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Status |
Public on Jun 21, 2021 |
Title |
Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing |
Organisms |
Homo sapiens; Human immunodeficiency virus 1 |
Experiment type |
Other
|
Summary |
Several prior reports have demonstrated that the epitranscriptomic addition of m6A to viral transcripts promotes the replication and pathogenicity of a wide range of viruses yet the underlying mechanism(s) causing this positive effect has remained unclear. It is known that m6A function is largely mediated by cellular m6A binding proteins or readers, however, how these m6A reader proteins contribute to the regulation of HIV-1 gene expression has remained controversial. Here, we confirm that m6A indeed enhances HIV-1 gene expression. We demonstrate that this effect is collectively mediated by the cytoplasmic reader YTHDF2, which increases HIV-1 transcript stability, and the nuclear m6A reader YTHDC1, which binds HIV-1 RNA at 7 distinct m6A methylated sites, regulating viral transcript alternative splicing.
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Overall design |
GFP (control) or YTHDC1 PAR-CLIP on HIV-1-infected CD4+ 293T cells.
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Contributor(s) |
Tsai K, Cullen BR |
Citation(s) |
34140354 |
Submission date |
Jan 25, 2021 |
Last update date |
Sep 20, 2021 |
Contact name |
Kevin Tsai |
E-mail(s) |
kevtsai@ibms.sinica.edu.tw
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Organization name |
Academia Sinica
|
Department |
Institute of Biomedical Sciences
|
Lab |
R414
|
Street address |
128 Sec. 2, Academia Rd. Nankang
|
City |
Taipei |
ZIP/Postal code |
115 |
Country |
Taiwan |
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Platforms (1) |
GPL18160 |
Illumina HiSeq 2000 (Homo sapiens; Human immunodeficiency virus 1) |
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Samples (3) |
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Relations |
BioProject |
PRJNA694663 |
SRA |
SRP303180 |