- 作者: Shu-Fen Chen, Yu-Chen Tsai and Seng-Sheen Fan
- 作者服務機構: Department of Life Science, Tunghai University, Taiwan, R.O.C
- 中文摘要: --
- 英文摘要:
Background: The 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.
Results: Drosophila 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 transloclates 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.
Conclusions: The results in this study delimit the novel function of Ktub in Rh1 endocytosis and retinal
degeneration. - 中文關鍵字: --
- 英文關鍵字: King-tubby, Rhabdomere, Phototransduction, Endocytosis, Retinal degeneration