Tomasselli A G, Hui J, Fisher J, Zürcher-Neely H, Reardon I M, Oriaku E, Kézdy F J, Heinrikson R L
Biopolymer Chemistry Unit, Upjohn Company, Kalamazoo, Michigan 49001.
J Biol Chem. 1989 Jun 15;264(17):10041-7.
The porcine pancreatic phospholipase A2-catalyzed hydrolysis of the water-soluble chromogenic substrate 4-nitro-3-octanoyloxybenzoate shows an initial latency phase similar to the one observed in the hydrolysis of aggregated phospholipids by the same enzyme. We report here that during the latency phase the enzyme undergoes a slow, autocatalytic, substrate-level acylation whereby in a few of the catalytic events the scissile octanoyl group of the substrate, normally transferred to water, is transferred to the epsilon-amino group of lysine 56. The N epsilon 56-octanoylphospholipase shows a strong tendency to dimerize in solution and thus may be separated from the monomeric native enzyme by gel filtration. Octanoylation of Lys-56 activates the enzyme some 180-fold toward 4-nitro-3-octanoyloxybenzoate and more than 100-fold toward monolayers of 1,2-didecanoyl-sn-glycero-3-phosphocholine. Acylation also attends the enzymatic hydrolysis of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine with the incorporation of 1 eq of palmitate. Kinetic analysis of the early phase of reaction with 4-nitro-3-octanoyloxybenzoate shows that in this initial step the rate of activation is first order with respect to enzyme and substrate. A much more rapid, autocatalytic activation occurs in the later phases of the reaction where the activation of the enzyme is catalyzed by the activated enzyme itself. These findings with porcine pancreatic phospholipase A2, together with those relative to a snake venom enzyme monomer (Cho, W., Tomasselli, A. G., Heinrikson, R. L., and Kézdy, F. J. (1988) J. Biol. Chem. 263, 11237-11241), strongly support the proposal that interfacial activation of monomeric phospholipases is due to substrate-level autoacylation resulting in fully potentiated dimeric enzymes.
猪胰磷脂酶A2催化水溶性显色底物4-硝基-3-辛酰氧基苯甲酸酯的水解反应,呈现出一个初始延迟期,这与该酶催化聚集磷脂水解时观察到的延迟期相似。我们在此报告,在延迟期内,该酶经历缓慢的、自催化的底物水平酰化过程,即在少数催化事件中,底物通常转移到水中的可裂解辛酰基转移到了赖氨酸56的ε-氨基上。Nε56-辛酰基磷脂酶在溶液中强烈倾向于二聚化,因此可通过凝胶过滤与单体天然酶分离。赖氨酸56的辛酰化使该酶对4-硝基-3-辛酰氧基苯甲酸酯的活性提高约180倍,对1,2-二癸酰-sn-甘油-3-磷酸胆碱单层膜的活性提高超过100倍。酰化作用也伴随着1,2-二棕榈酰-sn-甘油-3-磷酸胆碱的酶促水解,并掺入1当量的棕榈酸。对与4-硝基-3-辛酰氧基苯甲酸酯反应早期阶段的动力学分析表明,在这个初始步骤中,活化速率对酶和底物均为一级反应。在反应后期发生更快的自催化活化,此时酶的活化由活化后的酶自身催化。猪胰磷脂酶A2的这些发现,连同与蛇毒酶单体相关的发现(赵,W.,托马塞利,A. G.,海因里克森,R. L.,和凯兹迪,F. J.(1988年)《生物化学杂志》263,11237 - 11241),有力地支持了这样的提议,即单体磷脂酶的界面活化是由于底物水平的自酰化导致完全增强的二聚体酶。