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Updated: Aug 21, 2026

A Rhodopsin Transport Assay by High-Content Imaging Analysis
Published on: January 16, 2019
Coordinated changes in classes of ribosomal protein gene expression is associated with light-induced retinal
Ruby Grewal1, Jadwiga Stepczynski, Rhonda Kelln
1Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada. pwwong@ualbert.ca
Purpose:
To identify genes with altered expression levels in the degenerating retina in a light-induced retinal degeneration (LIRD) model.
Methods:
Adult Sprague-Dawley rats were exposed to intense green light for 4 hours. After this treatment, the retinas were excised, RNA was extracted, and a cDNA library was prepared. The cDNA library was differentially cross-screened with probes representing 0-hour and 4-hour light-exposed rat retina. Transcripts with altered expression levels were sequenced and expression was confirmed by Northern blot analysis. Gene-specific primers were designed and used to examine the expression levels of other genes involved in protein synthesis. Promoter sequences of the ribosomal-binding protein (Rbp) genes were analyzed for transcription-binding sites.
Results:
Of the 10,000 clones that were initially screened, 41 exhibited altered expression levels. Six of these corresponded to five known Rbp genes. Six additional Rbp genes were also examined. In total, 9 of 11 Rbp genes exhibited an increase in expression levels in response to a 4-hour light exposure. In contrast, the transcript levels of elongation factor 1alpha1 and 18S rRNA did not increase. The most abundant transcription factor-binding sites conserved in the promoter regions of all Rbp genes examined in this study include AP-1, Oct-1, V-myb, USF, Pax-4, and the FOX family of transcription factors.
Conclusions:
The results indicate that light-induced retinal degeneration (LIRD) is associated with increased expression of specific Rbp genes. These Rbp genes may be involved in mediating visual cell loss in LIRD through a translational or an extraribosomal mechanism.
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