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. 2019 Dec 12;20(24):6274. doi: 10.3390/ijms20246274

Figure 1.

Figure 1

Translation: normal procedure, at a premature stop codon (PTC) and in the presence of translational read-through inducing drugs (TRIDs). (A) During elongation of the translation process, the binding of a cognate aminoacyl-tRNA (tRNA; grey rounded square) and the elongation factor eEF1A (grey rectangle) to the mRNA triplet at the A site catalyses the peptide bond formation between the nascent polypeptide (dark blue) at the P site and the new amino acid. At the site of a stop codon (red) a termination complex (eRF1, eRF3 GTP, eIF4E, eIF4G, PABPC1; orange) is formed. Upon formation of the termination complex, the release of the nascent polypeptide chain from the tRNA is induced. (B) In-frame nonsense mutations introduce a stop codon into the genomic sequence resulting in PTC in the mRNA. Translation of the mRNA stops (red X) resulting in a shortened polypeptide. This truncated polypeptide can have deleterious effects to the cells, including gain-of-function and loss-of function effects. (C) Translational read-through inducing drugs (TRIDs, green octagon) bind to ribosomes and can thereby enhance the translational read-through of PTCs. This results in the expression of full-length proteins. Resulting proteins might have an altered amino acid (yellow) at the site of the PTC.