Abstract：
:N(6)-methyladenosine (m(6)A) is the most abundant internal modification in mammalian mRNA. This modification is reversible and non-stoichiometric and adds another layer to the dynamic control of mRNA metabolism. The stability of m(6)A-modified mRNA is regulated by an m(6)A reader protein, human YTHDF2, which recognizes m(6)A and reduces the stability of target transcripts. Looking at additional functional roles for the modification, we find that another m(6)A reader protein, human YTHDF1, actively promotes protein synthesis by interacting with translation machinery. In a unified mechanism of m(6)A-based regulation in the cytoplasm, YTHDF2-mediated degradation controls the lifetime of target transcripts, whereas YTHDF1-mediated translation promotion increases translation efficiency, ensuring effective protein production from dynamic transcripts that are marked by m(6)A. Therefore, the m(6)A modification in mRNA endows gene expression with fast responses and controllable protein production through these mechanisms.
journal_name
Celljournal_title
Cellauthors
Wang X,Zhao BS,Roundtree IA,Lu Z,Han D,Ma H,Weng X,Chen K,Shi H,He Cdoi
10.1016/j.cell.2015.05.014subject
Has Abstractpub_date
2015-06-04 00:00:00pages
1388-99issue
6eissn
0092-8674issn
1097-4172pii
S0092-8674(15)00562-0journal_volume
161pub_type
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