September 1998
Volume 39, Issue 10
Free
Articles  |   September 1998
Canine cone transducin-gamma gene and cone degeneration in the cd dog.
Author Affiliations
  • N B Akhmedov
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
  • N I Piriev
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
  • S Pearce-Kelling
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
  • G M Acland
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
  • G D Aguirre
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
  • D B Farber
    Jules Stein Eye Institute, University of California Los Angeles School of Medicine, 90095, USA.
Investigative Ophthalmology & Visual Science September 1998, Vol.39, 1775-1781. doi:
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      N B Akhmedov, N I Piriev, S Pearce-Kelling, G M Acland, G D Aguirre, D B Farber; Canine cone transducin-gamma gene and cone degeneration in the cd dog.. Invest. Ophthalmol. Vis. Sci. 1998;39(10):1775-1781.

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Abstract

PURPOSE: To characterize the cDNA and the organization of the gene encoding the cone-specific gamma subunit of transducin (Tgamma c) and to examine this gene as a candidate for the recessively inherited cone photoreceptor degeneration in the cd dog. METHODS: Canine Tgamma c cDNA was cloned and sequenced. Polymerase chain reaction (PCR) was used to define the Tgamma c gene structure, northern blot analysis to examine the level of expression of Tgamma c mRNA in control and cd-affected retinas, and immunocytochemistry to determine the presence and localization of Tgamma c in normal and cd retinas. RESULTS: Immunocytochemical results showed Tgamma c localized to cone photoreceptor outer segments in the normal retina, whereas no Tgamma c immunoreactivity was observed in the cd retinas. However, the level of transcription and the primary structure of the cloned cDNA coding for the 69-amino acid protein were identical in retinas from wild-type and affected dogs. CONCLUSIONS: Although Tgamma c immunoreactivity was specifically absent in the cd dog retina, no differences were detected between normal and cd retinas in the nucleotide sequence of Tgamma c mRNA or in its synthesis. These results indicate that a mutation in the Tgamma c gene may not be causally associated with the cd dog disease. These findings suggest that possible abnormalities in posttranslational modification of Tgamma c or defective assembly of the transducin alphabetagamma complex could lead to rapid degradation of Tgamma c.

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