Huang L, Montoya A L, Nester E W
J Biol Chem. 1975 Oct 10;250(19):7675-81.
In Bacillus subtilis shikimate kinase enzyme activity can be demonstrated when a small polypeptide forms a trifunctional complex with the bifunctional enzyme 3-deoxy-D-arabinoheptulosonate-7-phosphate synthetase-chorismate mutase. The shikimate kinase polypeptide whoch carries the catalytic site has been purified to homogeneity by a five-step procedure. The skikimate kinase was determined to have a molecular weight of 10,000 by superfine Sephadex G-75 thin layer chromatography and by calculation of the minimum chemical molecular weight from its amino acid composition. This number corresponds closely to the molecular weight determined by the mobility of the protein following electrophoresis on polyacrylamide gels containing sodium dodecyl sulfate. The enzyme aggregates with itself forming larger molecular weight proteins. Thes aggregational pattersn depend on protein concentration and sulfhydryl bridges. The enzyme activity is completely inhibited by EDTA and the requirement for Mg2+ can be partially replaced by Mn2+, Ca2+, and Co2+. The inhibition of shikimate kinase activity by p-hydroxymercuribenzoate is reversed completely when the enzyme complex is treated with dithiothreitol, suggesting the sulfhydryl groups may be involved with the active site. The trifunctional complex is relatively unstable, and the nonidentical subunits dissociate readily. This dissociation results in a 99% loss in shikimate kinase activity and a 30% decrease in the chorismate mutase-DAHP synthetase activities. Shikimate kinase activity is subject to a variety of controls. It is inhibited by the allosteric effectors chorismate and prephenate, the products of the reaction, ADP, and shikimate 5-phosphate. The activity responds to changes in the energy charge of the cell. Because of the variety of controls exerted on this enzyme, this member of the regulatory complex may represent the key enzyme in the allosteric control of the synthesis of the common precursors of aromatic acid synthesis.
在枯草芽孢杆菌中,当一种小多肽与双功能酶3-脱氧-D-阿拉伯庚酮糖-7-磷酸合成酶-分支酸变位酶形成三功能复合物时,莽草酸激酶的酶活性就可以得到证明。携带催化位点的莽草酸激酶多肽已通过五步纯化程序纯化至同质。通过超细葡聚糖G-75薄层色谱法以及根据其氨基酸组成计算最小化学分子量,确定莽草酸激酶的分子量为10,000。这个数字与在含有十二烷基硫酸钠的聚丙烯酰胺凝胶上电泳后根据蛋白质迁移率确定的分子量非常接近。该酶自身聚集形成分子量更大的蛋白质。这些聚集模式取决于蛋白质浓度和巯基桥。EDTA可完全抑制该酶的活性,Mg2+的需求可部分被Mn2+、Ca2+和Co2+替代。当用二硫苏糖醇处理酶复合物时,对羟基汞苯甲酸对莽草酸激酶活性的抑制作用可完全逆转,这表明巯基可能与活性位点有关。三功能复合物相对不稳定,不同的亚基很容易解离。这种解离导致莽草酸激酶活性损失99%,分支酸变位酶-DAHP合成酶活性降低30%。莽草酸激酶活性受到多种调控。它受到变构效应物分支酸和预苯酸、反应产物ADP以及5-磷酸莽草酸的抑制。其活性对细胞能量电荷的变化有反应。由于对这种酶施加了多种调控,调节复合物的这个成员可能代表了芳香酸合成共同前体合成变构控制中的关键酶。