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Susorov, D.

Publications and source records attributed to Susorov, D..

2 recordsLinked to original sources

Structural mechanism of mRNA decoding by mammalian GTPase GTPBP1

GTP-binding protein 1 (GTPBP1) is a widespread translational GTPase closely related to elongation factor eEF1A. The loss of GTPBP1 leads to errors in neuronal development in animals and is associated with neurodegenerative disorders in humans. Although linked to translation and quality control mechanisms, GTPBP1 functions remain largely obscure. Similarly to eEF1A, GTPBP1 delivers cognate aminoacyl-tRNA to the ribosomal A site in a GTP-dependent manner, but GTP hydrolysis is not followed by rapid peptide bond formation, and GTPBP1-mediated elongation is slow. To establish the basis for GTPBP1 function, we determined cryo-EM structures of 80S ribosomal complexes bound to GTPBP1*aa-tRNA with GTP or the non-hydrolysable analog GDPCP. They revealed that the unique GTPBP1 architecture, including the additional eIF1/IF3-like N-terminal domain and the shoulder-interacting H-loop in place of the 2 helix of canonical GTPases, is responsible for establishing GTPBP1-specific interactions with tRNA and the ribosome, leading to slow GTPBP1 dissociation after GTP hydrolysis and thus delayed tRNA accommodation. Slow dissociation correlates with an extended proofreading stage resulting in higher accuracy of GTPBP1-mediated decoding and potentially allows GTPBP1 to elicit its putative quality control functions. GTPBP1 visualization provides the foundation for mapping and elucidating GTPBP1 mutations associated with human diseases.

biochemistry↗

Ribosome inhibition by C9ORF72-ALS/FTD-associated poly-PR and poly-GR proteins revealed by cryo-EM

Toxic dipeptide repeat (DPR) proteins are produced from expanded G4C2 hexanucleotide repeats in the C9ORF72 gene, which cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Two DPR proteins, poly-PR and poly-GR, repress cellular translation but the molecular mechanism remains unknown. Here we show that poly-PR and poly-GR of [≥] 20 repeats inhibit the ribosomes peptidyl-transferase activity at nanomolar concentrations, comparable to specific translation inhibitors. High-resolution cryo-EM structures reveal that poly-PR and poly-GR block the polypeptide tunnel of the ribosome, extending into the peptidyl-transferase center. Consistent with these findings, the macrolide erythromycin, which binds in the tunnel, competes with the DPR proteins and restores peptidyl-transferase activity. Our results demonstrate that strong and specific binding of poly-PR and poly-GR in the ribosomal tunnel blocks translation, revealing the structural basis of their toxicity in C9ORF72-ALS/FTD.

biochemistry↗