Viruses utilize a number of translational control mechanisms to regulate the relative expression levels of viral proteins on polycistronic mRNAs. One such mechanism, that of termination-dependent reinitiation, has been described in a number of both negative- and positive-strand RNA viruses. Dicistronic RNAs which exhibit termination–reinitiation typically have a start codon of the 3′-ORF (open reading frame) proximal to the stop codon of the upstream ORF. For example, the segment 7 RNA of influenza B is dicistronic, and the stop codon of the M1 ORF and the start codon of the BM2 ORF overlap in the pentanucleotide UAAUG (the stop codon of M1 is shown in bold and the start codon of BM2 is underlined). Recent evidence has highlighted the potential importance of mRNA–rRNA interactions in reinitiation on caliciviral and influenza B viral RNAs, probably used to tether 40S ribosomal subunits to the RNA after termination in time for initiation factors to be recruited to the AUG of the downstream ORF. The present review summarizes how such interactions regulate reinitiation in an array of RNA viruses, and discusses what is known about reinitiation in viruses that do not rely on apparent mRNA–rRNA interactions.
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Conference Article| November 24 2010
Translational termination–reinitiation in RNA viruses
Michael L. Powell
Michael L. Powell 1
1Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, U.K.
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Biochem Soc Trans (2010) 38 (6): 1558–1564.
June 04 2010
Michael L. Powell; Translational termination–reinitiation in RNA viruses. Biochem Soc Trans 1 December 2010; 38 (6): 1558–1564. doi: https://doi.org/10.1042/BST0381558
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