期刊
CELL STEM CELL
卷 15, 期 6, 页码 707-719出版社
CELL PRESS
DOI: 10.1016/j.stem.2014.09.019
关键词
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资金
- California Institute for Regenerative Medicine
- NIH [R01-CA118750, DK090122]
- MGH Start-Up Funds
- MGH ECOR [2013A051178]
- Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA Research Award
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 30 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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