Q.23 Diphtheria toxin, tetracycline and streptomycin inhibit
- (A) DNA repair
- (B) DNA replication
- (C) transcription
- (D) translation
Diphtheria toxin, tetracycline, and streptomycin all inhibit translation (protein synthesis), targeting different stages of the ribosomal elongation cycle. This SEO-optimized article answers the MCQ: Diphtheria toxin, tetracycline and streptomycin inhibit (A) DNA repair, (B) DNA replication, (C) transcription, (D) translation—crucial for microbiology, pharmacology, and biotechnology students studying antibiotic mechanisms.
Correct Answer: Option (D) Translation
Diphtheria toxin ADP-ribosylates EF-2 (eukaryotic elongation factor 2), blocking translocation during translation.
Tetracycline binds 30S ribosomal subunit, preventing aminoacyl-tRNA entry into A-site.
Streptomycin binds 30S, causing mRNA misreading and inhibiting translocation.
All three target 70S (prokaryotic) or 80S (eukaryotic) ribosomes, halting protein synthesis essential for bacterial growth and toxin-mediated cell death.
Explanation of All Options
These antibiotics distinguish translation inhibition from other nucleic acid processes:
Option Process Targeted Diphtheria Toxin Tetracycline Streptomycin Correct/Incorrect (A) DNA repair Nucleotide excision No No No Incorrect (B) DNA replication DNA polymerase No No No Incorrect (C) Transcription RNA polymerase No No No Incorrect (D) Translation Ribosomes/EF-2 EF-2 30S A-site 30S misreading Correct Mechanisms by stage:
-
Initiation: None of these
-
Elongation: All three (different sites)
-
Termination: None of these
Biotechnology Relevance
Translation inhibitors validate balanced growth models (Q.12) by blocking μ during exponential phase. Tetracycline resistance genes serve as selectable markers in cloning vectors (Q.14 isoschizomers), hairy root transformation (Q.11), and microbial strain engineering. Understanding ribosomal targets aids recombinant protein production optimization (Q.5 animal cell culture, Q.19 chaperones).
-
