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HIV-1 Infection Reduces NAD Capping of Host Cell snRNA and snoRNA
B. Benoni, JF. Potužník, A. Škríba, R. Benoni, J. Trylcova, M. Tulpa, K. Spustová, K. Grab, MB. Mititelu, J. Pačes, J. Weber, D. Stanek, J. Kowalska, L. Bednarova, Z. Keckesova, P. Vopalensky, L. Gahurova, H. Cahova
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
- MeSH
- HIV infekce * virologie metabolismus MeSH
- HIV-1 * MeSH
- lidé MeSH
- malá jadérková RNA * metabolismus genetika MeSH
- NAD * metabolismus MeSH
- RNA čepičky metabolismus MeSH
- RNA malá jaderná * metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Nicotinamide adenine dinucleotide (NAD) is a critical component of the cellular metabolism and also serves as an alternative 5' cap on various RNAs. However, the function of the NAD RNA cap is still under investigation. We studied NAD capping of RNAs in HIV-1-infected cells because HIV-1 is responsible for the depletion of the NAD/NADH cellular pool and causing intracellular pellagra. By applying the NAD captureSeq protocol to HIV-1-infected and uninfected cells, we revealed that four snRNAs (e.g., U1) and four snoRNAs lost their NAD cap when infected with HIV-1. Here, we provide evidence that the presence of the NAD cap decreases the stability of the U1/HIV-1 pre-mRNA duplex. Additionally, we demonstrate that reducing the quantity of NAD-capped RNA by overexpressing the NAD RNA decapping enzyme DXO results in an increase in HIV-1 infectivity. This suggests that NAD capping is unfavorable for HIV-1 and plays a role in its infectivity.
1st Faculty of Medicine Charles University Kateřinská 32 121 08 Prague Czechia
Division of Biophysics Faculty of Physics University of Warsaw Pasteura 5 02 093 Warsaw Poland
Faculty of Science Department of Cell Biology Charles University Viničná 7 121 08 Prague 2 Czechia
Citace poskytuje Crossref.org
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- $a Nicotinamide adenine dinucleotide (NAD) is a critical component of the cellular metabolism and also serves as an alternative 5' cap on various RNAs. However, the function of the NAD RNA cap is still under investigation. We studied NAD capping of RNAs in HIV-1-infected cells because HIV-1 is responsible for the depletion of the NAD/NADH cellular pool and causing intracellular pellagra. By applying the NAD captureSeq protocol to HIV-1-infected and uninfected cells, we revealed that four snRNAs (e.g., U1) and four snoRNAs lost their NAD cap when infected with HIV-1. Here, we provide evidence that the presence of the NAD cap decreases the stability of the U1/HIV-1 pre-mRNA duplex. Additionally, we demonstrate that reducing the quantity of NAD-capped RNA by overexpressing the NAD RNA decapping enzyme DXO results in an increase in HIV-1 infectivity. This suggests that NAD capping is unfavorable for HIV-1 and plays a role in its infectivity.
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