The m^(6)A methylome of SARS-CoV-2 in host cells

查看全文 作　　者：Jun’e [1,2,3]Liu;Yan-Peng [4]Xu;Kai [1,5,6]Li;Qing [4]Ye;Hang-Yu [7]Zhou;Hanxiao [1]Sun;Xiaoyu [1]Li;Liu [4]Yu;Yong-Qiang [4]Deng;Rui-Ting [4]Li;Meng-Li [4]Cheng;Bo [5,6]He;Jia [4]Zhou;Xiao-Feng [4]Li;Aiping [7]Wu;Chengqi [1,6,8]Yi;Cheng-Feng [4]Qin

机构地区：[1]State Key Laboratory of Protein and Plant Gene Research,School of Life Sciences,Peking University,Beijing,100871,China;[2]Beijing Advanced Innovation Center for Genomics(ICG),Peking University,Beijing,100871,China;[3]Biomedical Pioneering Innovation Center,Ministry of Education Key Laboratory of Cell Proliferation and Differentiation,Beijing,100871,China;[4]State Key Laboratory of Pathogen and Biosecurity,Beijing Institute of Microbiology and Epidemiology,Academy of Military Medical Sciences,Beijing,100071,China;[5]Academy for Advanced Interdisciplinary Studies,Peking University,Beijing,100871,China;[6]Peking-Tsinghua Center for Life Sciences,Peking University,Beijing,100871,China;[7]Suzhou Institute of System Medicine,Chinese Academy of Medical Sciences&Peking Union Medical College,Suzhou,Jiangsu,215000,China;[8]Department of Chemical Biology and Synthetic and Functional Biomolecules Center,College of Chemistry and Molecular Engineering,Peking University,Beijing,100871,China

出　　处：《Cell Research》索引2021年第31卷第4期,共11页

基　　金：This work was supported by the National Natural Science Foundation of China(82041044,21825701,U1702282 and 91940304);National Key R&D Program(2020YFA0707801,2019YFA0110900 and 2019YFA0802200);Peking University Fund for SARS-CoV-2,International Innovation Resource Cooperation Project,Bejing Municipal Science and Technology Commission(Z201100008320024 to C.Y.);China Postdoctoral Science Foundation(2020M680217 to J.L.).C.-F.Q.was supported by the National Science Fund for Distinguished Young Scholar(81925025);the Innovative Research Group(81621005)from the NSFC,and the CAMS Innovation Fund for Medical Sciences(2019-I2M-5-049). 摘　　要：The newly identified Severe Acute Respiratory Syndrome Coronavirus 2(SARS-CoV-2)has resulted in a global health emergency because of its rapid spread and high mortality.The molecular mechanism of interaction between host and viral genomic RNA is yet unclear.We demonstrate herein that SARS-CoV-2 genomic RNA,as well as the negative-sense RNA,is dynamically N6-methyladenosine(m^(6)A)-modified in human and monkey cells.Combined RIP-seq and miCLIP analyses identified a total of 8 m^(6)A sites at single-base resolution in the genome.Especially,epidemic strains with mutations at these identified m^(6)A sites have emerged worldwide,and formed a unique cluster in the US as indicated by phylogenetic analysis.Further functional experiments showed that m^(6)A methylation negatively regulates SARS-CoV-2 infection.SARS-CoV-2 infection also triggered a global increase in host m^(6)A methylome,exhibiting altered localization and motifs of m^(6)A methylation in mRNAs.Altogether,our results identify m^(6)A as a dynamic epitranscriptomic mark mediating the virus–host interaction. 关键词：ACUTE MORTALITY

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The m^(6)A methylome of SARS-CoV-2 in host cells

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