METTL3 Gains R/W Access to the Epitranscriptome

Ulrike Schumann; Andrew Shafik; Thomas Preiss

doi:10.1016/j.molcel.2016.04.024

METTL3 Gains R/W Access to the Epitranscriptome

Mol Cell. 2016 May 5;62(3):323-324. doi: 10.1016/j.molcel.2016.04.024.

Authors

Ulrike Schumann¹, Andrew Shafik¹, Thomas Preiss²

Affiliations

¹ EMBL - Australia Collaborating Group, Department of Genome Sciences, The John Curtin School of Medical Research (JCSMR), The Australian National University, Acton (Canberra), ACT 2601, Australia.
² EMBL - Australia Collaborating Group, Department of Genome Sciences, The John Curtin School of Medical Research (JCSMR), The Australian National University, Acton (Canberra), ACT 2601, Australia; Victor Chang Cardiac Research Institute, Darlinghurst (Sydney), NSW 2010, Australia. Electronic address: thomas.preiss@anu.edu.au.

PMID: 27153530
DOI: 10.1016/j.molcel.2016.04.024

Abstract

Epitranscriptomic marks are dynamically placed on mRNA by "writer" or "eraser" enzymes, while "readers" modulate their function accordingly. Lin et al. (2016) now report that the N6-methyladenosine:RNA methyltransferase METTL3 is both a writer and a reader, directly enhancing mRNA translation.

Publication types

Comment

MeSH terms

Methyltransferases / genetics
RNA / genetics*
RNA, Messenger / genetics*

Substances

RNA, Messenger
RNA
Methyltransferases