Diphtheria toxin exerts its pathological effects via ADP-ribosylation. Identification of the specific molecular target helps explain the cardiac and neural toxicity. Which is the correct target?
- A Elongation factor G (EF-G) in prokaryotes
- B Adenylate cyclase in host cells
- C Elongation factor 2 (EF-2/EF-Tu) in eukaryotes, via modification of diphthamide residue ✓
- D Rho GTPase in epithelial cells
Explanation
The B fragment of diphtheria toxin binds to heparin-binding EGF receptor and delivers the A fragment into the cytoplasm. The A fragment is an ADP-ribosyltransferase that transfers ADP-ribose from NAD+ to a modified histidine residue called diphthamide in eukaryotic elongation factor 2 (EF-2), irreversibly inhibiting translocation of the ribosome and halting protein synthesis. Each toxin molecule can inactivate thousands of EF-2 molecules. Exotoxin A of Pseudomonas has the same mechanism but different receptor. Cholera toxin ADP-ribosylates adenylate cyclase Gs subunit.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.