Liu Rongfang, Groenewoud Nick J A, Peeters Miriam C, Lenselink Eelke B, IJzerman Ad P
Division of Medicinal Chemistry, Leiden Academic Centre for Drug Research, Leiden University, P.O. Box 9502, 2300 RA, Leiden, Netherlands.
Purinergic Signal. 2014 Sep;10(3):441-53. doi: 10.1007/s11302-014-9407-6. Epub 2014 Jan 26.
The expression of human G protein-coupled receptors (GPCRs) in Saccharomyces cerevisiae containing chimeric yeast/mammalian Gα subunits provides a useful tool for the study of GPCR activation. In this study, we used a one-GPCR-one-G protein yeast screening method in combination with molecular modeling and mutagenesis studies to decipher the interaction between GPCRs and the C-terminus of different α-subunits of G proteins. We chose the human adenosine A2B receptor (hA2BR) as a paradigm, a typical class A GPCR that shows promiscuous behavior in G protein coupling in this yeast system. The wild-type hA2BR and five mutant receptors were expressed in 8 yeast strains with different humanized G proteins, covering the four major classes: Gαi, Gαs, Gαq, and Gα12. Our experiments showed that a tyrosine residue (Y) at the C-terminus of the Gα subunit plays an important role in controlling the activation of GPCRs. Receptor residues R103(3.50) and I107(3.54) are vital too in G protein-coupling and the activation of the hA2BR, whereas L213(IL3) is more important in G protein inactivation. Substitution of S235(6.36) to alanine provided the most divergent G protein-coupling profile. Finally, L236(6.37) substitution decreased receptor activation in all G protein pathways, although to a different extent. In conclusion, our findings shed light on the selectivity of receptor/G protein coupling, which may help in further understanding GPCR signaling.
在含有嵌合酵母/哺乳动物Gα亚基的酿酒酵母中表达人类G蛋白偶联受体(GPCR),为研究GPCR激活提供了一个有用的工具。在本研究中,我们使用了一种一GPCR一G蛋白的酵母筛选方法,结合分子建模和诱变研究,来解读GPCR与不同G蛋白α亚基C末端之间的相互作用。我们选择人类腺苷A2B受体(hA2BR)作为范例,它是典型的A类GPCR,在该酵母系统中,其G蛋白偶联表现出混杂性。野生型hA2BR和五种突变受体在8种含有不同人源化G蛋白的酵母菌株中表达,这些G蛋白涵盖四大类:Gαi、Gαs、Gαq和Gα12。我们的实验表明,Gα亚基C末端的一个酪氨酸残基(Y)在控制GPCR激活中起重要作用。受体残基R103(3.50)和I107(3.54)在hA2BR的G蛋白偶联和激活中也至关重要,而L213(IL3)在G蛋白失活中更为重要。将S235(6.36)替换为丙氨酸产生了最不同的G蛋白偶联谱。最后,L236(6.37)替换在所有G蛋白途径中均降低了受体激活,尽管程度不同。总之,我们的研究结果揭示了受体/G蛋白偶联的选择性,这可能有助于进一步理解GPCR信号传导。