PUBLICATION

Cap-specific terminal N6-methylation of RNA by an RNA polymerase II-associated methyltransferase

Authors
Akichika, S., Hirano, S., Shichino, Y., Suzuki, T., Nishimasu, H., Ishitani, R., Sugita, A., Hirose, Y., Iwasaki, S., Nureki, O., Suzuki, T.
ID
ZDB-PUB-200522-32
Date
2019
Source
Science (New York, N.Y.)   363(6423): (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Transcription Initiation Site
  • Humans
  • Methylation
  • Nuclear Proteins/chemistry*
  • RNA Polymerase II/chemistry*
  • RNA Caps/chemistry*
  • Mass Spectrometry
  • HEK293 Cells
  • Methyltransferases/chemistry*
  • Gene Knockout Techniques
  • Protein Biosynthesis
  • Adaptor Proteins, Signal Transducing/chemistry*
  • Protein Domains
PubMed
30467178 Full text @ Science
Abstract
N6-methyladenosine (m6A), a major modification of messenger RNAs (mRNAs), plays critical roles in RNA metabolism and function. In addition to the internal m6A, N6, 2'-O-dimethyladenosine (m6Am) is present at the transcription start nucleotide of capped mRNAs in vertebrates. However, its biogenesis and functional role remain elusive. Using a reverse genetics approach, we identified PCIF1, a factor that interacts with the serine-5-phosphorylated carboxyl-terminal domain of RNA polymerase II, as a cap-specific adenosine methyltransferase (CAPAM) responsible for N6-methylation of m6Am. The crystal structure of CAPAM in complex with substrates revealed the molecular basis of cap-specific m6A formation. A transcriptome-wide analysis revealed that N6-methylation of m6Am promotes the translation of capped mRNAs. Thus, a cap-specific m6A writer promotes translation of mRNAs starting from m6Am.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
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Mapping