Department of Frontier Materials, Nagoya Institute of Technology, Nagoya, Japan.
Biophys J. 2011 Apr 20;100(8):1874-82. doi: 10.1016/j.bpj.2011.02.054.
G-protein-coupled receptors transmit stimuli (light, taste, hormone, neurotransmitter, etc.) to the intracellular signaling systems, and rhodopsin (Rh) is the most-studied G-protein-coupled receptor. Rh possesses an 11-cis retinal as the chromophore, and 11-cis to all-trans photoisomerization leads to the protein structural changes in the cytoplasmic loops to activate G-protein. Microbial rhodopsins are similar heptahelical membrane proteins that function as bacterial sensors, light-driven ion-pumps, or light-gated channels. Microbial rhodopsins possess an all-trans retinal, and all-trans to 13-cis photoisomerization triggers protein structural changes for each function. Despite these similarities, there is no sequence homology between visual and microbial rhodopsins, and microbial rhodopsins do not activate G-proteins. However, it was reported that bacteriorhodopsin (BR) chimeras containing the third cytoplasmic loop of bovine Rh are able to activate G-protein, suggesting a common mechanism of protein structural changes. Here we design chimeric proteins for Natronomonas pharaonis sensory rhodopsin II (SRII, also called pharaonis phoborhodopsin), which has a two-orders-of-magnitude slower photocycle than BR. Light-dependent transducin activation was observed for most of the nine SRII chimeras containing the third cytoplasmic loop of bovine Rh (from Y223, G224, Q225 to T251, R252, and M253), but the activation level was 30,000-140,000 times lower than that of bovine Rh. The BR chimera, BR/Rh223-253, activates a G-protein transducin, whereas the activation level was 37,000 times lower than that of bovine Rh. We interpret the low activation by the chimeric proteins as reasonable, because bovine Rh must have been optimized for activating a G-protein transducin during its evolution. On the other hand, similar activation level of the SRII and BR chimeras suggests that the lifetime of the M intermediates is not the simple determinant of activation, because SRII chimeras have two-orders-of-magnitude's slower photocycle than the BR chimera. Activation mechanism of visual and microbial rhodopsins is discussed on the basis of these results.
G 蛋白偶联受体将刺激(光、味道、激素、神经递质等)传递到细胞内信号系统,视紫红质(Rh)是研究最多的 G 蛋白偶联受体。Rh 具有 11-顺式视黄醛作为发色团,11-顺式到全反式光异构化导致细胞质环中的蛋白质结构变化,从而激活 G 蛋白。微生物视紫红质是类似的七螺旋膜蛋白,作为细菌传感器、光驱动离子泵或光门控通道发挥作用。微生物视紫红质具有全反式视黄醛,全反式到 13-顺式光异构化引发每种功能的蛋白质结构变化。尽管存在这些相似之处,但视觉和微生物视紫红质之间没有序列同源性,并且微生物视紫红质不能激活 G 蛋白。然而,据报道,包含牛 Rh 第三细胞质环的菌视紫红质(BR)嵌合体能够激活 G 蛋白,这表明蛋白质结构变化的共同机制。在这里,我们设计了纳氏盐沼红球菌感觉视紫红质 II(SRII,也称为盐沼嗜盐菌视紫红质)的嵌合蛋白,其光循环速度比 BR 慢两个数量级。观察到大多数包含牛 Rh 第三细胞质环的 9 种 SRII 嵌合体(从 Y223、G224、Q225 到 T251、R252 和 M253)的光依赖性转导蛋白激活,但激活水平比牛 Rh 低 30,000-140,000 倍。BR 嵌合体 BR/Rh223-253 激活 G 蛋白转导蛋白,但其激活水平比牛 Rh 低 37,000 倍。我们将嵌合蛋白的低激活解释为合理的,因为在进化过程中,牛 Rh 必须优化了激活 G 蛋白转导蛋白的能力。另一方面,SRII 和 BR 嵌合体的类似激活水平表明 M 中间体的寿命不是激活的简单决定因素,因为 SRII 嵌合体的光循环速度比 BR 嵌合体慢两个数量级。基于这些结果,讨论了视觉和微生物视紫红质的激活机制。