November 1986
Volume 27, Issue 11
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Articles  |   November 1986
Deficiency in light-dependent opsin phosphorylation in Irish setters with rod-cone dysplasia.
Investigative Ophthalmology & Visual Science November 1986, Vol.27, 1551-1559. doi:
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      S Y Schmidt, U P Andley, C A Heth, J Miller; Deficiency in light-dependent opsin phosphorylation in Irish setters with rod-cone dysplasia.. Invest. Ophthalmol. Vis. Sci. 1986;27(11):1551-1559.

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

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Abstract

A deficiency in light-dependent opsin phosphorylation and a slight reduction in opsin synthesis were observed during photoreceptor cell development (22-26 days) preceding photoreceptor cell loss in Irish setters with rod-cone dysplasia. In addition to opsin, two other phosphoprotein bands were found associated with the photoreceptor cell layer; synthesis and phosphorylation of one of these (band 3; 44-48 Kd) appeared reduced, while synthesis and phosphorylation of the other (band 1; 29-31 Kd) was within the normal range in 25-day-old affected setters. The deficiency in light-dependent opsin phosphorylation in affected setters was not due to a deficiency in opsin kinase, since soluble proteins from affected or normal outer segments catalyzed equally well opsin phosphorylation in partially kinase-depleted outer segment membranes from normal, while both kinase preparations failed to promote light-dependent opsin phosphorylation in those from affected setters. A deficiency in light-dependent opsin phosphorylation was also observed in rd/rd mice at all ages studied. In contrast, in Royal College of Surgeons (RCS) rats, light-dependent opsin phosphorylation was within the normal range prior to photoreceptor loss, and became nondetectable only after 50% or more of the photoreceptors had degenerated.

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