Difficulty: Easy
Correct Answer: It blocks the binding of aminoacyl-tRNA to the A site of ribosomes.
Explanation:
Introduction / Context:Tetracycline is a classic antibacterial drug used to inhibit bacterial (prokaryotic) protein synthesis. Understanding exactly which ribosomal step it targets is a high-yield concept in microbiology, pharmacology, and biochemistry because it explains both its spectrum of activity and typical resistance mechanisms.
Given Data / Assumptions:
Concept / Approach:
Tetracyclines bind reversibly to the 30S ribosomal subunit at a site that interferes with the docking of incoming aminoacyl-tRNA to the acceptor (A) site. This prevents codon-anticodon pairing for the next amino acid, stalling elongation before peptide-bond formation can proceed. They do not block the 50S peptidyl transferase center and do not inhibit translocation mediated by elongation factor-G; those are targeted by other antibiotics.
Step-by-Step Solution:
1) Identify candidate steps in elongation: aminoacyl-tRNA entry (A site), peptide-bond formation (peptidyl transferase), and translocation.2) Map known antibiotic actions: tetracycline → 30S A-site entry block; chloramphenicol/macrolides → 50S peptidyl transferase or exit tunnel; aminoglycosides → misreading/initiation interference; fusidic acid/EF-G → translocation.3) Conclude the specific action: prevent binding of aminoacyl-tRNA to the A site.Verification / Alternative check:
Clinical correlates include bacteriostatic activity and activity against intracellular pathogens due to good cell penetration. Resistance often involves efflux pumps or ribosomal protection proteins that dislodge tetracycline from the 30S A-site interface, which is consistent with the A-site mechanism.
Why Other Options Are Wrong:
Common Pitfalls:
Final Answer:
It blocks the binding of aminoacyl-tRNA to the A site of ribosomes.
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