| Literature DB >> 33563981 |
Sung-Yeon Hwang1,2, Hyunchul Jung3, Seyoung Mun4,5,6, Sungwon Lee1,2, Kiwon Park1,2, S Chan Baek1,2, Hyungseok C Moon7, Hyewon Kim1,2, Baekgyu Kim1,2, Yongkuk Choi1,2, Young-Hyun Go8, Wanxiangfu Tang9, Jongsu Choi10, Jung Kyoon Choi3, Hyuk-Jin Cha8, Hye Yoon Park7, Ping Liang9, V Narry Kim1,2, Kyudong Han11,12,13, Kwangseog Ahn14,15.
Abstract
L1 retrotransposons can pose a threat to genome integrity. The host has evolved to restrict L1 replication. However, mechanisms underlying L1 propagation out of the host surveillance remains unclear. Here, we propose an evolutionary survival strategy of L1, which exploits RNA m6A modification. We discover that m6A 'writer' METTL3 facilitates L1 retrotransposition, whereas m6A 'eraser' ALKBH5 suppresses it. The essential m6A cluster that is located on L1 5' UTR serves as a docking site for eukaryotic initiation factor 3 (eIF3), enhances translational efficiency and promotes the formation of L1 ribonucleoprotein. Furthermore, through the comparative analysis of human- and primate-specific L1 lineages, we find that the most functional m6A motif-containing L1s have been positively selected and became a distinctive feature of evolutionarily young L1s. Thus, our findings demonstrate that L1 retrotransposons hijack the RNA m6A modification system for their successful replication.Entities:
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Year: 2021 PMID： 33563981 PMCID： PMC7873242 DOI： 10.1038/s41467-021-21197-1
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919