Mechanistic basis for the failure of cone transducin to translocate: why cones are never blinded by light.
Mechanistic basis for the failure of cone transducin to translocate: why cones are never blinded by light.
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DOI：
10.1523/jneurosci.0613-10.2010
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发表时间：
2010-05-19
期刊：
影响因子：
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通讯作者：
Arshavsky VY
中科院分区：
文献类型：
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作者：
Lobanova ES;Herrmann R;Finkelstein S;Reidel B;Skiba NP;Deng WT;Jo R;Weiss ER;Hauswirth WW;Arshavsky VY
我们的视觉在不断变化的环境照明条件下发挥作用的非凡能力是由调节视杆细胞和视锥细胞光敏性的多种分子机制介导的。一种这样的机制涉及大量的易位信号蛋白，包括G蛋白转导，进出光敏感的光感受器外节隔室。Transducin易位扩大了杆的操作范围，但在锥transducin从来没有易位，这是令人费解的，因为锥通常在更明亮的光比杆的功能。使用基因操作的小鼠，其中transformin激活和失活的速率被改变，我们证明，像在杆，transformin易位在视锥细胞中可以被触发时，transformin激活超过一个临界水平，基本上饱和的光响应。然而，在野生型视锥细胞中从未达到该水平：它们严格控制转导蛋白活化和失活速率的上级能力，负责避免光饱和，也负责防止任何光强度下的转导蛋白易位。
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 prevention of transducin translocation at any light intensity.