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A Drosophila mutant defective in extracellular calcium-dependent photoreceptor deactivation and rapid desensitization

Nature volume 354, pages 230232 (21 November 1991) | Download Citation

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Abstract

CALCIUM is involved in the adaptation of vertebrate photoreceptors to light1,2 and may have a similar role in invertebrate phototransduction3,4. 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 photoreceptors5 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.

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Author information

Affiliations

  1. Howard Hughes Medical Institute and Department of Biology, University of California, San Diego, La Jolla, California 92093, USA

    • Rama Ranganathan
    • , Charles F. Stevens
    •  & Charles S. Zuker
  2. Howard Hughes Medical Institute and Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, USA

    • Charles F. Stevens
    •  & Charles S. Zuker
  3. Department of Biology and Molecular Biology Institute, San Diego State University, San Diego, California 92182, USA

    • Greg L. Harris
  4. Salk Institute for Biological Studies, La Jolla, California 92093, USA

    • Charles F. Stevens

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https://doi.org/10.1038/354230a0

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