Figure 4.
Schematic of Fap7-mediated QC step verifying translocation capability of the pre-40S subunit. (A) Fap7 releases Dim1 to allow pre-40S to continue their assembly only after confirming that the pre-40S can form the rotated state needed to maintain the reading frame during translation. Failure to pass this QC results in turnover of 80S-like intermediates. (B) Bypass of this QC using a weakly binding Dim1 mutant (yellow star) allows 40S subunits to continue maturation and causes −1 frameshifting during translation (Ghalei et al., 2017). (C) Structure of the 80S-like ribosome (gray, 60S is omitted for clarity) bound by Dim1 (yellow) and Tsr1 (blue; PDB accession no. 6WDR; Rai et al., 2021). Dim1_EKR (E93/K96/R97) is shown in red spheres. Dark blue spheres indicate residues in DIMT1 (P88A, P88T, D113N, N219T, and R228M) that are mutated in cancer and are predicted to bypass QC (TCGA www.cancer.gov/tcga, cBioPortal www.cbioportal.org).

Schematic of Fap7-mediated QC step verifying translocation capability of the pre-40S subunit. (A) Fap7 releases Dim1 to allow pre-40S to continue their assembly only after confirming that the pre-40S can form the rotated state needed to maintain the reading frame during translation. Failure to pass this QC results in turnover of 80S-like intermediates. (B) Bypass of this QC using a weakly binding Dim1 mutant (yellow star) allows 40S subunits to continue maturation and causes −1 frameshifting during translation (Ghalei et al., 2017). (C) Structure of the 80S-like ribosome (gray, 60S is omitted for clarity) bound by Dim1 (yellow) and Tsr1 (blue; PDB accession no. 6WDR; Rai et al., 2021). Dim1_EKR (E93/K96/R97) is shown in red spheres. Dark blue spheres indicate residues in DIMT1 (P88A, P88T, D113N, N219T, and R228M) that are mutated in cancer and are predicted to bypass QC (TCGA www.cancer.gov/tcga, cBioPortal www.cbioportal.org).

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