Thomas B, Wang Y, Stein R L
Department of Chemical Enzymology, DuPont Pharmaceuticals Company, Wilmington, Delaware 19880, USA.
Biochemistry. 2001 Dec 25;40(51):15811-23. doi: 10.1021/bi011368r.
High molecular weight penicillin-binding proteins (PBPs) are bifunctional enzymes that build bacterial cell walls from the glycopeptide lipid II [GlcNAc-MurNAc(L-Ala-gamma-D-Glu-L-Lys-D-Ala-D-Ala)-pyrophosphate-undecaprenol] by a process involving disaccharide polymerization and peptide cross-linking. The latter reaction involves acyl-transfer chemistry in which the penultimate (D)Ala first acylates the active-site serine, with release of the terminal (D)Ala, and is then transferred to the epsilon-amine of a Lys on a neighboring pentapeptide chain. These enzymes also catalyze hydrolysis of specific thioester substrates and acylation by beta-lactam antibiotics. In this paper, we explore these latter two reactions and report mechanistic experiments on the reaction of Streptococcus pneumoniae PBP 2x with N-benzoyl-(D)Ala-thioacetic acid [Bz-(D)Ala-(S)Gly] and penicillin G. For these experiments, we used PBP 2x, a soluble form of PBP 2x in which the transmembrane domain was deleted. The following results are significant: (1) pH dependencies for acylation of PBP 2x by penicillin G and Bz-(D)Ala-(S)Gly are identical, suggesting that the same ionizable residues are involved in both reactions and that these residues play the same catalytic role in the two processes. On the basis of these results, we propose a mechanistic model that is also consistent with recently published structural data [Gordon, E., et al. (2000) J. Mol. Biol. 299, 477-485]. (2) Pre-steady-state experiments for the PBP 2x-catalyzed hydrolysis of Bz-(D)Ala-(S)Gly at pH 6.5 indicate that k(c) is principally rate-limited by acylation with some contribution from deacylation. The contribution of these steps to rate limitation is pH-dependent, with acylation entirely rate-limiting at pH values less than 5.5 and deacylation principally rate-limiting above pH 8.5. (3) Results of solvent isotope effect and proton inventory experiments for acylation suggest a complex process that is at least partially rate-limited by chemistry with some involvement of changes in solvation and/or enzyme conformation. (4) Analysis of activation parameters suggests that during the acylation of PBP 2x by penicillin G the inherent chemical stability of penicillin's amide bond, as manifested in the enthalpy of activation, is offset by a favorable entropy term that reflects penicillin's rotationally constrained bicyclic system, which presumably allows a less energetically demanding entry into the transition state for acylation.
高分子量青霉素结合蛋白(PBPs)是双功能酶,可通过涉及二糖聚合和肽交联的过程,从糖肽脂质II [GlcNAc-MurNAc(L-Ala-γ-D-Glu-L-Lys-D-Ala-D-Ala)-焦磷酸-十一异戊烯醇]构建细菌细胞壁。后一反应涉及酰基转移化学,其中倒数第二个(D)Ala首先使活性位点丝氨酸酰化,释放末端(D)Ala,然后转移至相邻五肽链上Lys的ε-氨基。这些酶还催化特定硫酯底物的水解以及β-内酰胺抗生素的酰化反应。在本文中,我们探讨了后两个反应,并报告了肺炎链球菌PBP 2x与N-苯甲酰基-(D)Ala-硫代乙酸[Bz-(D)Ala-(S)Gly]和青霉素G反应的机理实验。对于这些实验,我们使用了PBP 2x,即一种缺失跨膜结构域的可溶性PBP 2x形式。以下结果具有重要意义:(1)青霉素G和Bz-(D)Ala-(S)Gly对PBP 2x的酰化反应的pH依赖性相同,这表明两个反应涉及相同的可电离残基,并且这些残基在两个过程中发挥相同的催化作用。基于这些结果,我们提出了一个机理模型,该模型也与最近发表的结构数据一致[Gordon,E.等人(2000年)《分子生物学杂志》299,477 - 485]。(2)在pH 6.5下对PBP 2x催化的Bz-(D)Ala-(S)Gly水解的预稳态实验表明,k(c)主要受酰化作用限速,脱酰化也有一定贡献。这些步骤对限速的贡献取决于pH,在pH值小于5.5时酰化完全限速,在pH值高于8.5时脱酰化主要限速。(3)酰化反应的溶剂同位素效应和质子累积实验结果表明这是一个复杂的过程,至少部分受化学作用限速,同时溶剂化和/或酶构象的变化也有一定参与。(4)活化参数分析表明,在青霉素G对PBP 2x的酰化过程中,青霉素酰胺键的固有化学稳定性(如活化焓所示)被一个有利的熵项抵消,该熵项反映了青霉素的旋转受限双环系统,这可能使得酰化进入过渡态所需的能量更低。