m3C32 tRNA modification controls serine codon-biased mRNA translation, cell cycle, and DNA-damage response
文献类型： 外文期刊
作者： Cui, Jia 1 ; Sendinc, Erdem 1 ; Liu, Qi 1 ; Kim, Sujin 1 ; Fang, Jaden Y. 1 ; Gregory, Richard I. 1 ;
作者机构： 1.Boston Childrens Hosp, Div Hematol Oncol, Stem Cell Program, Boston, MA 02115 USA
2.Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA
3.Guangdong Acad Agr Sci, Rice Res Inst, Guangzhou 510640, Guangdong, Peoples R China
4.Guangdong Key Lab New Technol Rice Breeding, Guangzhou 510640, Guangdong, Peoples R China
5.Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA
6.Harvard Initiat RNA Med, Boston, MA 02215 USA
7.Harvard Stem Cell Inst, Cambridge, MA 02138 USA
期刊名称：NATURE COMMUNICATIONS （ 影响因子：14.7； 五年影响因子：16.1 ）
ISSN：
年卷期： 2024 年 15 卷 1 期
页码：
收录情况： SCI
摘要： The epitranscriptome includes a diversity of RNA modifications that influence gene expression. N3-methylcytidine (m(3)C) mainly occurs in the anticodon loop (position C32) of certain tRNAs yet its role is poorly understood. Here, using HAC-Seq, we report comprehensive METTL2A/2B-, METTL6-, and METTL2A/2B/6-dependent m(3)C profiles in human cells. METTL2A/2B modifies tRNA-arginine and tRNA-threonine members, whereas METTL6 modifies the tRNA-serine family. However, decreased m(3)C32 on tRNA-Ser-GCT isodecoders is only observed with combined METTL2A/2B/6 deletion. Ribo-Seq reveals altered translation of genes related to cell cycle and DNA repair pathways in METTL2A/2B/6-deficient cells, and these mRNAs are enriched in AGU codons that require tRNA-Ser-GCT for translation. These results, supported by reporter assays, help explain the observed altered cell cycle, slowed proliferation, and increased cisplatin sensitivity phenotypes of METTL2A/2B/6-deficient cells. Thus, we define METTL2A/2B/6-dependent methylomes and uncover a particular requirement of m(3)C32 tRNA modification for serine codon-biased mRNA translation of cell cycle, and DNA repair genes.
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