Laboratory of Biological Chemistry, University of Ioannina Medical School, 45110 Ioannina, Greece.
J Biol Chem. 2010 Nov 5;285(45):35011-20. doi: 10.1074/jbc.M110.170415. Epub 2010 Aug 29.
Bacterial and fungal members of the ubiquitous nucleobase-ascorbate transporter (NAT/NCS2) family use the NAT signature motif, a conserved 11-amino acid sequence between amphipathic helices TM9a and TM9b, to define function and selectivity of the purine binding site. To examine the role of flanking helices TM9a, TM9b, and TM8, we employed Cys-scanning analysis of the xanthine-specific homolog YgfO from Escherichia coli. Using a functional mutant devoid of Cys residues (C-less), each amino acid residue in sequences (259)FLVVGTIYLLSVLEAVGDITATAMVSRRPIQGEEYQSRLKGGVLADGLVSVIASAV(314) and (342)TIAVMLVILGLFP(354) including these TMs (underlined) was replaced individually with Cys, except the irreplaceable Glu-272 and Asp-304, which had been studied previously. Of 67 single Cys mutants, 55 accumulate xanthine to 35-140% of the steady state observed with C-less, five (I265C, D276C, I277C, G299C, L350C) accumulate to low levels (10-20%) and seven (T278C, A279C, T280C, A281C, G305C, G351C, P354C) show negligible expression in the membrane. Extensive mutagenesis reveals that a carboxyl group is needed at Asp-276 for high activity and that D276E differs from wild type as it recognizes 8-methylxanthine (K(i) 79 μm) but fails to recognize 2-thioxanthine, 3-methylxanthine or 6-thioxanthine; bulky replacements of Ala-279 or Thr-280 and replacements of Gly-305, Gly-351, or Pro-354 impair activity or expression. Single Cys mutants V261C, A273C, G275C, and S284C are sensitive to inactivation by N-ethylmaleimide and sensitivity of G275C (IC(50) 15 μm) is enhanced in the presence of substrate. The data suggest that residues crucial for the transport mechanism cluster in two conserved motifs, at the cytoplasmic end of TM8 (EXXGDXXAT) and in TM9a (GXXXDG).
无处不在的核碱基-抗坏血酸转运体(NAT/NCS2)家族的细菌和真菌成员使用 NAT 特征基序,即跨膜螺旋 9a 和 9b 之间的保守 11 个氨基酸序列,来定义嘌呤结合位点的功能和选择性。为了研究侧翼螺旋 TM9a、TM9b 和 TM8 的作用,我们采用了大肠杆菌黄嘌呤特异性同源物 YgfO 的半胱氨酸扫描分析。使用缺乏半胱氨酸残基的功能突变体(无 C 型),除了先前研究过的不可替代的 Glu-272 和 Asp-304 之外,序列(259)FLVVGTIYLLSVLEAVGDITATAMVSRRPIQGEEYQSRLKGGVLADGLVSVIASAV(314)和(342)TIAVMLVILGLFP(354)中的每个氨基酸残基均被 Cys 取代,包括这些 TM(下划线)。在 67 个单个 Cys 突变体中,有 55 个积累黄嘌呤的量达到无 C 型观察到的稳态的 35-140%,5 个(I265C、D276C、I277C、G299C、L350C)积累到低水平(10-20%),7 个(T278C、A279C、T280C、A281C、G305C、G351C、P354C)在膜中表达可忽略不计。广泛的诱变表明,Asp-276 上的羧基是高活性所必需的,并且 D276E 与野生型不同,因为它识别 8-甲基黄嘌呤(K(i) 79 μm),但不能识别 2-硫代黄嘌呤、3-甲基黄嘌呤或 6-硫代黄嘌呤;Ala-279 或 Thr-280 的大取代以及 Gly-305、Gly-351 或 Pro-354 的取代会损害活性或表达。单个 Cys 突变体 V261C、A273C、G275C 和 S284C 对 N-乙基马来酰亚胺失活敏感,并且在存在底物时 G275C(IC(50) 15 μm)的敏感性增强。数据表明,对转运机制至关重要的残基聚集在两个保守基序中,一个在 TM8 的细胞质末端(EXXGDXXAT),另一个在 TM9a 中(GXXXDG)。