A Drosophila mutant defective in extracellular calcium-dependent photoreceptor deactivation and rapid desensitization.
CALCIUM is involved in the adaptation of vertebrate photoreceptors to light and may have a similar role in invertebrate phototransduction. But the molecular mechanisms mediating this stimulus-dependent regulation are not well understood in any G protein-coupled transduction system. We have developed a preparation of isolated Drosophila photoreceptors that has allowed us to carry out an electrophysiological characterization of the light-activated response in these sensory neurons using patch-clamp techniques. We report here that extracellular calcium entering through the light-activated conductance is a key regulator of both the activation and deactivation phases of the phototransduction cascade, and that inaC mutant photoreceptors are specifically defective in the calcium-dependent deactivation mechanism. These data suggest that the light-dependent calcium influx inactivates this cascade through a biochemical pathway that requires the inaC gene product, and that this mechanism represents a molecular basis for stimulus-dependent regulation of visual transduction in Drosophila photoreceptors.
Ranganathan
R
R
Howard Hughes Medical Institute, San Diego, La Jolla, California.
Harris
G L
GL
Stevens
C F
CF
Zuker
C S
CS
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides; D004305:Dose-Response Relationship, Drug; D004331:Drosophila melanogaster / Q000235:genetics / Q000502:physiology*; D004594:Electrophysiology; D010786:Photoreceptor Cells / Q000502:physiology*; D011189:Potassium Chloride / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology; D014325:Tromethamine / Q000494:pharmacology
D002712:Chlorides; D014325:Tromethamine; D002586:Cesium; D012965:Sodium Chloride; D011189:Potassium Chloride; C028019:cesium chloride; D002118:Calcium