Abstract
The mechanism leading to reinitiation of translation after termination of protein synthesis in eukaryotes has not yet been resolved in detail. One open question concerns the way the post-termination ribosome is tethered to the mRNA to allow binding of the necessary initiation factors. In caliciviruses, a family of positive strand RNA viruses, the capsid protein VP2 is translated via a termination/reinitiation process. VP2 of the feline calicivirus is encoded in the 3'-terminal open reading frame 3 (ORF3) that overlaps with the preceding ORF2 by four nucleotides. In transient expression studies, the efficiency of VP2 expression was 20 times lower than that of the ORF2 proteins. The close vicinity of the ORF2 termination signal and the ORF3 AUG codon was crucial, whereas the AUG could be replaced by alternative codons. Deletion mapping revealed that the 3'-terminal 69 nucleotides of ORF2 are crucial for VP2 expression. This sequence contains two essential sequence motifs. The first motif is conserved among caliciviruses and complementary to part of the 18 S rRNA. In conclusion, VP2 is expressed in a translation termination/reinitiation process that is special because it requires a sequence element that could prevent dissociation of post-termination ribosomes via hybridization with 18 S rRNA.
Highlights
Several alternative mechanisms have been identified that lead to the start of translation
Caliciviruses are special with regard to initiation of viral protein translation because they seem to use VPg as kind of a cap substitute that interacts with translation initiation factors [27,28,29]
VP1 Is Expressed with Much Higher Efficiency Than VP2— The FCV capsid proteins are encoded by two ORFs that overlap by four nucleotides and are contained in the genomic and the subgenomic mRNA (sg mRNA) (Fig. 1)
Summary
Caliciviruses are special with regard to initiation of viral protein translation because they seem to use VPg as kind of a cap substitute that interacts with translation initiation factors [27,28,29]. The small 3Ј-terminal ORF of rabbit hemorrhagic disease virus (RHDV) was shown to be translated according to a novel termination/reinitiation mechanism, dependent on an RNA element upstream of the start/stop site [25]. The present report shows that the 3Ј-terminal ORF3 of the feline calicivirus is initiated by a termination/reinitiation mechanism dependent on an upstream sequence element. Deletion analyses were conducted to identify crucial elements in this sequence, which were further characterized, so that a functional model could be proposed
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