Brain and Mind Research Institute, University of Sydney, Sydney, New South Wales 2050, Australia.
J Biol Chem. 2012 Jun 15;287(25):21244-52. doi: 10.1074/jbc.M111.337741. Epub 2012 Apr 25.
The glycine receptor (GlyR) exists either in homomeric α or heteromeric αβ forms. Its agonists bind at extracellular subunit interfaces. Unlike subunit interfaces from the homomeric α GlyR, subunit interfaces from the heteromeric αβ GlyR have not been characterized unambiguously because of the existence of multiple types of interface within single receptors. Here, we report that, by reconstituting β+/α- interfaces in a homomeric GlyR (αChb+a- GlyR), we were able to functionally characterize the αβ GlyR β+/α- interfaces. We found that the β+/α- interface had a higher agonist sensitivity than that of the α+/α- interface. This high sensitivity was contributed primarily by loop A. We also found that the β+/α- interface differentially modulates the agonist properties of glycine and taurine. Using voltage clamp fluorometry, we found that the conformational changes induced by glycine binding to the β+/α- interface were different from those induced by glycine binding to the α+/α- interface in the α GlyR. Moreover, the distinct conformational changes found at the β+/α- interface in the αChb+a- GlyR were also found in the heteromeric αβ GlyR, which suggests that the αChb+a- GlyR reconstitutes structural components and recapitulates functional properties, of the β+/α- interface in the heteromeric αβ GlyR. Our investigation not only provides structural and functional information about the GlyR β+/α- interface, which could direct GlyR β+/α- interface-specific drug design, but also provides a general methodology for unambiguously characterizing properties of specific protein interfaces from heteromeric proteins.
甘氨酸受体 (GlyR) 以同型的 α 或异型的 αβ 形式存在。其激动剂结合在细胞外亚基界面上。与同型的 α GlyR 的亚基界面不同,由于单个受体中存在多种类型的界面,异型的 αβ GlyR 的亚基界面尚未被明确表征。在这里,我们报告通过在同型 GlyR(αChb+a- GlyR)中重新构建β+/α-界面,我们能够对 αβ GlyR 的β+/α-界面进行功能表征。我们发现,β+/α-界面的激动剂敏感性高于α+/α-界面。这种高敏感性主要是由环 A 贡献的。我们还发现,β+/α-界面对甘氨酸和牛磺酸的激动剂特性具有不同的调节作用。使用电压钳荧光法,我们发现甘氨酸与β+/α-界面结合诱导的构象变化与甘氨酸与α+/α-界面结合在α GlyR 中诱导的构象变化不同。此外,在 αChb+a- GlyR 中β+/α-界面发现的独特构象变化也在异型的 αβ GlyR 中发现,这表明 αChb+a- GlyR 重新构建了异型的 αβ GlyR 中β+/α-界面的结构成分并再现了其功能特性。我们的研究不仅提供了关于 GlyR β+/α-界面的结构和功能信息,这可以指导 GlyR β+/α-界面特异性药物设计,而且还提供了一种明确表征异型蛋白中特定蛋白界面特性的通用方法。