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基于 N6-甲基腺苷的转录后表观遗传学机制调控 N-端甲基转移酶 1。

Modulation of N-terminal methyltransferase 1 by an N-methyladenosine-based epitranscriptomic mechanism.

机构信息

Environmental Toxicology Graduate Program, University of California, Riverside, United States.

Department of Chemistry, University of California, Riverside, United States.

出版信息

Biochem Biophys Res Commun. 2021 Mar 26;546:54-58. doi: 10.1016/j.bbrc.2021.01.088. Epub 2021 Feb 6.

Abstract

Protein α-N-methylation is an evolutionarily conserved type of post-translational modification; however, little is known about the regulatory mechanisms for this modification. Methylation at the N position of adenosine in mRNAs is dynamic and modulates their stability, splicing, and translational efficiency. Here, we found that the expression of N-terminal methyltransferase 1 (NTMT1) protein is altered by depletion of those genes encoding the reader/writer/eraser proteins of N-methyladenosine (mA). We also observed that MRG15 is N-terminally methylated by NTMT1, and this methylation could also be modulated by reader/writer/eraser proteins of mA. Together, these results revealed a novel mA-based epitranscriptomic mechanism in regulating protein N-terminal methylation.

摘要

蛋白质α-N-甲基化是一种进化上保守的翻译后修饰类型;然而,对于这种修饰的调控机制知之甚少。mRNA 中腺苷 N 位的甲基化是动态的,调节其稳定性、剪接和翻译效率。在这里,我们发现 N-端甲基转移酶 1(NTMT1)蛋白的表达因编码 N-甲基腺苷(mA)的读取器/写入器/擦除器蛋白的基因缺失而改变。我们还观察到 MRG15 被 NTMT1 进行 N 端甲基化,并且这种甲基化也可以被 mA 的读取器/写入器/擦除器蛋白调节。综上所述,这些结果揭示了一种新的基于 mA 的转录后修饰机制,用于调节蛋白质 N 端甲基化。

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