Epitranscriptomic addition of m⁶A regulates HIV-1 RNA stability and alternative splicing.

ABSTRACT: Previous work has demonstrated that the epitranscriptomic addition of m⁶A to viral transcripts can promote the replication and pathogenicity of a wide range of DNA and RNA viruses, including HIV-1, yet the underlying mechanisms responsible for this effect have remained unclear. It is known that m⁶A function is largely mediated by cellular m⁶A binding proteins or readers, yet how these regulate viral gene expression in general, and HIV-1 gene expression in particular, has been controversial. Here, we confirm that m⁶A addition indeed regulates HIV-1 RNA expression and demonstrate that this effect is largely mediated by the nuclear m⁶A reader YTHDC1 and the cytoplasmic m⁶A reader YTHDF2. Both YTHDC1 and YTHDF2 bind to multiple

SUBMITTER: Tsai K 

PROVIDER: S-EPMC8247604 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature