Laboratory of Biological Chemistry, University of Ioannina Medical School, 45110 Ioannina, Greece.
J Biol Chem. 2010 Jun 18;285(25):19422-33. doi: 10.1074/jbc.M110.120543. Epub 2010 Apr 20.
The nucleobase-ascorbate transporter (NAT) signature motif is a conserved 11-amino acid sequence of the ubiquitous NAT/NCS2 family, essential for function and selectivity of both a bacterial (YgfO) and a fungal (UapA) purine-transporting homolog. We examined the role of NAT motif in more detail, using Cys-scanning and site-directed alkylation analysis of the YgfO xanthine permease of Escherichia coli. Analysis of single-Cys mutants in the sequence 315-339 for sensitivity to inactivation by 2-sulfonatoethyl methanethiosulfonate (MTSES(-)) and N-ethylmaleimide (NEM) showed a similar pattern: highly sensitive mutants clustering at the motif sequence (323-329) and a short alpha-helical face downstream (332, 333, 336). In the presence of substrate, N325C is protected from alkylation with either MTSES(-) or NEM, whereas sensitivity of A323C to inactivation by NEM is enhanced, shifting IC(50) from 34 to 14 microM. Alkylation or sensitivity of the other mutants is unaffected by substrate; the lack of an effect on Q324C is attributed to gross inability of this mutant for high affinity binding. Site-directed mutants G333R and S336N at the alpha-helical face downstream the motif display specific changes in ligand recognition relative to wild type; G333R allows binding of 7-methyl and 8-methylxanthine, whereas S336N disrupts affinity for 6-thioxanthine. Finally, all assayable motif-mutants are highly accessible to MTSES(-) from the periplasmic side. The data suggest that the NAT motif region lines the solvent- and substrate-accessible inner cavity, Asn-325 is at the binding site, Ala-323 responds to binding with a specific conformational shift, and Gly-333 and Ser-336 form part of the purine permeation pathway.
核苷碱基-抗坏血酸转运体 (NAT) 特征基序是普遍存在的 NAT/NCS2 家族的一个保守的 11 个氨基酸序列,对细菌 (YgfO) 和真菌 (UapA) 嘌呤转运同源物的功能和选择性都很重要。我们使用大肠杆菌黄嘌呤通透酶的半胱氨酸扫描和定点烷基化分析更详细地研究了 NAT 基序的作用。对序列 315-339 中的单个半胱氨酸突变体进行分析,以确定其对 2-磺乙基甲硫基乙磺酸 (MTSES(-)) 和 N-乙基马来酰亚胺 (NEM) 失活的敏感性,结果显示出相似的模式:高度敏感的突变体聚集在基序序列 (323-329) 和下游的短α-螺旋面 (332、333、336)。在底物存在的情况下,N325C 可免受 MTSES(-) 或 NEM 的烷基化作用的影响,而 A323C 对 NEM 失活的敏感性增强,IC50 从 34 微摩尔变为 14 微摩尔。其他突变体的烷基化或敏感性不受底物影响;由于该突变体几乎不能高亲和力结合,因此对 Q324C 没有影响。基序下游α-螺旋面上的定点突变体 G333R 和 S336N 与野生型相比显示出配体识别的特异性变化;G333R 允许 7-甲基和 8-甲基黄嘌呤结合,而 S336N 破坏了与 6-硫代黄嘌呤的亲和力。最后,所有可检测的基序突变体都非常容易从周质侧与 MTSES(-) 结合。数据表明,NAT 基序区域构成了溶剂和底物可及的内腔,Asn-325 位于结合位点,Ala-323 对结合的响应是一个特定的构象转变,而 Gly-333 和 Ser-336 构成嘌呤渗透途径的一部分。