Jun Zhou

TL;DR: It is shown that mRNAs containing N(6)-methyladenosine (m(6)A) in their 5' UTR can be translated in a cap-independent manner, and that diverse cellular stresses induce a transcriptome-wide redistribution of m( 6)A, resulting in increased numbers of m RNAs with 5'UTR m(6), which bypasses 5' cap-binding proteins to promote translation under stresses.

TL;DR: The elucidation of the dynamic features of 5′UTR methylation and its critical role in cap-independent translation not only expands the breadth of physiological roles of m6A, but also uncovers a previously unappreciated translational control mechanism in heat shock response.

TL;DR: A base-resolution m1A profiling method is developed, based onm1A-induced misincorporation during reverse transcription, and distinct classes of m1 a methylome are revealed in the human transcriptome, providing a resource for functional studies of m 1A-mediated epitranscriptomic regulation.

TL;DR: It is reported that N6-methyladenosine (m6A) facilitates mRNA translation that is resistant to eIF4F inactivation, and ABCF1 is identified as a critical mediator of m6A-promoted translation under both stress and physiological conditions.

TL;DR: It is reported that, in response to amino acid starvation, the reinitiation of ATF4 is not only governed by the eIF2α signaling pathway, but is also subjected to regulation by mRNA methylation in the form of N6-methyladenosine (m6A).