N6-methyladenosine modification is not a general trait of viral RNA genomes

Belinda Baquero-Pérez, Ivaylo D. Yonchev, Anna Delgado-Tejedor, Rebeca Medina, Mireia Puig-Torrents, Ian Sudbery, Oguzhan Begik, Stuart A. Wilson (), Eva Maria Novoa () and Juana Díez ()
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Belinda Baquero-Pérez: Universitat Pompeu Fabra
Ivaylo D. Yonchev: The University of Sheffield, Firth Court, Western Bank
Anna Delgado-Tejedor: The Barcelona Institute of Science and Technology
Rebeca Medina: The Barcelona Institute of Science and Technology
Mireia Puig-Torrents: Universitat Pompeu Fabra
Ian Sudbery: The University of Sheffield, Firth Court, Western Bank
Oguzhan Begik: The Barcelona Institute of Science and Technology
Stuart A. Wilson: The University of Sheffield, Firth Court, Western Bank
Eva Maria Novoa: The Barcelona Institute of Science and Technology
Juana Díez: Universitat Pompeu Fabra

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract Despite the nuclear localization of the m6A machinery, the genomes of multiple exclusively-cytoplasmic RNA viruses, such as chikungunya (CHIKV) and dengue (DENV), are reported to be extensively m6A-modified. However, these findings are mostly based on m6A-Seq, an antibody-dependent technique with a high rate of false positives. Here, we address the presence of m6A in CHIKV and DENV RNAs. For this, we combine m6A-Seq and the antibody-independent SELECT and nanopore direct RNA sequencing techniques with functional, molecular, and mutagenesis studies. Following this comprehensive analysis, we find no evidence of m6A modification in CHIKV or DENV transcripts. Furthermore, depletion of key components of the host m6A machinery does not affect CHIKV or DENV infection. Moreover, CHIKV or DENV infection has no effect on the m6A machinery’s localization. Our results challenge the prevailing notion that m6A modification is a general feature of cytoplasmic RNA viruses and underscore the importance of validating RNA modifications with orthogonal approaches.

Date: 2024
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DOI: 10.1038/s41467-024-46278-9

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