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Mus musculus

ABSTRACT: m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (RNA-Seq)

PROVIDER: PRJNA262910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1596110_1.fastq.gz	Fastqsanger.gz
	SRR1596110_2.fastq.gz	Fastqsanger.gz
	SRR1596111_1.fastq.gz	Fastqsanger.gz
	SRR1596111_2.fastq.gz	Fastqsanger.gz
	SRR1596112_1.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (m6a-seq)

| PRJNA262906 | ENA

Mus musculus

Project description:m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (3p-Seq)

| PRJNA262905 | ENA

Mus musculus

Project description:m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (Ribo-seq)

| PRJNA262909 | ENA

m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation

Project description:m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation

| PRJNA262908 | ENA

METTL3-dependent m6A RNA Methylation Regulates Transposable Elements and Represses Human Naïve Pluripotency through Transposable Element-derived Enhancers

Project description:N6-methyladenosine (m6A) is the most prevalent mRNA modification with diverse regulatory roles in mammalian cells. While its functions are well-documented in mouse embryonic stem cells (mESCs), its role in human pluripotent stem cells (hPSCs) remains to be fully explored. METTL3 is the main enzyme responsible for m6A deposition. Here, using a METTL3 inducible knockout (iKO) system, we uncovered that, unlike in mESCs, METTL3 was indispensable for hPSC maintenance. Importantly, loss of METTL3 caused significant upregulation of pluripotency factors including naïve pluripotency genes and failure to exit pluripotency, thus impaired stem cell differentiation towards embryonic and extraembryonic cells including trophoblasts. Mechanistically, METTL3 iKO in hPSCs substantially increased expression and enhancer activities of two primate-specific transposable elements (TEs), SVA_D and HERVK/LTR5_Hs, which are normally modified by METTL3-dependent m6A. METTL3 loss activated SVA_D by lowering H3K9me3 deposition, and increased chromatin accessibility at LTR5_Hs through the naïve and other pluripotency factors. Conversely, we discovered that the activated SVA_D and LTR5_Hs loci positively regulated naïve gene expression by directly interacted with their promoters. These findings thus reveal that METTL3-dependent m6A RNA methylation has critical roles in suppressing TE expression and in the human pluripotency regulatory network.

2025-05-07 | PXD056046 | Pride

m6A RNA Methylation is Critical for Adequate Exit from Naïve Pluripotency and Execution of Mammalian Development (Ribo-seq)

Project description:In this study we identify Mettl3, an m6A RNA modification writer, as a critical regulator for terminating naïve pluripotency and a positive maintainer of primed pluripotency in vitro and in vivo. Remarkably, Mettl3 knockout pre-implantation epiblasts and naïve ES cells, entirely lack m6A on coding mRNAs and are viable. Yet, they fail to adequately terminate the naïve pluripotent state, and subsequently undergo aberrant priming and early lineage commitment at the post-implantation stage. A comprehensive functional and genomic analysis involving profiling of m6A, RNA transcription and translation in Mettl3 wild-type and knockout pluripotent and differentiated cells, identified m6A as a critical determinant that destabilizes secondary naïve specific pluripotency genes Esrrb, Klf4 and Nanog, and restrains their transcript stability and translation efficiency. In summary, our findings provide for the first time evidence for a critical role for an mRNA epigenetic modification in early mammalian development in vivo, and identify a mechanism that functionally regulates mouse naïve and primed pluripotency in an opposing manner. Ribosome footprint (Ribo-Seq) was measured from mouse embryonic stem cells and mouse embriod bodies, in WT and Mettl3-KO cell lines.

2014-11-02 | E-GEOD-61996 | biostudies-arrayexpress

m6A RNA Methylation is Critical for Adequate Exit from Naïve Pluripotency and Execution of Mammalian Development (RNA-Seq)

Project description:In this study we identify Mettl3, an m6A RNA modification writer, as a critical regulator for terminating naïve pluripotency and a positive maintainer of primed pluripotency in vitro and in vivo. Remarkably, Mettl3 knockout pre-implantation epiblasts and naïve ES cells, entirely lack m6A on coding mRNAs and are viable. Yet, they fail to adequately terminate the naïve pluripotent state, and subsequently undergo aberrant priming and early lineage commitment at the post-implantation stage. A comprehensive functional and genomic analysis involving profiling of m6A, RNA transcription and translation in Mettl3 wild-type and knockout pluripotent and differentiated cells, identified m6A as a critical determinant that destabilizes secondary naïve specific pluripotency genes Esrrb, Klf4 and Nanog, and restrains their transcript stability and translation efficiency. In summary, our findings provide for the first time evidence for a critical role for an mRNA epigenetic modification in early mammalian development in vivo, and identify a mechanism that functionally regulates mouse naïve and primed pluripotency in an opposing manner. polyA RNA-seq was measured in mouse embryonic stem cells (ESCs) and embroid bodies (EBs), each in WT and in Mettl3-KO cell lines. RNA-seq was measured also from WT mouse embronic fibroblasts (MEF). 3 biological replicates are available from ESCs and 2 from EBs. Replicate C in ESCs was measured alongside protein levels (SILAC) and was used for the analysis of that assay.

2014-11-02 | E-GEOD-61997 | biostudies-arrayexpress

Mus musculus

Project description:mRNA cap methylation in pluripotency and differentiation

| PRJNA322696 | ENA

m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (Ribo-seq)

Project description:Naïve and primed pluripotent states retain distinct molecular properties, yet limited knowledge exists on how their state transitions are regulated. Here we identify Mettl3, an N6-Methyladenosine (m6A) transferase, as a regulator for terminating murine naïve pluripotency. Mettl3 knockout pre-implantation epiblasts and naïve embryonic stem cells (ESCs) are depleted for m6A in mRNAs and yet, are viable. However, they fail to adequately terminate their naïve state, and subsequently undergo aberrant and restricted lineage priming at the post-implantation stage, leading to early embryonic lethality. m6A predominantly and directly reduces mRNA stability, including that of key naïve pluripotency promoting transcripts. This study highlights a critical role for an mRNA epigenetic modification in vivo, and identifies regulatory modules that functionally influence naïve and primed pluripotency in an opposing manner.

2014-11-02 | GSE61996 | GEO

m6A mRNA Methylation Facilitates Resolution of Naïve Pluripotency Towards Differentiation (RNA-Seq)

Project description:Naïve and primed pluripotent states retain distinct molecular properties, yet limited knowledge exists on how their state transitions are regulated. Here, we identify Mettl3, an N6-methyladenosine (m6A) transferase, as a regulator for terminating murine naïve pluripotency. Mettl3 knockout pre-implantation epiblasts and naïve embryonic stem cells (ESCs) are depleted for m6A in mRNAs and yet, are viable. However, they fail to adequately terminate their naïve state, and subsequently undergo aberrant and restricted lineage priming at the post-implantation stage, leading to early embryonic lethality. m6A predominantly and directly reduces mRNA stability, including that of key naïve pluripotency promoting transcripts. This study highlights a critical role for an mRNA epigenetic modification in vivo, and identifies regulatory modules that functionally influence naïve and primed pluripotency in an opposing manner.

2014-11-02 | GSE61997 | GEO

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