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The Journal of Neuroscience, January 15, 2003, 23(2):470-480

Light Stimulates a Transducin-Independent Increase of Cytoplasmic Ca²⁺ and Suppression of Current in Cones from the Zebrafish Mutant nof

Susan E. Brockerhoff¹, Fred Rieke², Hugh R. Matthews³, Michael R. Taylor¹, Breandan Kennedy¹, Irina Ankoudinova¹, Gregory A. Niemi¹, Chandra L. Tucker¹, Ming Xiao¹, Marianne C. Cilluffo⁴, Gordon L. Fain⁴, and James B. Hurley¹

Departments of ¹ Biochemistry and ² Physiology and Biophysics, University of Washington, Seattle, Washington 98195, ³ Physiological Laboratory, University of Cambridge, Cambridge CB2 3EG, United Kingdom, and ⁴ Departments of Physiological Science and Ophthalmology, University of California Los Angeles, Los Angeles, California 90095-1606

Transducins couple visual pigments to cGMP hydrolysis, the only recognized phototransduction pathway in vertebrate photoreceptors. Here we describe a zebrafish mutant, no optokinetic response f^w21 (nof), with a nonsense mutation in the gene encoding the  subunit of cone transducin. Retinal morphology and levels of phototransduction enzymes are normal in nof retinas, but cone transducin is undetectable. Dark current in nof cones is also normal, but it is insensitive to moderate intensity light. The nof cones do respond, however, to bright light. These responses are produced by a light-stimulated, but transducin-independent, release of Ca²⁺ into the cone cytoplasm. Thus, in addition to stimulating transducin, light also independently induces release of Ca²⁺ into the photoreceptor cytoplasm.

Key words: genetic analysis of phototransduction; transducin; cone photoreceptor physiology; light adaptation; photoreceptor mutations; G-protein-mediated signal transduction

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Copyright © 2003 Society for Neuroscience  0270-6474/03/232470-11$05.00/0

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