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. 2021 May 19;9:656849. doi: 10.3389/fcell.2021.656849

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Copyright © 2021 Sokpor, Xie, Nguyen and Tuoc.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of N⁶-methyladenosine (m⁶A) methylation on messenger RNA (mRNA) fate. (A) m⁶A modification regulates mRNA splicing and polyadenylation via YTHDC1 and its associating factors SRSF3, SRSF10, and CPSF6. (B) m⁶A modulates mRNA nuclear export through YTHDC1, SRSF3, and NXF1. (C) m⁶A regulates mRNA translation and stability via YTHDC2-mediated recruitment of the ribosome and the XRN1 exoribonuclease. (D) m⁶A marks are bound by IGFBPs, which can regulate a subset of mRNA translation, decay in P-body, and storage in stress granules. (E) m⁶A modification regulates mRNA degradation in P-body through associating with the YTHDF2-CCR4-NOT complex. (F) m⁶A marks on circRNA modulate its translation via recruiting YTHDF3. (G) m⁶A marks recruit YTHDF1/YTHDF3 to enhance translation in a Cap-dependent manner. (H) METTL3 serves as an m⁶A reader and increases translation via recruiting translation initiation complex independent of its methyltransferase activity. (I) m⁶A directly binds to eIF3 and increases translation in a Cap-independent manner.