Gesteira Tarsis Ferreira, Marforio Tainah Dorina, Mueller Jonathan Wolf, Calvaresi Matteo, Coulson-Thomas Vivien Jane
College of Optometry, University of Houston, Houston, Texas 77004, United States.
Dipartimento di Chimica "Giacomo Ciamician", Università di Bologna, Bologna 40126, Italy.
ACS Catal. 2021 Sep 3;11(17):10974-10987. doi: 10.1021/acscatal.1c03088. Epub 2021 Aug 18.
Heparan sulfate (HS) and heparin contain imprinted "sulfation codes", which dictate their diverse physiological and pathological functions. A group of orchestrated biosynthetic enzymes cooperate in polymerizing and modifying HS chains. The biotechnological development of enzymes that can recreate this sulfation pattern on synthetic heparin is challenging, primarily due to the paucity of quantitative data for sulfotransferase enzymes. Herein, we identified critical structural characteristics that determine substrate specificity and shed light on the catalytic mechanism of sugar sulfation of two HS sulfotransferases, 2-O-sulfotransferase (HS2ST) and 6-O-sulfotransferase (HS6ST). Two sets of molecular clamps in HS2ST recognize appropriate substrates; these clamps flank the acceptor binding site on opposite sides. The hexuronic epimers, and not their puckers, have a critical influence on HS2ST selectivity. In contrast, HS6ST recognizes a broader range of substrates. This promiscuity is granted by a conserved tryptophan residue, W210, that positions the acceptor within the active site for catalysis by means of strong electrostatic interactions. Lysines K131 and K132 act in concert with a second tryptophan, W153, shedding water molecules from within the active site, thus providing HS6ST with a binding preference toward 2-O-sulfated substrates. QM/MM calculations provided valuable mechanistic insights into the catalytic process, identifying that the sulfation of both HS2ST and HS6ST follows a SN2-like mechanism. When they are taken together, our findings reveal the molecular basis of how these enzymes recognize different substrates and catalyze sugar sulfation, enabling the generation of enzymes that could create specific heparin epitopes.
硫酸乙酰肝素(HS)和肝素含有印记“硫酸化密码”,这些密码决定了它们多样的生理和病理功能。一组精心编排的生物合成酶协同作用,使HS链聚合并进行修饰。能够在合成肝素上重现这种硫酸化模式的酶的生物技术开发具有挑战性,主要是由于硫酸转移酶的定量数据匮乏。在此,我们确定了决定底物特异性的关键结构特征,并阐明了两种HS硫酸转移酶,即2-O-硫酸转移酶(HS2ST)和6-O-硫酸转移酶(HS6ST)的糖硫酸化催化机制。HS2ST中的两组分子钳识别合适的底物;这些钳位于受体结合位点的两侧。己糖醛酸差向异构体而非其构象对HS2ST的选择性有关键影响。相比之下,HS6ST识别更广泛的底物。这种通用性是由保守的色氨酸残基W210赋予的,它通过强烈的静电相互作用将受体定位在活性位点内以进行催化。赖氨酸K131和K132与第二个色氨酸W153协同作用,从活性位点内去除水分子,从而使HS6ST对2-O-硫酸化底物具有结合偏好。量子力学/分子力学(QM/MM)计算为催化过程提供了有价值的机制见解,确定HS2ST和HS6ST的硫酸化均遵循类似SN2的机制。综合来看,我们的研究结果揭示了这些酶如何识别不同底物并催化糖硫酸化的分子基础,从而能够生成可产生特定肝素表位的酶。