APOBEC3B drives PKR-mediated translation shutdown and protects stress granules in response to viral infection

Lavanya Manjunath, Sunwoo Oh, Pedro Ortega, Alexis Bouin, Elodie Bournique, Ambrocio Sanchez, Pia Møller Martensen, Ashley A. Auerbach, Jordan T. Becker, Marcus Seldin, Reuben S. Harris, Bert L. Semler and Rémi Buisson ()
Additional contact information
Lavanya Manjunath: University of California Irvine
Sunwoo Oh: University of California Irvine
Pedro Ortega: University of California Irvine
Alexis Bouin: University of California Irvine
Elodie Bournique: University of California Irvine
Ambrocio Sanchez: University of California Irvine
Pia Møller Martensen: Aarhus University
Ashley A. Auerbach: University of Texas Health San Antonio
Jordan T. Becker: University of Minnesota – Twin Cities
Marcus Seldin: University of California Irvine
Reuben S. Harris: University of Texas Health San Antonio
Bert L. Semler: University of California Irvine
Rémi Buisson: University of California Irvine

Nature Communications, 2023, vol. 14, issue 1, 1-19

Abstract: Abstract Double-stranded RNA produced during viral replication and transcription activates both protein kinase R (PKR) and ribonuclease L (RNase L), which limits viral gene expression and replication through host shutoff of translation. In this study, we find that APOBEC3B forms a complex with PABPC1 to stimulate PKR and counterbalances the PKR-suppressing activity of ADAR1 in response to infection by many types of viruses. This leads to translational blockage and the formation of stress granules. Furthermore, we show that APOBEC3B localizes to stress granules through the interaction with PABPC1. APOBEC3B facilitates the formation of protein-RNA condensates with stress granule assembly factor (G3BP1) by protecting mRNA associated with stress granules from RNAse L-induced RNA cleavage during viral infection. These results not only reveal that APOBEC3B is a key regulator of different steps of the innate immune response throughout viral infection but also highlight an alternative mechanism by which APOBEC3B can impact virus replication without editing viral genomes.

Date: 2023
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-023-36445-9 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-36445-9

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-36445-9

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().