Department of Physiology, The Geffen School of Medicine at University of California, Los Angeles, California 90095-1751, USA.
Am J Physiol Cell Physiol. 2012 May 1;302(9):C1293-305. doi: 10.1152/ajpcell.00397.2011. Epub 2011 Dec 7.
The Na(+)-glucose cotransporter hSGLT1 is a member of a class of membrane proteins that harness Na(+) electrochemical gradients to drive uphill solute transport. Although hSGLT1 belongs to one gene family (SLC5), recent structural studies of bacterial Na(+) cotransporters have shown that Na(+) transporters in different gene families have the same structural fold. We have constructed homology models of hSGLT1 in two conformations, the inward-facing occluded (based on vSGLT) and the outward open conformations (based on Mhp1), mutated in turn each of the conserved gates and ligand binding residues, expressed the SGLT1 mutants in Xenopus oocytes, and determined the functional consequences using biophysical and biochemical assays. The results establish that mutating the ligand binding residues produces profound changes in the ligand affinity (the half-saturation concentration, K(0.5)); e.g., mutating sugar binding residues increases the glucose K(0.5) by up to three orders of magnitude. Mutation of the external gate residues increases the Na(+) to sugar transport stoichiometry, demonstrating that these residues are critical for efficient cotransport. The changes in phlorizin inhibition constant (K(i)) are proportional to the changes in sugar K(0.5), except in the case of F101C, where phlorizin K(i) increases by orders of magnitude without a change in glucose K(0.5). We conclude that glucose and phlorizin occupy the same binding site and that F101 is involved in binding to the phloretin group of the inhibitor. Substituted-cysteine accessibility methods show that the cysteine residues at the position of the gates and sugar binding site are largely accessible only to external hydrophilic methanethiosulfonate reagents in the presence of external Na(+), demonstrating that the external sugar (and phlorizin) binding vestibule is opened by the presence of external Na(+) and closes after the binding of sugar and phlorizin. Overall, the present results provide a bridge between kinetics and structural studies of cotransporters.
钠-葡萄糖协同转运蛋白 hSGLT1 是一类膜蛋白的成员,它利用 Na+电化学梯度来驱动溶质的 uphill 转运。尽管 hSGLT1 属于一个基因家族(SLC5),但最近对细菌 Na+协同转运蛋白的结构研究表明,不同基因家族的 Na+转运蛋白具有相同的结构折叠。我们构建了 hSGLT1 的两种构象的同源模型,即内向封闭构象(基于 vSGLT)和外向开放构象(基于 Mhp1),依次突变了保守的门控和配体结合残基,在非洲爪蟾卵母细胞中表达 SGLT1 突变体,并使用生物物理和生化测定来确定其功能后果。结果表明,突变配体结合残基会导致配体亲和力发生深刻变化(半饱和浓度,K0.5);例如,突变糖结合残基会使葡萄糖 K0.5 增加多达三个数量级。突变外门控残基会增加 Na+与糖的转运计量比,表明这些残基对高效协同转运至关重要。苦芪素抑制常数(K i)的变化与糖 K0.5 的变化成正比,除了 F101C 的情况,其中苦芪素 K i 增加了几个数量级,而葡萄糖 K0.5 没有变化。我们得出结论,葡萄糖和苦芪素占据相同的结合位点,并且 F101 参与与抑制剂的 phloretin 基团结合。取代半胱氨酸可及性方法表明,只有在存在外部 Na+的情况下,门控和糖结合位点的半胱氨酸残基才能被外部亲水性甲硫基磺酸盐试剂大量进入,这表明外部糖(和苦芪素)结合前庭是由外部 Na+的存在打开的,并且在糖和苦芪素结合后关闭。总体而言,本研究结果为协同转运蛋白的动力学和结构研究提供了桥梁。