Key result
Structural analysis reveals that the Taura syndrome virus IRES initiates translation by placing a tRNA-mRNA-like structure in the ribosomal A site, leaving the P site unoccupied.
The study reveals a novel, initiator tRNA-independent mechanism of translation initiation by the Taura syndrome virus IRES.
Novel IRES mechanism bypasses initiator tRNA; leaves open its conservation and therapeutic relevance in viral translation.
In cap-dependent translation initiation, the open reading frame (ORF) of mRNA is established by the placement of the AUG start codon and initiator tRNA in the ribosomal peptidyl (P) site. Internal ribosome entry sites (IRESs) promote translation of mRNAs in a cap-independent manner. We report two structures of the ribosome-bound Taura syndrome virus (TSV) IRES belonging to the family of Dicistroviridae intergenic IRESs. Intersubunit rotational states differ in these structures, suggesting that ribosome dynamics play a role in IRES translocation. Pseudoknot I of the IRES occupies the ribosomal decoding center at the aminoacyl (A) site in a manner resembling that of the tRNA anticodon-mRNA codon. The structures reveal that the TSV IRES initiates translation by a previously unseen mechanism, which is conceptually distinct from initiator tRNA-dependent mechanisms. Specifically, the ORF of the IRES-driven mRNA is established by the placement of the preceding tRNA-mRNA-like structure in the A site, whereas the 40S P site remains unoccupied during this initial step.
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Koh et al. (2014) studied this question. Structural analysis reveals that the Taura syndrome virus IRES initiates translation by placing a tRNA-mRNA-like structure in the ribosomal A site, leaving the P site unoccupied.
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