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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE282841 | GEO | 2026/03/20

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.

2026-03-23 | GSE283382 | GEO

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

2026-03-23 | GSE282543 | GEO

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

2026-03-23 | GSE325527 | GEO

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

2026-03-23 | GSE282840 | GEO

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

Project description:N6-methyladenosine modulate second cell fate decision by enhancing mRNA stability of pivotal transcription factors during primitive endoderm development

| PRJNA1190595 | ENA

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

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

| PRJNA1193564 | ENA

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

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

| PRJNA1189118 | ENA

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

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

| PRJNA1440409 | ENA

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

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

| PRJNA1190591 | ENA

N6-methyladenosine triggers renal fibrosis via enhancing translation and stability of ZEB2 mRNA.

Project description:In recent years, a surge in studies investigating N6-methyladenosine (m6A) modification in human diseases has occurred. However, the specific roles and mechanisms of m6A in kidney disease remain incompletely understood. This study revealed that m6A plays a positive role in regulating renal fibrosis (RF) by inducing epithelial-to-mesenchymal phenotypic transition (EMT) in renal tubular cells. Through comprehensive analyses, including m6A sequencing, RNA-seq, and functional studies, we confirmed the pivotal involvement of zinc finger E-box binding homeobox 2 (ZEB2) in m6A-mediated RF and EMT. Notably, the m6A-modified coding sequence of ZEB2 mRNA significantly enhances its translational elongation and mRNA stability by interacting with the YTHDF1/eEF-2 complex and IGF2BP3, respectively. Moreover, targeted demethylation of ZEB2 mRNA using the dm6ACRISPR system substantially decreases ZEB2 expression and disrupts the EMT process in renal tubular epithelial cells. In vivo and clinical data further support the positive influence of m6A/ZEB2 on RF progression. Our findings highlight the m6A-mediated regulation of RF through ZEB2, revealing a novel therapeutic target for RF treatment and enhancing our understanding of the impact of mRNA methylation on kidney disease.

| S-EPMC11381876 | biostudies-literature

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