General physiology: pertussis toxin and Gi: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · General physiology: pertussis toxin and Gi

Sample item

A 4-month-old unvaccinated infant has paroxysmal coughing ending in an inspiratory whoop. The toxin of the causative organism ADP-ribosylates the alpha subunit of a G protein and keeps it in the GDP-bound state. What is the cellular consequence?

AGs coupling is lost, so cAMP falls and relaxation of smooth muscle failsBGq signalling is lost, so phospholipase C produces less IP3CReceptor-mediated inhibition of adenylyl cyclase is lost, so cAMP risesDGs is locked in the active state, so adenylyl cyclase stays switched on

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

C. Receptor-mediated inhibition of adenylyl cyclase is lost, so cAMP rises

Pertussis toxin modifies the alpha subunit of Gi so that it cannot exchange GDP for GTP. Receptors that normally inhibit adenylyl cyclase through Gi can no longer do so, and cAMP rises. Cholera toxin does the opposite kind of damage by locking Gs on.

Option by option

A. Gs coupling is lost, so cAMP falls and relaxation of smooth muscle fails
Gs is not the target here, and losing Gs would lower cAMP, the opposite of the real effect.
B. Gq signalling is lost, so phospholipase C produces less IP3
Pertussis toxin does not target Gq, so the phospholipase C pathway is unaffected.
C. Receptor-mediated inhibition of adenylyl cyclase is lost, so cAMP rises (correct)
Correct. Gi cannot be activated, so inhibition of adenylyl cyclase is lost and cAMP rises.
D. Gs is locked in the active state, so adenylyl cyclase stays switched on
This is the mechanism of cholera toxin, which keeps Gs active; pertussis toxin acts on Gi.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is C, Receptor-mediated inhibition of adenylyl cyclase is lost, so cAMP rises. Pertussis toxin modifies the alpha subunit of Gi so that it cannot exchange GDP for GTP.

Why is "Gs coupling is lost, so cAMP falls and relaxation of smooth muscle fa…" not the answer?

Gs is not the target here, and losing Gs would lower cAMP, the opposite of the real effect.

Why is "Gq signalling is lost, so phospholipase C produces less IP3" not the answer?

Pertussis toxin does not target Gq, so the phospholipase C pathway is unaffected.

Why is "Gs is locked in the active state, so adenylyl cyclase stays switched…" not the answer?

This is the mechanism of cholera toxin, which keeps Gs active; pertussis toxin acts on Gi.

What concept does this question test?

It tests General physiology: pertussis toxin and Gi in Physiology. Receptors that normally inhibit adenylyl cyclase through Gi can no longer do so, and cAMP rises. Cholera toxin does the opposite kind of damage by locking Gs on.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study General physiology: pertussis toxin and Gi?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.