Vibrio cholerae O1 El Tor produces cholera toxin. The action of the A1 subunit of cholera toxin that causes profuse watery diarrhoea is:
- A Inhibitory ADP-ribosylation of Gi protein, reducing cAMP production
- B Stimulatory ADP-ribosylation of Gs protein, causing constitutive adenylate cyclase activation and cAMP accumulation ✓
- C RNA N-glycosidase activity cleaving 28S rRNA
- D Inhibition of the sodium-glucose co-transporter (SGLT1)
Explanation
Cholera toxin A1 subunit is an ADP-ribosyltransferase that permanently activates the stimulatory G-protein (Gs-alpha) by ADP-ribosylation, blocking its GTPase activity. Constitutively active Gs stimulates adenylate cyclase continuously, massively elevating intracellular cAMP, which activates CFTR chloride channels — causing profuse secretory ('rice-water') diarrhoea. E. coli LT has the same mechanism. Gi inhibition (lowering cAMP) is the mechanism of pertussis toxin. SGLT1 inhibition would impair ORS efficacy (this is why ORS works — it uses intact SGLT1).
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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