Institut für Medizinische Physik und Biophysik - CC2, Charité - Universitätsmedizin Berlin, Charitéplatz 1, D-10117 Berlin, Germany.
Nature. 2011 Mar 31;471(7340):651-5. doi: 10.1038/nature09789. Epub 2011 Mar 9.
G-protein-coupled receptors (GPCRs) are seven transmembrane helix (TM) proteins that transduce signals into living cells by binding extracellular ligands and coupling to intracellular heterotrimeric G proteins (Gαβγ). The photoreceptor rhodopsin couples to transducin and bears its ligand 11-cis-retinal covalently bound via a protonated Schiff base to the opsin apoprotein. Absorption of a photon causes retinal cis/trans isomerization and generates the agonist all-trans-retinal in situ. After early photoproducts, the active G-protein-binding intermediate metarhodopsin II (Meta II) is formed, in which the retinal Schiff base is still intact but deprotonated. Dissociation of the proton from the Schiff base breaks a major constraint in the protein and enables further activating steps, including an outward tilt of TM6 and formation of a large cytoplasmic crevice for uptake of the interacting C terminus of the Gα subunit. Owing to Schiff base hydrolysis, Meta II is short-lived and notoriously difficult to crystallize. We therefore soaked opsin crystals with all-trans-retinal to form Meta II, presuming that the crystal's high concentration of opsin in an active conformation (Ops*) may facilitate all-trans-retinal uptake and Schiff base formation. Here we present the 3.0 Å and 2.85 Å crystal structures, respectively, of Meta II alone or in complex with an 11-amino-acid C-terminal fragment derived from Gα (GαCT2). GαCT2 binds in a large crevice at the cytoplasmic side, akin to the binding of a similar Gα-derived peptide to Ops* (ref. 7). In the Meta II structures, the electron density from the retinal ligand seamlessly continues into the Lys 296 side chain, reflecting proper formation of the Schiff base linkage. The retinal is in a relaxed conformation and almost undistorted compared with pure crystalline all-trans-retinal. By comparison with early photoproducts we propose how retinal translocation and rotation induce the gross conformational changes characteristic for Meta II. The structures can now serve as models for the large GPCR family.
G 蛋白偶联受体(GPCRs)是一种七次跨膜螺旋(TM)蛋白,通过与细胞外配体结合并与细胞内异三聚体 G 蛋白(Gαβγ)偶联,将信号转导到活细胞中。光感受器视紫红质与转导蛋白偶联,并通过质子化的席夫碱将其配体 11-顺式视黄醛共价结合到视蛋白脱辅基蛋白上。吸收光子会导致视黄醛顺/反异构化,并在原位生成激动剂全反式视黄醛。在早期光产物之后,形成活性 G 蛋白结合中间产物视紫红质 II(Meta II),其中视黄醛席夫碱仍然完整但去质子化。席夫碱中质子的解离打破了蛋白质中的主要限制,并使进一步的激活步骤成为可能,包括 TM6 的向外倾斜和形成用于摄取 Gα 亚基相互作用的 C 末端的大细胞质裂隙。由于席夫碱水解,Meta II 是短寿命的,并且众所周知难以结晶。因此,我们用全反式视黄醛浸泡视蛋白晶体以形成 Meta II,假设晶体中高浓度的处于活性构象的视蛋白(Ops*)可能有助于全反式视黄醛摄取和席夫碱形成。在这里,我们分别呈现了单独的 Meta II 或与源自 Gα(GαCT2)的 11 个氨基酸 C 末端片段形成复合物的 Meta II 的 3.0Å 和 2.85Å 晶体结构。GαCT2 结合在细胞质侧的一个大裂隙中,类似于类似的 Gα 衍生肽与 Ops*的结合(参考文献 7)。在 Meta II 结构中,来自视黄醛配体的电子密度无缝地延续到 Lys296 侧链,反映了席夫碱键的正确形成。与纯结晶全反式视黄醛相比,视黄醛处于松弛构象且几乎未变形。通过与早期光产物进行比较,我们提出了视黄醛易位和旋转如何诱导 Meta II 特征的大构象变化。这些结构现在可以作为大型 GPCR 家族的模型。