Toxins – E. coli heat-labile enterotoxin (LT) The heat-labile enterotoxin (LT) of enterotoxigenic Escherichia coli (ETEC) primarily activates which host cell enzyme/signaling pathway?

Introduction / Context:
ETEC expresses two principal toxins with distinct mechanisms: LT (heat-labile) and ST (heat-stable). Exam questions often test whether you can differentiate their intracellular signaling targets.

Given Data / Assumptions:

• LT resembles cholera toxin in structure and action.
• LT increases intestinal secretion of chloride and water, causing watery diarrhea.
• The effect is mediated by cyclic nucleotides.

Concept / Approach:
LT ADP-ribosylates the Gs alpha subunit, locking it in the active form. This persistently stimulates adenylate cyclase to raise intracellular cAMP. Elevated cAMP activates protein kinase A, which phosphorylates transporters such as CFTR, promoting chloride secretion and reducing sodium absorption. ST, by contrast, activates guanylate cyclase C to raise cGMP.

Step-by-Step Solution:
Recall mechanistic similarity to cholera toxin (both target cAMP via Gs–adenylate cyclase).Map downstream effects to secretory diarrhea.Select “Adenylate cyclase (cAMP pathway).”

Verification / Alternative check:
Pharmacologic inhibition and genetic studies of Gs/adenylate cyclase confirm the cAMP dependence of LT-mediated secretion.

Why Other Options Are Wrong:

• Guanylate cyclase: that is the ST pathway.
• Both equally: mechanistically incorrect for LT.
• None/Tyrosine kinase: not the primary route for LT's effect.

Common Pitfalls:
Mixing up LT and ST targets; use the mnemonic “LT → cAMP, ST → cGMP.”

Final Answer:
Adenylate cyclase (cAMP pathway).