATA6 at shared regulatory elements underlie specification of divergent cell fates [RNA-seq]

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Rapid redistribution and extensive co-binding of NANOG and GATA6 at shared regulatory elements underlie specification of divergent cell fates [CUT&TAG, CUT&RUN]

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Rapid redistribution and extensive cobinding of NANOG and GATA6 at shared regulatory elements underlie specification of divergent cell fates [reChIP]

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Rapid redistribution and extensive co-binding of NANOG and GATA6 at shared regulatory elements underlie specification of divergent cell fates [Hi-C]

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Rapid redistribution and extensive co-binding of NANOG and GATA6 at shared regulatory elements underlie specification of divergent cell fates [ChIP-seq]

2021-07-30 | GSE181097 | GEO

Molecular and epistatic interactions between pioneer transcription factors shape nucleosome dynamics and cell differentiation [MNase-seq]

Project description:Pioneer transcription factors (TF) bind nucleosome-embedded DNA motifs to activate new regulatory elements and promote differentiation. However, the complexity, binding dependencies and temporal effects of their action remain unclear. Here, we dissect how ectopic induction of the pioneer TF GATA6 triggers Primitive Endoderm (PrE) differentiation from pluripotent cells. We show that transient GATA6 binding exploits accessible regions to decommission enhancers and promote pluripotency gene silencing. Simultaneously, GATA6 targets closed chromatin and initiates extensive remodeling culminating in the establishment of fragile nucleosomes flanked by ordered nucleosome arrays and increased accessibility. This is enhanced by rapidly expressed PrE TFs (SOX17) and by pluripotency TFs repurposed for differentiation (OCT4/SOX2). Accordingly, depletion of OCT4 during GATA6 induction decreases Gata6 expression, alters GATA6 and SOX17 binding and impairs differentiation. Therefore, pioneer TFs orchestrate complex regulatory networks involving many if not all available pioneer TFs, including those required to support the original identity of differentiating cells.

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