Literature DB >> 21546531

Misexpression of the constitutive Rpgr(ex1-19) variant leads to severe photoreceptor degeneration.

Rachel N Wright1, Dong-Hyun Hong, Brian Perkins.   

Abstract

PURPOSE: Mutations in the retinitis pigmentosa GTPase regulator (RPGR) gene are a frequent cause of X-linked retinitis pigmentosa. The RPGR transcript undergoes complex alternative splicing to express both constitutive (Rpgr(ex1-19)) and Rpgr(ORF15) variants. Both variants localize to photoreceptor connecting cilia and are believed to play roles in ciliary function. This study examined variability in isoform expression and tested whether the constitutive variant could substitute for Rpgr function in photoreceptors.
METHODS: Rpgr(ex1-19) and Rpgr(ORF15) expression during retinal development were compared using immunoblot analysis and immunohistochemistry, and ciliary affinity in adult photoreceptors was assessed by protein fractionation. Transgenic mice expressing either the full-length Rpgr(ex1-19) or Rpgr(ORF15) variant were studied using light and electron microscopy and immunofluorescence imaging. The results were compared with those of wild-type and Rpgr(-/-) mice.
RESULTS: Rpgr expression undergoes dynamic temporal regulation during retinal development, and variants exhibit variability for ciliary localization in adult photoreceptors. Transgenic expression of both variants grossly exceeded endogenous Rpgr expression in photoreceptors. Although both variants exhibited normal ciliary localization, overexpression of the Rpgr(ex1-19) variant resulted in atypical accumulation of Rpgr in photoreceptor outer segments, abnormal photoreceptor morphology, and severe retinal degeneration.
CONCLUSIONS: The Rpgr isoform ratio in the adult retina is critical to photoreceptor integrity. The utilization of distinct Rpgr variants at different stages of photoreceptor maturation suggests independent roles in photoreceptor function. Finally, misexpression of Rpgr(ex1-19) causes retinal degeneration that is considerably more severe than that caused by Rpgr knockout but photoreceptors tolerate overexpression of Rpgr(ORF15) without evidence of degeneration.

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Year:  2011        PMID: 21546531      PMCID: PMC3176051          DOI: 10.1167/iovs.11-7470

Source DB:  PubMed          Journal:  Invest Ophthalmol Vis Sci        ISSN: 0146-0404            Impact factor:   4.799


  29 in total

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2.  Complex expression pattern of RPGR reveals a role for purine-rich exonic splicing enhancers.

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3.  Retinitis pigmentosa GTPase regulator (RPGRr)-interacting protein is stably associated with the photoreceptor ciliary axoneme and anchors RPGR to the connecting cilium.

Authors:  D H Hong; G Yue; M Adamian; T Li
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4.  Glial cell line derived neurotrophic factor delays photoreceptor degeneration in a transgenic rat model of retinitis pigmentosa.

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5.  The retinitis pigmentosa GTPase regulator (RPGR) interacts with novel transport-like proteins in the outer segments of rod photoreceptors.

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6.  Identification of a novel protein interacting with RPGR.

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9.  The retinitis pigmentosa GTPase regulator (RPGR)- interacting protein: subserving RPGR function and participating in disk morphogenesis.

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10.  A retinitis pigmentosa GTPase regulator (RPGR)-deficient mouse model for X-linked retinitis pigmentosa (RP3).

Authors:  D H Hong; B S Pawlyk; J Shang; M A Sandberg; E L Berson; T Li
Journal:  Proc Natl Acad Sci U S A       Date:  2000-03-28       Impact factor: 11.205

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10.  RPGR, a prenylated retinal ciliopathy protein, is targeted to cilia in a prenylation- and PDE6D-dependent manner.

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