RT Journal Article SR Electronic T1 Mettl14 is required for mouse post-implantation development by facilitating epiblast maturation JF bioRxiv FD Cold Spring Harbor Laboratory SP 294926 DO 10.1101/294926 A1 Tie-Gang Meng A1 Xukun Lu A1 Lei Guo A1 Guan-Mei Hou A1 Xue-Shan Ma A1 Qian-Nan Li A1 Lin Huang A1 Li-Hua Fan A1 Zheng-Hui Zhao A1 Xiang-Hong Ou A1 Ying-Chun OuYang A1 Heide Schatten A1 Lei Li A1 Zhen-Bo Wang A1 Qing-Yuan Sun YR 2018 UL http://biorxiv.org/content/early/2018/04/04/294926.abstract AB N6-methyladenosine (m6A) is the most prevalent and reversible internal modification of mammalian messenger and noncoding RNAs mediated by specific m6A writer, reader, and eraser proteins. As an m6A writer, the METTL3–METTL14-WTAP complex dynamically regulates m6A modification and plays important roles in diverse biological processes. However, our knowledge about the complete functions of this RNA methyltransferase complex, the contributions of each component to the methylation and their impacts on different biological pathways, are still very limited. Here, by employing both in vivo and in vitro models, we report that METTL14 was indispensable for post-implantation embryonic development by facilitating the conversion from naïve to primed state of the epiblast. Depletion of Mettl14 lead to conspicuous embryonic growth retardation from E6.5 mainly as a result of resistance to differentiation, which further lead to embryonic lethality early in gestation. Our data highlight the critical function of METTL14, as an m6A modification regulator, in orchestrating early mouse embryogenesis.