| Literature DB >> 35511947 |
Jiangbo Wei1,2, Xianbin Yu1,2, Lei Yang3,4, Xuelian Liu3, Boyang Gao1,2, Boxian Huang5, Xiaoyang Dou1,2, Jun Liu1,2, Zhongyu Zou1,2, Xiao-Long Cui1,2, Li-Sheng Zhang1,2, Xingsen Zhao6,7, Qinzhe Liu1,2, P Cody He1,2, Caraline Sepich-Poore1,2, Nicole Zhong1,2, Wenqiang Liu4, Yanhe Li4, Xiaochen Kou3, Yanhong Zhao3, You Wu3, Xuejun Cheng6,7, Chuan Chen3, Yiming An3, Xueyang Dong1,2, Huanyu Wang1,2, Qiang Shu6, Ziyang Hao1,2, Tao Duan4, Yu-Ying He8, Xuekun Li6,7, Shaorong Gao3,4, Yawei Gao3, Chuan He1,2.
Abstract
N6-methyladenosine (m6A) is the most abundant internal modification on mammalian messenger RNA. It is installed by a writer complex and can be reversed by erasers such as the fat mass and obesity-associated protein FTO. Despite extensive research, the primary physiological substrates of FTO in mammalian tissues and development remain elusive. Here, we show that FTO mediates m6A demethylation of long-interspersed element-1 (LINE1) RNA in mouse embryonic stem cells (mESCs), regulating LINE1 RNA abundance and the local chromatin state, which in turn modulates the transcription of LINE1-containing genes. FTO-mediated LINE1 RNA m6A demethylation also plays regulatory roles in shaping chromatin state and gene expression during mouse oocyte and embryonic development. Our results suggest broad effects of LINE1 RNA m6A demethylation by FTO in mammals.Entities:
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Year: 2022 PMID： 35511947 DOI： 10.1126/science.abe9582
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 63.714