May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
DNA binding activity of activator protein–1 (AP1) in canine inherited retinal degenerations
Author Affiliations & Notes
  • D. Gu
    School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA
  • G.M. Acland
    Baker Institute, Cornell University, Ithaca, NY
  • A. Kukekova
    Baker Institute, Cornell University, Ithaca, NY
  • G. Aguirre
    Baker Institute, Cornell University, Ithaca, NY
  • Footnotes
    Commercial Relationships  D. Gu, None; G.M. Acland, None; A. Kukekova, None; G. Aguirre, None.
  • Footnotes
    Support  EY13132, EY13729, EY06855, Morris Animal Fdn./TSE, Van Sloun Fund, Foundation Fighting Blindness
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2490. doi:
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      D. Gu, G.M. Acland, A. Kukekova, G. Aguirre; DNA binding activity of activator protein–1 (AP1) in canine inherited retinal degenerations . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2490.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Because the transcription factor AP–1 is activated by photic damage to the rodent retina, prior to the onset of morphological photoreceptor degeneration, we measured the DNA binding activity of AP–1 in several canine retinal diseases (erd, prcd, XLPRA1, XLPRA2), to gain a better understanding of the molecular regulation of retinal degeneration in these diseases. Methods: DNA binding activity of AP–1 was examined by electrophoretic mobility shift assay (EMSA). Retinal nuclear protein extracts from normal and diseased dogs of different ages were hybridized with labeled AP–1 consensus oligonucleotide, and analyzed on 2–20% gradient polyacrylamide gels. The DNA binding activity of AP–1 was assessed by evaluating the intensity of the shifted bands, representing the AP–1/oligonucleotide complex. Results: No significant AP–1 DNA binding activity was found in prcd, XLPRA1 or XLPRA2 at any age tested, nor in erd at 6, 8, 9 or 15 weeks postnatal. In contrast, distinctly increased AP–1 binding, to almost 10 times normal, was present in erd–affected retinas at 11 weeks of age. Conclusions: Analysis of retinal nuclear protein samples indicated that DNA binding activity of AP–1 was transiently, specifically and dramatically induced in erd at the disease stage immediately prior to the previously described sudden and rapid onset of photoreceptor degeneration. This observation is specific for erd, as it is not found in other early (XLPRA2) or late (prcd, XLPRA1) onset disorders. In further studies we are investigating the cause of induction of AP–1 DNA binding activity, the composition of the protein complex, and the target genes transactivated by AP–1. This will provide insights into the molecular mechanism of retinal disease caused by this novel retinal disease locus.

Keywords: retinal degenerations: hereditary • photoreceptors • transcription factors 

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