ArticleJournal of biomedical science2012
Drosophila king tubby (ktub) mediates light-induced rhodopsin endocytosis and retinal degeneration.
Article in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Progressive mitochondrial dysfunction impairs visual signal transduction and induces retinal degeneration inFrontiers in insect science · 2025Article
- A novel homozygous TUB mutation associated with autosomal recessive retinitis pigmentosa in a consanguineous Chinese family.BMC medical genomics · 2023Article
- TheeLife · 2019Article
- Effects of Modest Hypoxia and Exercise on Cardiac Function, Sleep-Activity, Negative Geotaxis Behavior of Aged FemaleFrontiers in physiology · 2019Article
- Genetic architecture of natural variation in visual senescence in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Disease Protein Tulp1 Is Essential for Periactive Zone Endocytosis in Photoreceptor Ribbon Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Diverse cell type-specific mechanisms localize G protein-coupled receptors to Caenorhabditis elegans sensory cilia.Genetics · 2014Article
- dTULP, the Drosophila melanogaster homolog of tubby, regulates transient receptor potential channel localization in cilia.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe tubby (tub) and tubby-like protein (tulp) 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 Drosophila king tubby (ktub) in rhodopsin 1 (Rh1) endocytosis and retinal degeneration upon light stimulation.
resultsDrosophila ktub 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 ktub mutants, the majority of Rh1 remains at the rhabdomere, and only a few RLVs appear in the cytoplasm of photoreceptor cells. Mutation of norpA allele causes massive Rh1 endocytosis in light stimulation. In ktub and norpA double mutants, however, Rh1 endocytosis is blocked under light stimulation. This study also shows that ktub and norpA double mutants rescue the light-induced norpA retinal degeneration. Deletion constructs further demonstrate that the Tubby domain of the Ktub protein participates in an important role in Rh1 endocytosis.
conclusionsThe results in this study delimit the novel function of Ktub in Rh1 endocytosis and retinal degeneration.
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