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Volume 17, Number 15, Issue of August 1, 1997 pp. 5881-5890
Copyright ©1997 Society for Neuroscience

Mammalian Homolog of Drosophila retinal degeneration B Rescues the Mutant Fly Phenotype

Received March 11, 1997; revised May 12, 1997; accepted May 22, 1997.

Jinghua T. Chang1, Scott Milligan4, Yuanyuan Li1, Christina E. Chew1, Janey Wiggs5, Neal G. Copeland6, Nancy A. Jenkins6, Peter A. Campochiaro1, 2, David R. Hyde4, and Donald J. Zack1, 2, 3

1 Wilmer Eye Institute and Departments of 2 Neuroscience and 3 Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-9289, 4 Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556, 5 New England Eye Center, Tufts University School of Medicine, Boston, Massachusetts 02111, and 6 Mammalian Genetics Laboratory, ABL-Frederick Cancer Research and Development Center, Frederick, Maryland 21702

Mutations in the Drosophila rdgB gene, which encodes a transmembrane phosphatidylinositol transfer protein (PITP), cause a light-enhanced retinal degeneration. Cloning of mammalian rdgB orthologs (mrdgB) reveal predicted proteins that are 39% identical to rdgB, with highest homology in the N-terminal PITP domain (62%) and in a region near the C terminus (65%). The human mrdgB gene spans ~12 kb and maps to 11q13.1, a locus where several retinal diseases have also been mapped. Murine mrdgB maps to a syntenic region on the proximal region of chromosome 19. MrdgB is specifically expressed in the retina and brain. In the retina, MrdgB protein is localized to photoreceptor inner segments and the outer and inner plexiform layers. Expression of murine mrdgB in mutant flies fully rescues both the rdgB-dependent retinal degeneration and abnormal electroretinogram. These results suggest the existence of similarities between the invertebrate and mammalian retina that were not previously appreciated and also identify mrdgB as a candidate gene for retinal diseases that map to 11q13.1.

Key words: retina; retinal degeneration; phosphatidylinositol transfer protein; photoreceptors; phototransduction; retinal degeneration B




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