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首页> 外文期刊>Nature structural & molecular biology >RNA cytosine methylation by Dnmt2 and NSun2 promotes tRNA stability and protein synthesis
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RNA cytosine methylation by Dnmt2 and NSun2 promotes tRNA stability and protein synthesis

机译：Dnmt2和NSun2的RNA胞嘧啶甲基化促进tRNA稳定性和蛋白质合成

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The function of cytosine-C5 methylation, a widespread modification of tRNAs, has remained obscure, particularly in mammals. We have now developed a mouse strain defective in cytosine-C5 tRNA methylation, by disrupting both the Dnmt2 and the NSun2 tRNA methyltransferases. Although the lack of either enzyme alone has no detectable effects on mouse viability, double mutants showed a synthetic lethal interaction, with an underdeveloped phenotype and impaired cellular differentiation. tRNA methylation analysis of the double-knockout mice demonstrated complementary target-site specificities for Dnmt2 and NSun2 and a complete loss of cytosine-C5 tRNA methylation. Steady-state levels of unmethylated tRNAs were substantially reduced, and loss of Dnmt2 and NSun2 was further associated with reduced rates of overall protein synthesis. These results establish a biologically important function for cytosine-C5 tRNA methylation in mammals and suggest that this modification promotes mouse development by supporting protein synthesis.
机译：胞嘧啶-C5甲基化（tRNA的广泛修饰）的功能仍然不清楚，特别是在哺乳动物中。现在，我们通过破坏Dnmt2和NSun2 tRNA甲基转移酶，开发了胞嘧啶C5 tRNA甲基化缺陷的小鼠品系。尽管单独缺少这两种酶都无法检测到对小鼠生存力的影响，但双突变体显示出合成的致命相互作用，具有不发达的表型和受损的细胞分化。对双敲除小鼠的tRNA甲基化分析表明，Dnmt2和NSun2具有互补的靶位点特异性，并且胞嘧啶-C5 tRNA甲基化完全丧失。未甲基化的tRNA的稳态水平大大降低，Dnmt2和NSun2的丧失进一步与总体蛋白质合成速率降低有关。这些结果为哺乳动物的胞嘧啶-C5 tRNA甲基化建立了生物学上重要的功能，并表明这种修饰通过支持蛋白质合成促进小鼠发育。

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