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...

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Bibliographic Details
Published in:	Nature (London) 1991-11, Vol.354 (6350), p.230-232
Main Authors:	Ranganathan, R, Harris, G.L, Stevens, C.F, Zuker, C.S
Format:	Article
Language:	eng
Subjects:	Animals Biochemistry Biochemistry. Physiology. Immunology Biological and medical sciences Biological control systems Calcium Calcium - pharmacology Cesium - pharmacology Chlorides Dose-Response Relationship, Drug Drosophila Drosophila melanogaster - genetics Drosophila melanogaster - physiology Electrophysiology Fundamental and applied biological sciences. Psychology Insecta Invertebrates Light mutants Nervous system Photoreceptor Cells - physiology Photoreceptors Physiological aspects Physiology. Development Potassium Chloride - pharmacology Signal Transduction - drug effects Sodium Chloride - pharmacology Tromethamine - pharmacology
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Summary:	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.
ISSN:	0028-0836 1476-4687