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METTL3-dependent m6A modification programs human neural progenitor cell proliferation

ABSTRACT: METTL3-dependent m6A modification programs human neural progenitor cell proliferation

PROVIDER: PRJNA1013796 | ENA |

REPOSITORIES: ENA

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METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RIP-seq]

Project description:METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RIP-seq]

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METTL3-dependent m6A modification programs human neural progenitor cell proliferation [MeRIP-seq]

Project description:METTL3-dependent m6A modification programs human neural progenitor cell proliferation [MeRIP-seq]

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METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RNA-seq]

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METTL3-mediated m6A modification is required for cerebellar development m6A modification and cerebellar development

Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant modification on mRNAs and plays important roles in various biological processes. The formation of m6A is catalyzed by a methyltransferase complex including methyltransferase like 3 (METTL3) as a key factor. However, the in vivo functions of METTL3 and m6A modification in mammalian development remain unclear. Here we show that specific inactivation of Mettl3 in mouse nervous system causes severe developmental defects in the brain. Mettl3 conditional knockout mice manifest cerebellar hypoplasia caused by drastically enhanced apoptosis of new born cerebellar granule cells (CGCs) in the external granular layer (EGL). METTL3 depletion induced loss of m6A modification causes extended RNA half-lives and aberrant splicing events, consequently leading to dysregulation of transcriptome-wide gene expression and premature CGC death. Our findings reveal a critical role of METTL3-mediated m6A in regulating the development of mammalian cerebellum.

2018-07-15 | GSE100528 | GEO

Examing the m6A modification in control or METTL3 knockdown BGC823 cells

Project description:To investigate the role of METTL3-mediated m6A modification, we performed m6A-sequencing to map the m6A modification in control or METTL3 knockdown BGC823 cells.

2019-10-29 | GSE133132 | GEO

m6A RNA modification controls cell fate transition in mammalian embryonic stem cells (RNA methylation)

Project description:Here we determine the map of RNA methylation (m6A) in mouse embrionic stem cells, and Mettl3 knock out cells Examination of m6A modification sites on the transcriptome of mouse Embryonic stem cells and Embryonic Mettl3 knock out cells, using a m6A specific antibody.

2014-10-16 | E-GEOD-52662 | biostudies-arrayexpress

METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RNA-seq]

Project description:To investigate whether the role of METTL3 in hNPCs is dependent on its m6A activity,samples form neural progenitor cell (NPC) differentiation in the small molecule-assisted shut-off (SMASh) tagged hESC groups were collected. Gene expression levels were quantitated by RNA-seq analysis, and the potential target genes were identified by MeRIP-seq analysis and RIP-seq.

2023-11-22 | GSE242521 | GEO

METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RIP-seq]

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METTL3-dependent m6A modification programs human neural progenitor cell proliferation [MeRIP-seq]

2023-11-22 | GSE242519 | GEO

Mettl3-m6A-YTHDF1 axis promotion of mitochondrial dysfunction in metabolic dysfunction–associated steatotic liver disease (MASLD)

Project description:The N6-methyladenosine (m6A) mRNA modification and the mitochondrial respiratory chain (MRC) hold paramount importance in the advancement of MASLD. This study thoroughly investigates the relationship and impact of m6A mRNA modification and mitochondrial function in the progression of MASLD. Here we report that the mRNA and protein levels of mitochondrial respiratory chain (MRC) subunits showed inconsistent trends in vivo experiments. Abnormal m6A modification and mitochondrial dysfunction in MASLD were attributed to the upregulation of methyltransferase like 3 (Mettl3) and the downregulation of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) induced by high-fat foods. Mettl3 promoted the MRC's function. However, knockout of the reader protein YTHDF1, which plays a crucial role in the m6A modification process, counteracted the effect of Mettl3 and suppressed MRC. In MASLD, damage to the MRC may be regulated by the Mettl3-m6A-YTHDF1 complex axis, especially by the role of YTHDF1. Our research has offered a novel perspective on the involvement of m6A mRNA methylation in the pathogenesis of MASLD.

2024-09-20 | PXD047819 | Pride

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