In prokaryotic protein synthesis, what is the specific molecular action of the antibiotic tetracycline on the ribosome? Choose the option that best states the step it blocks at the ribosomal binding sites.

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:

  • Target organism: prokaryotes (bacteria).
  • Process: translation on 70S ribosomes (30S + 50S subunits).
  • Focus: which step tetracycline inhibits.


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:

  • Blocks translocation: that is typically affected by macrolides or certain toxins, not tetracycline.
  • Blocks peptidyl transferase: chloramphenicol binds the 50S catalytic center, not tetracycline.
  • Not known with certainty: the A-site binding mechanism is well established.


Common Pitfalls:

  • Confusing 30S-acting drugs: aminoglycosides cause misreading and initiation complex problems, whereas tetracycline blocks A-site entry.
  • Assuming bactericidal action; tetracyclines are mainly bacteriostatic.


Final Answer:

It blocks the binding of aminoacyl-tRNA to the A site of ribosomes.

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