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. 2016 May 9;5:e13567. doi: 10.7554/eLife.13567

Figure 3. CrPV-IRES conformation induced by the binding of eEF2.

Figure 3.

(A) Overview of the complex with the area of interest highlighted. (B) Superposition of the CrPV-IRES (green) with tRNAs in canonical configurations (grey, PDB-ID 2WDG). Ribosomal sites A, P and E are indicated to show how the ASL-like element of the IRES PKI occupies a position between the A and P sites as it interacts with domain IV of eEF2 (red). (C) Relative displacement of PKI in a comparison of the conformation in the present reconstruction (green) with the one adopted in the CrPV-IRES/80S complex (grey). CrPV-IRES superposition has been computed excluding PKI. (D) View down the axis of the PKI stem in the CrPV-IRES/40S complex (top-left), in the pre-translocated CrPV-IRES/80S complex (top-right Fernández et al., 2014), in the 80S/CrPV-IRES/eEF2 complex (bottom-right) and finally, in the post-translocated 80S/CrPV-IRES complex (bottom-left, adapted from Muhs et al. (2015)). Ribosomal sites A and P are depicted as dotted lines. The CrPV-IRES PKI (green) is inserted in the A-site in the isolated interaction with the 40S (yellow) as well as in the pre-translocated 80S/CrPV-IRES complex. The interaction with domain IV of eEF2 (red) displaces it towards the P site so it occupies an intermediate position between the A and P sites.

DOI: http://dx.doi.org/10.7554/eLife.13567.014