Which translation termination mechanism is exploited by aminoglycoside antibiotics (e.g., gentamicin) causing readthrough therapy potential in premature stop codon diseases?

• A Aminoglycosides inhibit release factor eRF1, blocking stop codon recognition
• B Aminoglycosides bind the 30S (prokaryotic) or 18S (eukaryotic) rRNA A-site, inducing misreading that can suppress UAG/UAA/UGA stop codons ✓
• C Aminoglycosides promote ribosome frameshifting past stop codons
• D Aminoglycosides activate nonsense-mediated mRNA decay, reducing premature termination

Explanation

Aminoglycosides bind the decoding centre of 16S rRNA (prokaryotes) or the homologous region of 18S rRNA (eukaryotes), inducing conformational changes that reduce the fidelity of codon-anticodon discrimination. At therapeutic concentrations they can cause misreading of premature stop codons (nonsense codons), allowing near-cognate tRNA to insert an amino acid and read through the stop — 'readthrough therapy'. This is being explored for diseases like Duchenne muscular dystrophy (DMD) with premature UAA/UAG mutations, though clinical efficacy varies.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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