Journal
CELL RESEARCH
Volume 31, Issue 4, Pages 404-414Publisher
SPRINGERNATURE
DOI: 10.1038/s41422-020-00465-7
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Funding
- National Natural Science Foundation of China [82041044, 21825701, U1702282, 91940304]
- National Key RD Program [2020YFA0707801, 2019YFA0110900, 2019YFA0802200]
- Peking University Fund for SARS-CoV-2
- International Innovation Resource Cooperation Project, Bejing Municipal Science and Technology Commission [Z201100008320024]
- China Postdoctoral Science Foundation [2020M680217]
- National Science Fund for Distinguished Young Scholar [81925025]
- NSFC [81621005]
- CAMS Innovation Fund for Medical Sciences [2019-I2M-5-049]
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The study found that SARS-CoV-2 genomic RNA is dynamically N-6-methyladenosine (m(6)A)-modified in human and monkey cells, and the m(6)A methylation negatively regulates SARS-CoV-2 infection. SARS-CoV-2 infection triggers a global increase in host m(6)A methylome.
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-6-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.
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