Schröter Grit, Mann Daniel, Kötting Carsten, Gerwert Klaus
From the Biophysics Department, Ruhr-University Bochum, 44801 Bochum, Germany.
From the Biophysics Department, Ruhr-University Bochum, 44801 Bochum, Germany
J Biol Chem. 2015 Jul 10;290(28):17085-95. doi: 10.1074/jbc.M115.651190. Epub 2015 May 15.
Gα subunits are central molecular switches in cells. They are activated by G protein-coupled receptors that exchange GDP for GTP, similar to small GTPase activation mechanisms. Gα subunits are turned off by GTP hydrolysis. For the first time we employed time-resolved FTIR difference spectroscopy to investigate the molecular reaction mechanisms of Gαi1. FTIR spectroscopy is a powerful tool that monitors reactions label free with high spatio-temporal resolution. In contrast to common multiple turnover assays, FTIR spectroscopy depicts the single turnover GTPase reaction without nucleotide exchange/Mg(2+) binding bias. Global fit analysis resulted in one apparent rate constant of 0.02 s(-1) at 15 °C. Isotopic labeling was applied to assign the individual phosphate vibrations for α-, β-, and γ-GTP (1243, 1224, and 1156 cm(-1), respectively), α- and β-GDP (1214 and 1134/1103 cm(-1), respectively), and free phosphate (1078/991 cm(-1)). In contrast to Ras · GAP catalysis, the bond breakage of the β-γ-phosphate but not the Pi release is rate-limiting in the GTPase reaction. Complementary common GTPase assays were used. Reversed phase HPLC provided multiple turnover rates and tryptophan fluorescence provided nucleotide exchange rates. Experiments were complemented by molecular dynamics simulations. This broad approach provided detailed insights at atomic resolution and allows now to identify key residues of Gαi1 in GTP hydrolysis and nucleotide exchange. Mutants of the intrinsic arginine finger (Gαi1-R178S) affected exclusively the hydrolysis reaction. The effect of nucleotide binding (Gαi1-D272N) and Ras-like/all-α interface coordination (Gαi1-D229N/Gαi1-D231N) on the nucleotide exchange reaction was furthermore elucidated.
Gα亚基是细胞中的核心分子开关。它们由G蛋白偶联受体激活,该受体将GDP交换为GTP,这类似于小GTP酶的激活机制。Gα亚基通过GTP水解而关闭。我们首次采用时间分辨傅里叶变换红外差光谱法来研究Gαi1的分子反应机制。傅里叶变换红外光谱法是一种强大的工具,可在无标记的情况下以高时空分辨率监测反应。与常见的多周转测定法不同,傅里叶变换红外光谱法描绘了无核苷酸交换/Mg(2+)结合偏差的单周转GTP酶反应。全局拟合分析得出在15°C下的一个表观速率常数为0.02 s(-1)。应用同位素标记来确定α-、β-和γ-GTP(分别为1243、1224和1156 cm(-1))、α-和β-GDP(分别为1214和1134/1103 cm(-1))以及游离磷酸根(1078/991 cm(-1))的各个磷酸振动。与Ras·GAP催化不同,β-γ-磷酸键的断裂而非Pi的释放是GTP酶反应中的限速步骤。使用了互补的常规GTP酶测定法。反相高效液相色谱法提供多周转速率,色氨酸荧光提供核苷酸交换速率。实验通过分子动力学模拟得到补充。这种广泛的方法在原子分辨率上提供了详细的见解,现在能够识别Gαi1在GTP水解和核苷酸交换中的关键残基。内在精氨酸指(Gαi1-R178S)的突变体仅影响水解反应。此外还阐明了核苷酸结合(Gαi1-D272N)和Ras样/全α界面配位(Gαi1-D229N/Gαi1-D231N)对核苷酸交换反应的影响。