Cahill Thomas J, Thomsen Alex R B, Tarrasch Jeffrey T, Plouffe Bianca, Nguyen Anthony H, Yang Fan, Huang Li-Yin, Kahsai Alem W, Bassoni Daniel L, Gavino Bryant J, Lamerdin Jane E, Triest Sarah, Shukla Arun K, Berger Benjamin, Little John, Antar Albert, Blanc Adi, Qu Chang-Xiu, Chen Xin, Kawakami Kouki, Inoue Asuka, Aoki Junken, Steyaert Jan, Sun Jin-Peng, Bouvier Michel, Skiniotis Georgios, Lefkowitz Robert J
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Department of Biochemistry, Duke University Medical Center, Durham, NC 27710.
Proc Natl Acad Sci U S A. 2017 Mar 7;114(10):2562-2567. doi: 10.1073/pnas.1701529114. Epub 2017 Feb 21.
β-Arrestins (βarrs) interact with G protein-coupled receptors (GPCRs) to desensitize G protein signaling, to initiate signaling on their own, and to mediate receptor endocytosis. Prior structural studies have revealed two unique conformations of GPCR-βarr complexes: the "tail" conformation, with βarr primarily coupled to the phosphorylated GPCR C-terminal tail, and the "core" conformation, where, in addition to the phosphorylated C-terminal tail, βarr is further engaged with the receptor transmembrane core. However, the relationship of these distinct conformations to the various functions of βarrs is unknown. Here, we created a mutant form of βarr lacking the "finger-loop" region, which is unable to form the core conformation but retains the ability to form the tail conformation. We find that the tail conformation preserves the ability to mediate receptor internalization and βarr signaling but not desensitization of G protein signaling. Thus, the two GPCR-βarr conformations can carry out distinct functions.
β-抑制蛋白(βarrs)与G蛋白偶联受体(GPCRs)相互作用,使G蛋白信号脱敏,自身启动信号传导,并介导受体内吞作用。先前的结构研究揭示了GPCR-βarr复合物的两种独特构象:“尾部”构象,其中βarr主要与磷酸化的GPCR C末端尾部偶联;以及“核心”构象,除了磷酸化的C末端尾部外,βarr还与受体跨膜核心进一步结合。然而,这些不同构象与βarrs各种功能之间的关系尚不清楚。在这里,我们创建了一种缺乏“指环”区域的βarr突变形式,该区域无法形成核心构象,但保留了形成尾部构象的能力。我们发现,尾部构象保留了介导受体内化和βarr信号传导的能力,但不能使G蛋白信号脱敏。因此,两种GPCR-βarr构象可以执行不同的功能。