ATP mediates rapid reversal of cyclic GMP phosphodiesterase activation in visual receptor membranes.
Weak or strong lights will activate visual receptor rod disk membrane (RDM) cyclic GMP phosphodiesterase (PDE) in the presence of GTP cofactor. A similarly activated GTPase can exhaust small amounts of initially present GTP to deactivate the PDE. However, further additions of GTP reactivate PDE without more light, and deactivation by simple GTP depletion takes minutes or more, even at GTP concentrations 100 to 1,000 times lower than physiological levels. A more rapid deactivation mechanism must exist if modulation of cytoplasmic cyclic GMP by light is to play a role on the time scale (seconds) of events in vision. We report here that ATP is essential to such rapid control and that its presence permits multiple cycles of activation-deactivation. The complete control mechanism seems to involve gamma phosphate transfer from both ATP and GTP.
D015106:3',5'-Cyclic-GMP Phosphodiesterases / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002417:Cattle; D004789:Enzyme Activation / Q000187:drug effects; D020558:GTP Phosphohydrolases / Q000378:metabolism; D007700:Kinetics; D008027:Light; D010766:Phosphorylation; D010786:Photoreceptor Cells / Q000201:enzymology*; D012243:Rhodopsin / Q000378:metabolism; D012374:Rod Cell Outer Segment / Q000201:enzymology* / Q000528:radiation effects
D000255:Adenosine Triphosphate; D012243:Rhodopsin; D015106:3',5'-Cyclic-GMP Phosphodiesterases; D020558:GTP Phosphohydrolases