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. Author manuscript; available in PMC: 2021 Mar 5.
Published in final edited form as: Cell Rep. 2020 Dec 8;33(10):108476. doi: 10.1016/j.celrep.2020.108476

Figure 7. The P-Site-Stabilizing Interaction of PKI and Activities of Hybrid HalV/CrPV IGR IRESs.

Figure 7.

(A) Left: model of the HalV IGR PKI structure, showing nucleotides targeted for substitution to assay a stabilizing interaction of PKI in the P site. Right: binding of 80S ribosomes to the indicated HalV IGR IRES mutants, assayed by toe-printing.

(B, C, E, and F) Ribosomal binding, one-cycle elongation and release factor binding on WT and hybrid HalV/CrPV IGR IRESs (shown schematically in each panel) in the presence of the indicated translational components, assayed by toe-printing. The positions of ribosomal complexes are shown.

(D) Ribosome-binding activity of the L2 deletion/insertion HalV IGR IRES mutants, assayed by toe-printing. Separation of lanes by white lines indicates that they were juxtaposed from the same gel. (A–F) The positions of ribosomal complexes are indicated. (A, B, and F) Lanes C, T, A, and G depict CrPV or HalV sequences.