<it>Drosophila king tubby (ktub)</it> mediates light-induced rhodopsin endocytosis and retinal degeneration
<p>Background</p> <p>The <it>tubby</it> (<it>tub)</it> and <it>tubby-like protein (tulp)</it> genes encode a small family of proteins found in many organisms. Previous studies have shown that TUB and TULP genes in mammalian involve in obesity, ne...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2012-12-01
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| Series: | Journal of Biomedical Science |
| Subjects: | |
| Online Access: | http://www.jbiomedsci.com/content/19/1/101 |
| Summary: | <p>Background</p> <p>The <it>tubby</it> (<it>tub)</it> and <it>tubby-like protein (tulp)</it> genes encode a small family of proteins found in many organisms. Previous studies have shown that TUB and TULP genes in mammalian involve in obesity, neural development, and retinal degeneration. The purpose of this study was to investigate the role of <it>Drosophila king tubby (ktub)</it> in rhodopsin 1 (Rh1) endocytosis and retinal degeneration upon light stimulation.</p> <p>Results</p> <p><it>Drosophila ktub</it> mutants were generated using imprecise excision. Wild type and mutant flies were raised in dark or constant light conditions. After a period of light stimulation, retinas were dissected, fixed and stained with anti-Rh1 antibody to reveal Rh1 endocytosis. Confocal and transmission electron microscope were used to examine the retinal degeneration. Immunocytochemical analysis shows that Ktub is expressed in the rhabdomere domain under dark conditions. When flies receive light stimulation, the Ktub translocates from the rhabdomere to the cytoplasm and the nucleus of the photoreceptor cells. Wild type photoreceptors form Rh1-immunopositive large vesicles (RLVs) shortly after light stimulation. In light-induced <it>ktub</it> mutants, the majority of Rh1 remains at the rhabdomere, and only a few RLVs appear in the cytoplasm of photoreceptor cells. Mutation of <it>norpA</it> allele causes massive Rh1 endocytosis in light stimulation. In <it>ktub</it> and <it>norpA</it> double mutants, however, Rh1 endocytosis is blocked under light stimulation. This study also shows that <it>ktub</it> and <it>norpA</it> double mutants rescue the light-induced <it>norpA</it> retinal degeneration. Deletion constructs further demonstrate that the Tubby domain of the Ktub protein participates in an important role in Rh1 endocytosis.</p> <p>Conclusions</p> <p>The results in this study delimit the novel function of Ktub in Rh1 endocytosis and retinal degeneration.</p> |
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| ISSN: | 1021-7770 1423-0127 |