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T. Nakao, M. Tsujikawa, Y. Tano; Phototransduction and Photoreceptor Cell Death Are Closely Related in a Zebrafish Model. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4398.
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© ARVO (1962-2015); The Authors (2016-present)
Many mutations on the genes of phototransduction signal cascades cause inherited retinal diseases. However, the effect of phototransduction on photoreceptor cell death in such diseases remains unknown. We previously demonstrated that shutdown of phototransduction upstream of phosphodiesterase reduces photoreceptor cell death in ovl mutants. The purpose of our study was to determine whether the phosphodiesterase is associated with photoreceptor cell death.
The zebrafish mutation locus oval (ovl) encodes IFT88, which is involved in transport processes in the connecting cilium. This locus causes mislocalization of visual pigments and photoreceptor cell death within 3 days after fertilization. Because of this phenotype, ovl is regarded as an animal model of human inherited retinal diseases. We determined the number of surviving photoreceptors in ovl mutants while the rod cGMP-phosphodiesterase beta subunit (PDE6B) was being suppressed by antisense morpholinos. Photoreceptors were visualized in the zebrafish rhodopsin promoter-driven green fluorescent protein (GFP) fish line, and the surviving photoreceptors on the cryosections were counted by means of fluorescent microscopy.
Suppression of PDE6B did not affect the number of surviving photoreceptor cells in either the ovl or the wild-type zebrafish retina 96 hours after fertilization.
Suppression of phosphodiesterase in ovl mutants did not have a protective effect on disease photoreceptors. Under abnormal conditions resulting in visual pigment mislocalization, initiation of phototransduction cascades accelerates photoreceptor cell death. However, the pathway of photoreceptor cell death may not pass through PDE6B.
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