G. B. Bietti Foundation, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), 00198, Rome, Italy,
Adv Exp Med Biol. 2014;801:559-66. doi: 10.1007/978-1-4614-3209-8_71.
Light-activated movement of transducin-α (Gαt1) from rod photoreceptor outer segments (ROS) into inner segments (IS) enables rods to rapidly adapt to changes in light intensity. The threshold light intensity at which Gαt1 translocates from ROS into IS is primarily determined by the rates of activation and inactivation of Gαt1. Loss- of- expression of the retina specific cell surface protein, retinoschsin (Rs1-KO), led to a dramatic 3-10 fold increase, depending on age, in the luminance threshold for transducin translocation from ROS into IS compared with wild-type control. In contrast, arrestin translocated from IS into ROS at the same light intensity both in WT and Rs1-KO mice. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Gαt1 translocation in Rs1-KO mice. These changes in Rs1-KO mice were also associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.
视紫红质转导蛋白-α（Gαt1）从视杆细胞外节（ROS）向内节（IS）的光激活运动使视杆细胞能够快速适应光强度的变化。Gαt1 从 ROS 向 IS 易位的阈值光强度主要取决于 Gαt1 的激活和失活速率。视网膜特异性细胞表面蛋白 retinoschsin（Rs1-KO）的表达缺失导致视紫红质转导蛋白-α（Gαt1）从 ROS 向 IS 易位的亮度阈值显著增加 3-10 倍，这取决于年龄，与野生型对照相比。相比之下，在 WT 和 Rs1-KO 小鼠中，相同光照强度下视黄醛从 IS 向 ROS 易位。生化变化，包括转导蛋白水平降低和转导蛋白 GTPase 活性增强，解释了 Rs1-KO 小鼠中 Gαt1 易位光强度阈值的变化。这些 Rs1-KO 小鼠的变化也与光感受器形态和转录因子表达的年龄相关改变有关，表明光感受器成熟延迟。
