Mechanistic Basis for the Failure of Cone Transducin to Translocate: Why Cones Are Never Blinded by Light

被引:49
作者
Lobanova, Ekaterina S. [1 ]
Herrmann, Rolf [1 ]
Finkelstein, Stella [1 ]
Reidel, Boris [1 ]
Skiba, Nikolai P. [1 ]
Deng, Wen-Tao [2 ]
Jo, Rebecca [3 ]
Weiss, Ellen R. [3 ]
Hauswirth, William W. [2 ]
Arshavsky, Vadim Y. [1 ]
机构
[1] Duke Univ, Ctr Eye, Albert Eye Res Inst, Durham, NC 27710 USA
[2] Univ Florida, Dept Ophthalmol, Gainesville, FL 32610 USA
[3] Univ N Carolina, Dept Cell & Dev Biol, Chapel Hill, NC 27599 USA
基金
美国国家卫生研究院;
关键词
VISUAL PIGMENT PHOSPHORYLATION; PHOTORECEPTOR DARK-ADAPTATION; GTPASE ACCELERATING PROTEIN; DRIVEN RETINAL RESPONSES; ROD PHOTORECEPTORS; KNOCKOUT MOUSE; ALPHA-SUBUNIT; RAT RETINA; VERTEBRATE PHOTORECEPTORS; RHODOPSIN PHOSPHORYLATION;
D O I
10.1523/JNEUROSCI.0613-10.2010
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The remarkable ability of our vision to function under ever-changing conditions of ambient illumination is mediated by multiple molecular mechanisms regulating the light sensitivity of rods and cones. One such mechanism involves massive translocation of signaling proteins, including the G-protein transducin, into and out of the light-sensitive photoreceptor outer segment compartment. Transducin translocation extends the operating range of rods, but in cones transducin never translocates, which is puzzling because cones typically function in much brighter light than rods. Using genetically manipulated mice in which the rates of transducin activation and inactivation were altered, we demonstrate that, like in rods, transducin translocation in cones can be triggered when transducin activation exceeds a critical level, essentially saturating the photoresponse. However, this level is never achieved in wild-type cones: their superior ability to tightly control the rates of transducin activation and inactivation, responsible for avoiding saturation by light, also accounts for the prevention of transducin translocation at any light intensity.
引用
收藏
页码:6815 / 6824
页数:10
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