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Mettl3-dependent m6A modification in postnatal liver

ABSTRACT: Mettl3-dependent m6A modification in postnatal liver

PROVIDER: PRJNA812059 | ENA |

REPOSITORIES: ENA

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Mettl3-dependent m6A modification and mRNA expression in postnatal liver

Project description:Mettl3-dependent m6A modification and mRNA expression in postnatal liver

| PRJNA812055 | ENA

Mettl3-dependent m6A modification in postnatal liver

Project description:Liver-specific deficiency of Mettl3 causes liver injury. By performing RNA sequencing (RNA-seq) analysis on the Mettl3-deficient versus control livers, we identified the potential target genes that were closely associated with the liver phenotype in liver-specific Mettl3 knockout mice. RNA-seq analysis revealed extensive metabolic reprogramming in Mettl3-deficient livers. These results demonstrated that Mettl3 coordinates metabolic homeostasis and functional maturation during postnatal liver development.

2022-03-09 | GSE197799 | GEO

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

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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.

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Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

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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-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

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M6A-seq analysis of wild type and Mettl3-cKO liver tissues' transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in liver, we performed m6A-sequencing to map the m6A modification in liver tissues of wild type (WT) and liver-sepcific Mettl3-KO mice.

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

Project description:N6-methyl-adenosine (m6A) is the most abundant modification on messenger RNAs and is linked to human diseases, but its functions in mammalian development are poorly understood. Here we reveal the evolutionary conservation and function of m6A by mapping the m6A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m6A modification, including transcripts encoding core pluripotency transcription factors. m6A is enriched over 3M-bM-^@M-^Y untranslated regions at defined sequence motifs, and marks unstable transcripts, including transcripts turned over upon differentiation. Genetic inactivation or depletion of mouse and human Mettl3, one of the m6A methylases, led to m6A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESCM-bM-^@M-^Ys exit from self-renewal towards differentiation into several lineages in vitro and in vivo. Thus, m6A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages. Examing m6A modification differences in two different cell types

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