Zouhar J, Vévodová J, Marek J, Damborský J, Su X D, Brzobohatý B
Department of Functional Genomics and Proteomics, Faculty of Science, Masaryk University, Kotláská 2, CZ-61137 Brno, Czech Republic.
Plant Physiol. 2001 Nov;127(3):973-85.
The maize (Zea mays) beta-glucosidase Zm-p60.1 has been implicated in regulation of plant development by the targeted release of free cytokinins from cytokinin-O-glucosides, their inactive storage forms. The crystal structure of the wild-type enzyme was solved at 2.05-A resolution, allowing molecular docking analysis to be conducted. This indicated that the enzyme specificity toward substrates with aryl aglycones is determined by aglycone aromatic system stacking with W373, and interactions with edges of F193, F200, and F461 located opposite W373 in a slot-like aglycone-binding site. These aglycone-active site interactions recently were hypothesized to determine substrate specificity in inactive enzyme substrate complexes of ZM-Glu1, an allozyme of Zm-p60.1. Here, we test this hypothesis by kinetic analysis of F193I/Y/W mutants. The decreased K(m) of all mutants confirmed the involvement of F193 in determining enzyme affinity toward substrates with an aromatic aglycone. It was unexpected that a 30-fold decrease in k(cat) was found in F193I mutant compared with the wild type. Kinetic analysis and computer modeling demonstrated that the F193-aglycone-W373 interaction not only contributes to aglycone recognition as hypothesized previously but also codetermines catalytic rate by fixing the glucosidic bond in an orientation favorable for attack by the catalytic pair, E186 and E401. The catalytic pair, assigned initially by their location in the structure, was confirmed by kinetic analysis of E186D/Q and E401D/Q mutants. It was unexpected that the E401D as well as C205S and C211S mutations dramatically impaired the assembly of a catalysis-competent homodimer, suggesting novel links between the active site structure and dimer formation.
玉米(Zea mays)β-葡萄糖苷酶Zm-p60.1通过从细胞分裂素-O-葡萄糖苷(它们的无活性储存形式)中靶向释放游离细胞分裂素来参与植物发育的调控。野生型酶的晶体结构在2.05埃分辨率下解析出来,从而能够进行分子对接分析。这表明,该酶对具有芳基糖苷配基的底物的特异性是由糖苷配基的芳香体系与W373堆积,以及与位于类似狭缝状糖苷配基结合位点中与W373相对的F193、F200和F461边缘的相互作用所决定的。最近有人推测,这些糖苷配基-活性位点相互作用决定了Zm-p60.1的一种同工酶ZM-Glu1的无活性酶-底物复合物中的底物特异性。在这里,我们通过对F193I/Y/W突变体的动力学分析来检验这一假设。所有突变体的K(m)降低证实了F193参与决定酶对具有芳香糖苷配基的底物的亲和力。出乎意料的是,与野生型相比,F193I突变体的k(cat)降低了30倍。动力学分析和计算机建模表明,F193-糖苷配基-W373相互作用不仅如先前假设的那样有助于糖苷配基识别,还通过将糖苷键固定在有利于催化对E186和E401攻击的方向来共同决定催化速率。最初根据它们在结构中的位置确定的催化对,通过对E186D/Q和E401D/Q突变体的动力学分析得到了证实。出乎意料的是,E401D以及C205S和C211S突变极大地损害了具有催化活性的同型二聚体的组装,这表明活性位点结构与二聚体形成之间存在新的联系。