Human Molecular Genetics, 2000, Vol. 9, No. 4 645-651
© 2000 Oxford University Press
Mutation of the receptor tyrosine kinase gene Mertk in the retinal dystrophic RCS rat
Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305-5120, USA and 1Departments of Anatomy and Ophthalmology, University of California, San Francisco School of Medicine, San Francisco, CA 94143-0730, USA
Vertebrate photoreceptor cells are the basic sensory apparatus of the retina, capable of converting the energy of absorbed photons into neuronal signals. The proximal portions of mammalian photoreceptor outer segments are synthesized daily by cell bodies, and outer segment tips are shed with a circadian rhythm, resulting in a complete turnover of outer segments about every 9 days. The shed outer segments are phagocytosed by adjacent retinal pigment epithelial (RPE) cells, and metabolites are recycled to photoreceptors. The Royal College of Surgeons (RCS) rat is a widely studied, classic model of recessively inherited retinal degeneration in which the RPE fails to phagocytose shed outer segments, and photoreceptor cells subsequently die. We have used a positional cloning approach to study the rdy (retinal dystrophy) locus of the RCS rat. Within a 0.3 cM genetic inclusion interval, we have discovered a small deletion of RCS DNA that disrupts the gene encoding the receptor tyrosine kinase Mertk. The deletion includes the splice acceptor site upstream of the second coding exon of Mertk and results in a shortened transcript that lacks this exon. The aberrant transcript joins the first and third coding exons, leading to a frameshift and a translation termination signal 20 codons after the AUG. The concordance of these and other data indicate that Mertk is probably the gene for rdy. Our results provide genetic evidence for an essential role of a receptor tyrosine kinase in a specialized form of phagocytosis and suggest a molecular model for ingestion of outer segments by RPE cells.
+ Present address: Genset Genomic Research Center, RN 7, 91030 Evry cedex, France
§ To whom correspondence should be addressed. Tel: +1 650 723 3290; Fax: +1 650 723 7016; Email: vollrath@genome.stanford.edu
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H. Yamada, E. Yamada, A. Ando, N. Esumi, N. Bora, J. Saikia, C.-H. Sung, D. J. Zack, and P. A. Campochiaro Fibroblast Growth Factor-2 Decreases Hyperoxia-Induced Photoreceptor Cell Death in Mice Am. J. Pathol., September 1, 2001; 159(3): 1113 - 1120. [Abstract] [Full Text] [PDF]
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R. D. Lund, P. Adamson, Y. Sauve, D. J. Keegan, S. V. Girman, S. Wang, H. Winton, N. Kanuga, A. S. L. Kwan, L. Beauchene, et al. Subretinal transplantation of genetically modified human cell lines attenuates loss of visual function in dystrophic rats PNAS, August 14, 2001; 98(17): 9942 - 9947. [Abstract] [Full Text] [PDF]
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M. M. Jablonski, J. Tombran-Tink, D. A. Mrazek, and A. Iannaccone Pigment Epithelium-Derived Factor Supports Normal Development of Photoreceptor Neurons and Opsin Expression after Retinal Pigment Epithelium Removal J. Neurosci., October 1, 2000; 20(19): 7149 - 7157. [Abstract] [Full Text] [PDF]
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D. Vollrath, W. Feng, J. L. Duncan, D. Yasumura, P. M. D'Cruz, A. Chappelow, M. T. Matthes, M. A. Kay, and M. M. LaVail Correction of the retinal dystrophy phenotype of the RCS rat by viral gene transfer of Mertk PNAS, October 23, 2001; 98(22): 12584 - 12589. [Abstract] [Full Text] [PDF]
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