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M6A RNA modification controls cell fate transition in mouse embryonic stem cells (gene expression analysis)

ABSTRACT: Here we determine the map of RNA methylation (m6A) in mouse embryonic stem cells, and embryoid bodies.

ORGANISM(S): Mus musculus

PROVIDER: GSE52680 | GEO | 2014/10/16

SECONDARY ACCESSION(S): PRJNA229783

REPOSITORIES: GEO

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m6A RNA modification controls cell fate transition in mouse embryonic stem cells (gene expression analysis)

Project description:Here we determine the map of RNA methylation (m6A) in mouse embryonic stem cells, and embryoid bodies. Gene expression analysis: To establish the impact of METTL3 loss of function on gene expression in mESC. RNA hybridized to GeneChip Mouse Exon 1.0 ST Array

2014-10-16 | E-GEOD-52680 | biostudies-arrayexpress

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.

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

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2014-10-16 | GSE52662 | GEO

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 3’ 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 ESC’s 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.

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-16 | E-GEOD-52681 | biostudies-arrayexpress

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

Project description:m6A RNA modification controls cell fate transition in mouse embryonic stem cells

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-10-16 | GSE52681 | GEO

m(6)A RNA modification controls cell fate transition in mammalian embryonic stem cells.

Project description:N6-methyl-adenosine (m(6)A) 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 m(6)A by mapping the m(6)A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m(6)A modification, including transcripts encoding core pluripotency transcription factors. m(6)A is enriched over 3' 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 m(6)A methylases, led to m(6)A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESC exit from self-renewal toward differentiation into several lineages in vitro and in vivo. Thus, m(6)A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages.

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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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