m6 A修饰在病毒感染宿主细胞中的调节作用
The Regulatory Role of m6A Modification in Viral Infection of Host Cells
夏月平 1黄芬1
作者信息
- 1. 昆明理工大学生命科学与技术学院&医学院,昆明 650500
- 折叠
摘要
N6-甲基腺苷(N6-methyladenosine,m6A)是指RNA分子腺嘌呤第6位氮原子上发生的甲基化修饰,是信使RNA(mRNA)和非编码RNA(ncRNA)中最常见的转录后修饰.m6A修饰在RNA循环的所有阶段,包括RNA稳定、剪接、核输出、折叠、翻译和降解等过程中发挥重要作用,这一过程需甲基转移酶(writers)、去甲基酶(erasers)和m6A阅读蛋白(readers)的参与.随着RNA高通量测序技术的不断发展,m6A修饰参与病毒与宿主互作中的研究不断涌现.研究表明m6A修饰发生在多种RNA病毒中,影响病毒感染、复制及子代病毒粒子的生成.病毒也可通过改变宿主细胞转录物组的m6A修饰影响病毒的感染性或宿主对病毒的抵抗性.本文对呼吸道病毒、反转录病毒、疱疹病毒等感染宿主细胞造成的m6A修饰进行概述,并针对m6A修饰对病毒的复制及对宿主免疫反应的调节作用进行综述,为了解病毒与宿主互作机制研究及抗病毒药物筛选供理论基础.
Abstract
N6-methyladenosine(m6A)is a methylation modification on the 6th nitrogen atom of the RNA molecule adenine,and is the most common post-transcriptional modification in messenger RNA(mRNA)and non-coding RNA(ncRNA).m6A modification plays a crucial role in all stage of RNA cy-cle,including RNA stabilization,splicing,nuclear export,folding,translation and degradation.m6A modification requires the participation of methyltransferase(writers),demethylase(erasers)and m6 A readers.The important roles of m6A modification involved in virus-host interactions have been largely ex-plored based on the rapid development of high-throughput RNA sequencing technology.Studies have shown that m6A modification participates in a variety of viral RNAs,and is associated with viral en-trance,replication and progeny virion release.Viruses can also alter host transcriptome by m6A modifica-tion to impact viral infectivity or host resistance.This review explored the role of m6A modification in re-spiratory virus,retrovirus and herpes virus,etc.infected cells,and the regulatory effects of m6A modifi-cations on viral replication and host immune response.It will help to further clarify the mechanisms of vi-rus-host interactions and benefit the development of antiviral drugs.
关键词
N6-methyladenosine(m6A)/m6A甲基转移酶/m6A去甲基酶/m6A阅读蛋白/病毒Key words
N6-methyladenosine(m6A)/m6A methyltransferase/m6A demethylase/m6A reading pro-teins/virus引用本文复制引用
基金项目
国家自然科学基金资助项目(82260396)
云南省自然科学基金资助项目(202401AS070057)
出版年
2024