C2.1 Chemical signalling (HL)

The question asks what happens after GDP→GTP exchange on the α subunit and after the α subunit has dissociated from the βγ dimer. This places us at Step 3 (Signal Propagation) of the GPCR cascade.

Once free, the GTP-bearing α subunit diffuses within the inner leaflet of the plasma membrane and directly interacts with and activates adenylyl cyclase, a membrane-bound enzyme.

Adenylyl cyclase catalyses the conversion of ATP → cyclic AMP (cAMP), which then acts as a second messenger to activate protein kinase A (PKA).

The first intracellular event after α subunit dissociation is stimulation of adenylyl cyclase → cAMP production, making option A correct. GTP hydrolysis (termination) occurs later, and nuclear entry is characteristic of steroid hormones, not GPCRs.

The question asks for the immediate next event after the activated GTP-bound α subunit has separated from the βγ dimer in GPCR signalling.

GTP hydrolysis by the α subunit's intrinsic GTPase activity occurs after the α subunit has already activated its effector, not immediately upon dissociation. This is the termination step, not the propagation step.

Nuclear translocation and binding to hormone response elements (HREs) is the mechanism of intracellular (steroid hormone) receptors, not G protein α subunits, which remain membrane-associated.

Tyrosine phosphorylation is characteristic of receptor tyrosine kinases (RTKs) such as the insulin receptor. G proteins do not possess tyrosine kinase activity.

By elimination, the α subunit stimulates adenylyl cyclase to convert ATP into cyclic AMP is correct. This is the canonical signal propagation step in Gs-coupled GPCR pathways.

This question tests quorum sensing in Vibrio fischeri — specifically why bioluminescence only occurs at high population density (inside the squid's light organ) and not in open seawater.

Each V. fischeri cell continuously releases acyl-homoserine lactone (AHL) autoinducers. In open seawater, the density is too low for AHL to accumulate to a critical threshold.

Inside the squid's light organ, bacteria are highly concentrated. AHL accumulates until it diffuses back into cells and binds the cytoplasmic regulator LuxR. The LuxR–AHL complex activates the lux operon, encoding bioluminescent proteins including luciferase.

Option A accurately describes the quorum sensing mechanism: density-dependent autoinducer accumulation → LuxR activation → lux operon expression → bioluminescence. This is the correct answer.

The question asks for the mechanistic explanation of density-dependent bioluminescence in V. fischeri, a classic example of quorum sensing.

This option incorrectly attributes bioluminescence to host enzymes acting on bacteria. The light-producing mechanism is entirely bacterial, involving the bacteria's own luciferase encoded by the lux operon — the squid does not chemically induce light production.

Free-living V. fischeri do possess the lux operon — the genes are present in all V. fischeri regardless of location. The difference is in gene expression, controlled by autoinducer concentration, not gene acquisition.

While oxygen is indeed a substrate for the luciferase reaction, it is not the controlling signal for gene expression. Luciferase is only produced when the lux operon is activated by LuxR — an oxygen-rich environment alone does not turn on the genes.

Option A is correct: autoinducer accumulation at high density → threshold reached → LuxR activated → lux operon switched on → luciferase produced → bioluminescence.