Abstract
Weak or strong lights activate visual receptor rod disk membrane (RDM) cGMP phosphodiesterase (PDE) in the presence of GTP cofactor. A similarly activated GTPase can exhaust small amounts of initially present GTP to deactivate the PDE. Further additions of GTP reactivate PDE without more light. Deactivation by simple GTP depletion takes several minutes, even at GTP concentrations 100-1000 times lower than physiological levels. A more rapid deactivation mechanism must exist if modulation of cytoplasmic cGMP by light is to play a role on the time scale (seconds) of events in vision. ATP was essential to rapid control in bovine retinal suspensions. Its presence permited multiple cycles of activation-deactivation. The complete control mechanism seems to involve .gamma. phosphate transfer from ATP and GTP.