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m(6)A RNA modification controls cell fate transition in mammalian embryonic stem cells.
Batista, Pedro J; Molinie, Benoit; Wang, Jinkai; Qu, Kun; Zhang, Jiajing; Li, Lingjie; Bouley, Donna M; Lujan, Ernesto; Haddad, Bahareh; Daneshvar, Kaveh; Carter, Ava C; Flynn, Ryan A; Zhou, Chan; Lim, Kok-Seong; Dedon, Peter; Wernig, Marius; Mullen, Alan C; Xing, Yi; Giallourakis, Cosmas C; Chang, Howard Y.
Affiliation
  • Batista PJ; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Molinie B; Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
  • Wang J; Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  • Qu K; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Zhang J; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Li L; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Bouley DM; Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Lujan E; Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Haddad B; Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Daneshvar K; Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
  • Carter AC; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Flynn RA; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Zhou C; Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
  • Lim KS; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Dedon P; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Wernig M; Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
  • Mullen AC; Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
  • Xing Y; Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: yxing@ucla.edu.
  • Giallourakis CC; Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Electronic address: cgiallourakis@mgh.harvard.edu.
  • Chang HY; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: howchang@stanford.edu.
Cell Stem Cell ; 15(6): 707-19, 2014 Dec 04.
Article in En | MEDLINE | ID: mdl-25456834
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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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Adenine / Homeodomain Proteins / Embryonic Stem Cells / Methyltransferases Limits: Animals / Female / Humans Language: En Journal: Cell Stem Cell Year: 2014 Document type: Article Affiliation country: United States Country of publication: United States
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Adenine / Homeodomain Proteins / Embryonic Stem Cells / Methyltransferases Limits: Animals / Female / Humans Language: En Journal: Cell Stem Cell Year: 2014 Document type: Article Affiliation country: United States Country of publication: United States