tetano
Editor, Senior Moderator
Cell Res
. 2021 Jan 28.
doi: 10.1038/s41422-020-00465-7. Online ahead of print.
The m [SUP]6[/SUP] A methylome of SARS-CoV-2 in host cells
Jun'e Liu[SUP] #[/SUP][SUP] 1 2 3 [/SUP], Yan-Peng Xu[SUP] #[/SUP][SUP] 4 [/SUP], Kai Li[SUP] #[/SUP][SUP] 1 5 6 [/SUP], Qing Ye[SUP] #[/SUP][SUP] 4 [/SUP], Hang-Yu Zhou[SUP] #[/SUP][SUP] 7 [/SUP], Hanxiao Sun[SUP] 1 [/SUP], Xiaoyu Li[SUP] 1 [/SUP], Liu Yu[SUP] 4 [/SUP], Yong-Qiang Deng[SUP] 4 [/SUP], Rui-Ting Li[SUP] 4 [/SUP], Meng-Li Cheng[SUP] 4 [/SUP], Bo He[SUP] 5 6 [/SUP], Jia Zhou[SUP] 4 [/SUP], Xiao-Feng Li[SUP] 4 [/SUP], Aiping Wu[SUP] 7 [/SUP], Chengqi Yi[SUP] 8 9 10 [/SUP], Cheng-Feng Qin[SUP] 11 [/SUP]
Affiliations
Abstract
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 N[SUP]6[/SUP]-methyladenosine (m[SUP]6[/SUP]A)-modified in human and monkey cells. Combined RIP-seq and miCLIP analyses identified a total of 8 m[SUP]6[/SUP]A sites at single-base resolution in the genome. Especially, epidemic strains with mutations at these identified m[SUP]6[/SUP]A sites have emerged worldwide, and formed a unique cluster in the US as indicated by phylogenetic analysis. Further functional experiments showed that m[SUP]6[/SUP]A methylation negatively regulates SARS-CoV-2 infection. SARS-CoV-2 infection also triggered a global increase in host m[SUP]6[/SUP]A methylome, exhibiting altered localization and motifs of m[SUP]6[/SUP]A methylation in mRNAs. Altogether, our results identify m[SUP]6[/SUP]A as a dynamic epitranscriptomic mark mediating the virus-host interaction.
. 2021 Jan 28.
doi: 10.1038/s41422-020-00465-7. Online ahead of print.
The m [SUP]6[/SUP] A methylome of SARS-CoV-2 in host cells
Jun'e Liu[SUP] #[/SUP][SUP] 1 2 3 [/SUP], Yan-Peng Xu[SUP] #[/SUP][SUP] 4 [/SUP], Kai Li[SUP] #[/SUP][SUP] 1 5 6 [/SUP], Qing Ye[SUP] #[/SUP][SUP] 4 [/SUP], Hang-Yu Zhou[SUP] #[/SUP][SUP] 7 [/SUP], Hanxiao Sun[SUP] 1 [/SUP], Xiaoyu Li[SUP] 1 [/SUP], Liu Yu[SUP] 4 [/SUP], Yong-Qiang Deng[SUP] 4 [/SUP], Rui-Ting Li[SUP] 4 [/SUP], Meng-Li Cheng[SUP] 4 [/SUP], Bo He[SUP] 5 6 [/SUP], Jia Zhou[SUP] 4 [/SUP], Xiao-Feng Li[SUP] 4 [/SUP], Aiping Wu[SUP] 7 [/SUP], Chengqi Yi[SUP] 8 9 10 [/SUP], Cheng-Feng Qin[SUP] 11 [/SUP]
Affiliations
- PMID: 33510385
- DOI: 10.1038/s41422-020-00465-7
Abstract
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 N[SUP]6[/SUP]-methyladenosine (m[SUP]6[/SUP]A)-modified in human and monkey cells. Combined RIP-seq and miCLIP analyses identified a total of 8 m[SUP]6[/SUP]A sites at single-base resolution in the genome. Especially, epidemic strains with mutations at these identified m[SUP]6[/SUP]A sites have emerged worldwide, and formed a unique cluster in the US as indicated by phylogenetic analysis. Further functional experiments showed that m[SUP]6[/SUP]A methylation negatively regulates SARS-CoV-2 infection. SARS-CoV-2 infection also triggered a global increase in host m[SUP]6[/SUP]A methylome, exhibiting altered localization and motifs of m[SUP]6[/SUP]A methylation in mRNAs. Altogether, our results identify m[SUP]6[/SUP]A as a dynamic epitranscriptomic mark mediating the virus-host interaction.