Final answer:
Gsα is activated by cholera toxin through ADP-ribosylation, leading to persistent stimulation of adenylyl cyclase and increased cAMP levels.
Step-by-step explanation:
The G protein, Gsα, is locked in an active state by cholera toxin through the mechanism of ADP-ribosylation, which results in elevated levels of cAMP.
This modification occurs when the cholera toxin catalyzes the transfer of an ADP-ribose moiety onto the Gsα subunit, preventing GTP hydrolysis and keeping the G protein in an active state.
Consequently, the active Gsα persistently stimulates adenylyl cyclase to convert ATP into cAMP, leading to prolonged signaling events, such as the activation of protein kinase A, which can then phosphorylate other targets and lead to changes in cell function.