Structural Glycobiology Section, National Institutes of Health, Frederick, Maryland 21702; Basic Research Program, SAIC-Frederick, Inc., Center for Cancer Research Nanobiology Program, Center for Cancer Research, NCI, National Institutes of Health, Frederick, Maryland 21702.
Structural Glycobiology Section, National Institutes of Health, Frederick, Maryland 21702.
J Biol Chem. 2010 May 14;285(20):15619-15626. doi: 10.1074/jbc.M109.099564. Epub 2010 Mar 17.
The beta1,4-galactosyltransferase-7 (beta4Gal-T7) enzyme, one of seven members of the beta4Gal-T family, transfers in the presence of manganese Gal from UDP-Gal to an acceptor sugar (xylose) that is attached to a side chain hydroxyl group of Ser/Thr residues of proteoglycan proteins. It exhibits the least protein sequence similarity with the other family members, including the well studied family member beta4Gal-T1, which, in the presence of manganese, transfers Gal from UDP-Gal to GlcNAc. We report here the crystal structure of the catalytic domain of beta4Gal-T7 from Drosophila in the presence of manganese and UDP at 1.81 A resolution. In the crystal structure, a new manganese ion-binding motif (HXH) has been observed. Superposition of the crystal structures of beta4Gal-T7 and beta4Gal-T1 shows that the catalytic pocket and the substrate-binding sites in these proteins are similar. Compared with GlcNAc, xylose has a hydroxyl group (instead of an N-acetyl group) at C2 and lacks the CH(2)OH group at C5; thus, these protein structures show significant differences in their acceptor-binding site. Modeling of xylose in the acceptor-binding site of the beta4Gal-T7 crystal structure shows that the aromatic side chain of Tyr(177) interacts strongly with the C5 atom of xylose, causing steric hindrance to any additional group at C5. Because Drosophila Cd7 has a 73% protein sequence similarity to human Cd7, the present crystal structure offers a structure-based explanation for the mutations in human Cd7 that have been linked to Ehlers-Danlos syndrome.
β1,4-半乳糖基转移酶-7(β4Gal-T7)酶是β4Gal-T 家族的七个成员之一,在锰的存在下,从 UDP-Gal 将 Gal 转移到连接到蛋白聚糖蛋白丝氨酸/苏氨酸残基侧链羟基的受体糖(木糖)上。它与其他家族成员,包括研究得很好的β4Gal-T1 成员,表现出最小的蛋白质序列相似性,β4Gal-T1 在锰的存在下,从 UDP-Gal 将 Gal 转移到 GlcNAc。我们在此报告来自果蝇的β4Gal-T7 催化结构域在锰和 UDP 存在下的晶体结构,分辨率为 1.81Å。在晶体结构中,观察到一个新的锰离子结合基序(HXH)。β4Gal-T7 和β4Gal-T1 的晶体结构叠加表明这些蛋白质的催化口袋和底物结合位点相似。与 GlcNAc 相比,木糖在 C2 位有一个羟基(而不是 N-乙酰基),并且在 C5 位缺少 CH(2)OH 基团;因此,这些蛋白质结构在受体结合位点表现出明显的差异。在β4Gal-T7 晶体结构的受体结合位点中对木糖进行建模表明,Tyr(177)的芳香侧链与木糖的 C5 原子强烈相互作用,导致 C5 上任何额外基团的空间位阻。因为果蝇 Cd7 与人类 Cd7 有 73%的蛋白质序列相似性,所以目前的晶体结构为与埃勒斯-当洛斯综合征相关的人类 Cd7 突变提供了基于结构的解释。