June 1994
Volume 35, Issue 7
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Articles  |   June 1994
Downregulation of cGMP phosphodiesterase induced by expression of GTPase-deficient cone transducin in mouse rod photoreceptors.
Author Affiliations
  • C J Raport
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • J Lem
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • C Makino
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • C K Chen
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • C L Fitch
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • A Hobson
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • D Baylor
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • M I Simon
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
  • J B Hurley
    Department of Biochemistry and Howard Hughes Medical Institute, Seattle, Washington 98195.
Investigative Ophthalmology & Visual Science June 1994, Vol.35, 2932-2947. doi:
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    • Get Citation

      C J Raport, J Lem, C Makino, C K Chen, C L Fitch, A Hobson, D Baylor, M I Simon, J B Hurley; Downregulation of cGMP phosphodiesterase induced by expression of GTPase-deficient cone transducin in mouse rod photoreceptors.. Invest. Ophthalmol. Vis. Sci. 1994;35(7):2932-2947.

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Abstract

PURPOSE: Photoexcitation of vertebrate retinal rod photoreceptors stimulates GTP binding to the transducin alpha subunit. Like other GTP-binding proteins, transducin restores itself to an inactive form by hydrolyzing its bound GTP. The role of GTP hydrolysis in phototransduction was investigated. METHODS: A mutant form of cone transducin alpha deficient in its ability to hydrolyze bound GTP was expressed in mouse rod photoreceptors. RESULTS: Expression of the mutant cone transducin alpha at levels threefold to sixfold higher than endogenous rod transducin alpha led to a specific depletion of the transducin target, cGMP phosphodiesterase, and a decrease in the cGMP level. Suction electrode recordings revealed abnormally prolonged flash responses, decreased maximal response amplitudes, and a shift in the stimulus-response relation to higher flash strengths. CONCLUSIONS: Rods expressing high levels of GTPase-deficient cone transduction alpha have reduced levels of phosphodiesterase catalytic subunits and cGMP. These changes are associated with prolonged flash responses, reduced dark current, and decreased sensitivity to light.

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