Translation initiation by factor-independent binding of eukaryotic ribosomes to internal ribosomal entry sites - 01/01/05
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Abstract |
Two exceptional mechanisms of eukaryotic translation initiation have recently been identified that differ fundamentally from the canonical factor-mediated, end-dependent mechanism of ribosomal attachment to mRNA. Instead, ribosomal 40S subunits bind in a factor-independent manner to the internal ribosomal entry site (IRES) in an mRNA. These two mechanisms are exemplified by initiation on the unrelated ~300 nt.-long Hepatitis C virus (HCV) IRES and the ~200 nt.-long cricket paralysis virus (CrPV) intergenic region (IGR) IRES, respectively. Ribosomal binding involves interaction with multiple non-contiguous sites on these IRESs, and therefore also differs from the factor-independent attachment of prokaryotic ribosomes to mRNA, which involves base-pairing to the linear Shine-Dalgarno sequence. The HCV IRES binds to the solvent side of the 40S subunit, docks a domain of the IRES into the ribosomal exit (E) site and places the initiation codon in the ribosomal peptidyl (P) site. Subsequent binding of eIF3 and the eIF2-GTP/initiator tRNA complex to form a 48S complex is followed by subunit joining to form an 80S ribosome. The CrPV IRES binds to ribosomes in a very different manner, by occupying the ribosomal E and P sites in the intersubunit cavity, thereby excluding initiator tRNA. Ribosomes enter the elongation stage of translation directly, without any involvement of initiator tRNA or initiation factors, following recruitment of aminoacyl-tRNA to the ribosomal aminoacyl (A) site and translocation of it to the P site. To cite this article: A.V. Pisarev et al., C. R. Biologies 328 (2005).
Le texte complet de cet article est disponible en PDF.Keywords : Classical swine fever virus, Cricket paralysis virus, Hepatitis C virus, IRES, Ribosome, Translation initiation
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Vol 328 - N° 7
P. 589-605 - juillet 2005 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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