Next Article in Journal
HBV-Integration Studies in the Clinic: Role in the Natural History of Infection
Next Article in Special Issue
Serological and Molecular Investigation of Batai Virus Infections in Ruminants from the State of Saxony-Anhalt, Germany, 2018
Previous Article in Journal
Liquid Biomolecular Condensates and Viral Lifecycles: Review and Perspectives
Previous Article in Special Issue
Recent Advances in Bunyavirus Glycoprotein Research: Precursor Processing, Receptor Binding and Structure
Open AccessArticle

The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing

1
Division of Biological Sciences, University of Montana, Missoula, MT 59812, USA
2
Department of Chemistry and Biochemistry, University of Montana, Missoula, MT 59812, USA
3
Center for Biomolecular Structure and Dynamics, University of Montana, Missoula, MT 59812, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editors: Esther Schnettler and Benjamin Brennan
Viruses 2021, 13(3), 367; https://doi.org/10.3390/v13030367
Received: 16 January 2021 / Revised: 16 February 2021 / Accepted: 22 February 2021 / Published: 26 February 2021
(This article belongs to the Special Issue Bunyavirus 2020)
In recent years, transcriptome profiling studies have identified changes in host splicing patterns caused by viral invasion, yet the functional consequences of the vast majority of these splicing events remain uncharacterized. We recently showed that the host splicing landscape changes during Rift Valley fever virus MP-12 strain (RVFV MP-12) infection of mammalian cells. Of particular interest, we observed that the host mRNA for Rio Kinase 3 (RIOK3) was alternatively spliced during infection. This kinase has been shown to be involved in pattern recognition receptor (PRR) signaling mediated by RIG-I like receptors to produce type-I interferon. Here, we characterize RIOK3 as an important component of the interferon signaling pathway during RVFV infection and demonstrate that RIOK3 mRNA expression is skewed shortly after infection to produce alternatively spliced variants that encode premature termination codons. This splicing event plays a critical role in regulation of the antiviral response. Interestingly, infection with other RNA viruses and transfection with nucleic acid-based RIG-I agonists also stimulated RIOK3 alternative splicing. Finally, we show that specifically stimulating alternative splicing of the RIOK3 transcript using a morpholino oligonucleotide reduced interferon expression. Collectively, these results indicate that RIOK3 is an important component of the mammalian interferon signaling cascade and its splicing is a potent regulatory mechanism capable of fine-tuning the host interferon response. View Full-Text
Keywords: Rift Valley fever virus; MP-12; RIOK3; innate immune response; alternative splicing; morpholino oligonucleotide Rift Valley fever virus; MP-12; RIOK3; innate immune response; alternative splicing; morpholino oligonucleotide
Show Figures

Figure 1

MDPI and ACS Style

Havranek, K.E.; White, L.A.; Bisom, T.C.; Lanchy, J.-M.; Lodmell, J.S. The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing. Viruses 2021, 13, 367. https://doi.org/10.3390/v13030367

AMA Style

Havranek KE, White LA, Bisom TC, Lanchy J-M, Lodmell JS. The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing. Viruses. 2021; 13(3):367. https://doi.org/10.3390/v13030367

Chicago/Turabian Style

Havranek, Katherine E.; White, Luke A.; Bisom, Thomas C.; Lanchy, Jean-Marc; Lodmell, J. S. 2021. "The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing" Viruses 13, no. 3: 367. https://doi.org/10.3390/v13030367

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop