Cotton F A, Hazen E E, Legg M J
Proc Natl Acad Sci U S A. 1979 Jun;76(6):2551-5. doi: 10.1073/pnas.76.6.2551.
The structure of the staphylococcal nuclease (EC 3.1.4.7)-thymidine 3',5'-bisphosphate-Ca(2+) (enzyme-inhibitor) complex has been extended to 1.5-A resolution by using much additional data and a phase refinement scheme based on an electron-density map modification procedure. By correlating this structure with the known properties of the enzyme, a mechanism of action is proposed that involves nucleophilic attack on phosphorus by a water molecule, which is bound to Glu-43, in line with the 5'-CH(2)O(H) leaving group. The carboxylate of Glu-43 promotes this attack by acting as a general base for the abstraction of a proton from the attacking water molecule. Nucleophilic attack is further facilitated by polarization of the phosphodiester by an ionic interaction between a Ca(2+) ion and a phosphate oxygen atom and by four hydrogen bonds to phosphate oxygen atoms from guanidinium ions of Arg-35 and Arg-87. These interactions may also catalyze the reaction by lowering the energy of a trigonal bipyramidal transition state. The hydrolysis of nucleic acid substrate proceeds by cleavage of the 5'-P-O bond to yield a free 5'-hydroxyl group and a terminal, 3'-phosphate monoester group. In the inhibitor complex the only general acid group found in a position to donate a proton to the leaving 5'-oxygen is the guanidinium ion of Arg-87. Alternative proton donors, presently lacking direct structural support, could be the phenolic hydroxyl group of Tyr-113 or a water molecule. The precision and rigidity of the location of the reactants at the active site and the probable dual binding and catalytic roles of the guanidinium ions of Arg-35 and Arg-87 are especially noteworthy.
通过使用大量额外数据以及基于电子密度图修正程序的相位细化方案,葡萄球菌核酸酶(EC 3.1.4.7)-胸苷3',5'-二磷酸-Ca(2+)(酶-抑制剂)复合物的结构已扩展至1.5埃分辨率。通过将此结构与该酶的已知特性相关联,提出了一种作用机制,该机制涉及与Glu-43结合的水分子对磷进行亲核攻击,这与5'-CH(2)O(H)离去基团一致。Glu-43的羧酸盐通过作为从攻击水分子中夺取质子的通用碱来促进这种攻击。Ca(2+)离子与磷酸氧原子之间的离子相互作用以及来自Arg-35和Arg-87的胍离子与磷酸氧原子形成的四个氢键使磷酸二酯极化,从而进一步促进亲核攻击。这些相互作用还可能通过降低三角双锥过渡态的能量来催化反应。核酸底物的水解通过5'-P-O键的断裂进行,产生一个游离的5'-羟基和一个末端的3'-磷酸单酯基团。在抑制剂复合物中,唯一处于能够向离去的5'-氧提供质子位置的通用酸基团是Arg-87的胍离子。目前缺乏直接结构支持的替代质子供体可能是Tyr-113的酚羟基或一个水分子。反应物在活性位点的定位精度和刚性以及Arg-35和Arg-87的胍离子可能的双重结合和催化作用尤其值得注意。